The DOI matches its Crossref record; 220 of the 227 references it cites were found in a registry or an index; 15 of the 385 sources its claims cite were checked for support.
Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease
Open accessAbstract
The most prevalent chronic neurodegenerative illness in the world is Alzheimer’s disease (AD). It results in mental symptoms including behavioral abnormalities and cognitive impairment, which have a substantial financial and psychological impact on the relatives of the patients. The review discusses various pathophysiological mechanisms contributing to AD, including amyloid beta, tau protein, inflammation, and other factors, while emphasizing the need for effective disease-modifying therapeutics that alter disease progression rather than merely alleviating symptoms. This review mainly covers medications that are now being studied in clinical trials or recently approved by the FDA that fall under the disease-modifying treatment (DMT) category, which alters the progression of the disease by targeting underlying biological mechanisms rather than merely alleviating symptoms. DMTs focus on improving patient outcomes by slowing cognitive decline, enhancing neuroprotection, and supporting neurogenesis. Additionally, the review covers amyloid-targeting therapies, tau-targeting therapies, neuroprotective therapies, and others. This evaluation specifically looked at studies on FDA-approved novel DMTs in Phase II or III development that were carried out between 2021 and 2024. A thorough review of the US government database identified clinical trials of biologics and small molecule drugs for 14 agents in Phase I, 34 in Phase II, and 11 in Phase III that might be completed by 2028.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review summarizes Alzheimer’s disease pathophysiology and disease-modifying therapies, focusing on amyloid-, tau-, and neuroprotective strategies and recent FDA-approved or clinical-stage agents. It reports the 2024 AD drug development pipeline and highlights challenges including disease heterogeneity, blood–brain barrier penetration, biomarkers, and regulation.
Key findings
- The 2024 AD drug development pipeline included 164 trials, of which 127 were testing possible treatments or medicines; 41% targeted disease-modifying small molecules and 34% targeted disease-modifying biological agents, with the remaining trials focused on cognitive or neuropsychiatric symptoms.
- A review of the US government clinical trials database identified disease-modifying biologic and small-molecule trials for 14 agents in Phase I, 34 in Phase II, and 11 in Phase III that might be completed by 2028. Section 3.2 separately reports Phase I: 26 trials assessing 25 agents; Phase II: 90 studies of 81 medicines; Phase III: 48 trials testing 32 medications.
- Lecanemab reduced total brain amyloid plaque burden versus placebo at 79 weeks, with a mean difference of −73.5 centiloids and −0.31 standardized uptake value ratio (SUVR) units; the treatment effect was dose- and exposure-dependent, and the study suggested a 20%–40% risk reduction in clinical symptom progression.
- Aducanumab showed inconsistent results in the Phase III EMERGE and ENGAGE trials; FDA expedited approval was based on the EMERGE trial’s amyloid reduction. Both aducanumab and lecanemab slowed cognitive decline and reduced amyloid plaques but were more likely to cause amyloid-related imaging abnormalities (ARIAs), especially ARIA-E with aducanumab.
Methods
- Narrative review of AD pathophysiology, disease-modifying therapeutic mechanisms, current treatments, clinical trials, and emerging therapies; no formal systematic review or meta-analysis is described.
- The evaluation focused on studies of FDA-approved novel DMTs in Phase II or III development conducted between 2021 and 2024, and a thorough review of the US government clinical trials database identified disease-modifying biologic and small-molecule agents across phases.
- Findings are presented in narrative text and in Tables 2 and 3, which summarize clinical trials of disease-modifying biological agents and disease-modifying small-molecule drugs, respectively.
Limitations
- Stated challenges include disease heterogeneity complicating diagnosis, treatment, and trial design; blood–brain barrier penetration limits drug delivery, with the text noting impermeability to 98% of small molecules and around 100% of large molecules in relevant quantities; lack of validated diagnostic biomarkers and low clinical diagnostic specificity can require larger trials and inclusion of “slow/no progressors”; regulatory obstacles include inconsistent review levels and restrictions on biobanking and repository research.
- The conclusion states that only a small percentage of AD patients benefit from the two currently approved DMTs, that more research comparing DMTs with diverse therapeutic targets and across patient groups is needed, and that natural compounds require clinical trials to verify safety and efficacy.
- Evident from the text: this is a narrative review without a described systematic search strategy, inclusion/exclusion criteria, or risk-of-bias assessment; trial-count figures in the abstract and Section 3.2 differ, which may reflect different database snapshots or definitions.
Model-written summary. Check it against the paper before relying on it.
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Figures
![Figure 1 Pathophysiology of the AD hypothesis [8]. Reproduced with permission from Jifa Zhang, Yinglu Zhang, Jiaxing Wang, Yilin Xia, Jiaxian Zhang, and Lei Chen, in the journal Signal Transduction and Targeted Therapy; published by Springer Nature, 2024, licensed under CC BY 4.0.](/paper-figures/96e0143d1ef448fe8ee19762f0705b3a/recent-advances-in-therapeutics-for-the-treatment-of-alzheimers-disease-figure-1.jpg)
Verification
Claims the paper makes
137 Not checked yet · 7 Own interpretation · 5 Partly supported · 2 Supported so far · 1 Supported · 1 Own result · 1 No basis given · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The AD risk is greatly increased by the APOE ε4 allele.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Supportedcites [42] Narayan, 2020, PICALM Rescues Endocytic Defects Caused by the Alzheimer’s Disease Risk Factor APOE4, Cell Rep. source
The Introduction describes APOE ε4 as a major genetic risk factor for late-onset Alzheimer’s disease and says that carriers of one APOE4 allele are 3–4 times more likely to develop AD than noncarriers. This supports the claim that the allele greatly increases AD risk. (LLM, conf=0.94)
- Supportedcites [43] Fu, 2023, The role of genetic risk factors of Alzheimer’s disease in synaptic dysfunction, Semin. Cell Dev. Biol. source
Section 1.2, “Astrocytic genes” (page not supplied), calls APOE the most significant genetic risk factor for AD and says APOE ε4 carriers are more susceptible to AD. This supports the claim that the allele greatly increases AD risk. (LLM, conf=0.92)
- Partly supportedcites [44] Flores-Cordero, J.A., Pérez-Pérez, A., Jiménez-Cortegana, C., Alba, G., Flores-Barragán, A., and Sánchez-Margalet, V. (2022). Obesity as a Risk Factor for Dementia and Alzheimer’s Disease: The Role of Leptin. Int. J. Mol. Sci., 23. sourceExperimental — accuracy not yet measured
Section 6 identifies APOE4 as the best-known genetic variant associated with increased Alzheimer’s disease risk. It does not describe the size of that increase, so it does not establish the claim’s “greatly” qualifier. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“After 79 weeks, lecanemab was found to have a lower total brain amyloid plaque burden than a placebo (Study 201).”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [187] Mukhopadhyay, 2021, A Primer on the Evolution of Aducanumab: The First Antibody Approved for Treatment of Alzheimer’s Disease, J. Alzheimer’s Dis. source
- Supportedcites [188] Swanson, 2021, A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer’s disease with lecanemab, an anti-Aβ protofibril antibody, Alzheimer’s Res. Ther. source
The Results > Efficacy section reports lower brain amyloid PET values with lecanemab than with placebo at 18 months, approximately 79 weeks. This finding comes from the optional PET substudy; the paper reports amyloid PET measurements rather than a direct count of plaques. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“They may also be the cause of neuroinflammation by activating microglia and producing inflammatory cytokines.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Partly supportedcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. sourceExperimental — accuracy not yet measured
Section 5.1.2 links PSEN1 and PSEN2 mutations to Aβ accumulation, and Section 3.1 says Aβ plaques can stimulate microglia. The review does not state that these mutations cause neuroinflammation through microglial activation and inflammatory-cytokine production; that proposed mechanism goes beyond what the cited passages establish. Page numbers are unavailable in our copy. (LLM, conf=0.82)
- Could not verifycites [213] AlMansoori, M.E., Jemimah, S., Abuhantash, F., and AlShehhi, A. (2024). Predicting early Alzheimer’s with blood biomarkers and clinical features. Sci. Rep., 14. sourceExperimental — accuracy not yet measured
The Results section on SHAP-prioritized genetic features discusses other genes, including NMNAT1, ABHD6 and SLC2A4RG, but does not address PSEN1 or PSEN2 mutations causing neuroinflammation. Searches for PSEN1/PSEN2, microglial activation and inflammatory cytokines found no passage in our copy supporting the proposed mechanism. (LLM, conf=0.76)
- Not checked yetcites [214] Kesu, S.M.R., Sinha, N., and Ramasangu, H. (2024). Cellular Automata Framework for Dementia Classification Using Explainable AI. Eng. Proc., 68. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the healthy aging human brain, amyloid-β plaques have the ability to cause persistent inflammation in microglia, which are the brain’s resident immune cells.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Partly supportedcites [202] Yang, 2020, TREM2 ectodomain and its soluble form in Alzheimer’s disease, J. Neuroinflamm. sourceExperimental — accuracy not yet measured
The “Microglial activation and innate immune system” section describes chronic neuroinflammation in Alzheimer’s disease and reports that some studies find protein overload induces an inflammatory response. It does not establish persistent plaque-caused microglial inflammation in the healthy aging human brain; it says the relationship between protein deposition and inflammation is conflicting. (LLM, conf=0.87)
- Partly supportedcites [203] Huang, W., Huang, J., Huang, N., and Luo, Y. (2023). The role of TREM2 in Alzheimer’s disease: From the perspective of Tau. Front. Cell Dev. Biol., 11. sourceExperimental — accuracy not yet measured
Section 2 (page unavailable) identifies TREM2 as a microglial receptor for Aβ, and Section 3 links microglial regulation to neuroinflammation in Alzheimer’s disease. Neither passage says that amyloid-β plaques cause persistent microglial inflammation in healthy aging human brains; that setting, duration, and causal claim are unsupported. (LLM, conf=0.78)
- Partly supportedcites [204] Shi, Q., Gutierrez, R.A., and Bhat, M.A. (2024). Microglia, Trem2, and Neurodegeneration. Neuroscientist, 10738584241254118. sourceExperimental — accuracy not yet measured
The Figure 3 caption in “Mechanisms Linking TREM2 Variants to AD” says that accumulating amyloid-β plaques during Alzheimer disease progression can lead to excessive microglial activation and release of proinflammatory factors. “Microglia—Specialized Neuroimmune Cells” identifies microglia as the brain’s resident immune cells and links chronic inflammation to neurodegenerative disease. The paper does not establish this plaque-driven persistent inflammation specifically in the healthy aging human brain. (LLM, conf=0.87)
- Partly supportedcites [205] Pocock, 2024, Microglia and TREM2, Neuropharmacology sourceExperimental — accuracy not yet measured
The paper’s discussion of TREM2 and NLRP3 inflammasome activation says that exposure to amyloid-β can activate an inflammasome and release proinflammatory cytokines. It does not establish that amyloid-β plaques cause persistent microglial inflammation in healthy aging human brains. The Conclusions identify microglia as immune cells of the brain. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“One example of this is rasagiline, which combines neuroprotective and amyloid-processing properties with monoamine oxidase B inhibition [217].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Supportedcites [217] Cummings, 2019, Treatment Combinations for Alzheimer’s Disease: Current and Future Pharmacotherapy Options, J. Alzheimer’s Dis. source
The TYPES OF COMBINATION THERAPIES section explicitly identifies rasagiline as an MAO B inhibitor with neuroprotective effects and effects on amyloid processing. The Phase II add-on and combination treatments section further describes its neuroprotective action and modulation of AβPP cleavage. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“As an illustration, ongoing clinical trials combine novel DMT- or symptomatic-based treatments with standard-of-care medications (such as memantine or cholinesterase inhibitors) [217,218,219].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Supportedcites [217] Cummings, 2019, Treatment Combinations for Alzheimer’s Disease: Current and Future Pharmacotherapy Options, J. Alzheimer’s Dis. source
The Types of Combination Therapies section states that current add-on trials generally pair a new DMT or symptomatic agent with a standard-of-care cholinesterase inhibitor or memantine. The Conclusions section likewise describes ongoing trials investigating these agents as add-ons to background standard-of-care therapy. (LLM, conf=0.94)
- Not checked yetcites [218] Horani, 2015, Anticancer Prodrugs—Three Decades of Design, World J. Pharm. Pharm. Sci.
- Partly supportedcites [219] Dudchenko, 2024, Combination Drug Therapy for the Management of Alzheimer’s Disease, Russ. J. Geriatr. Med. sourceExperimental — accuracy not yet measured
The ‘Treatment of Alzheimer’s disease’ section (page not specified) describes clinical research on new disease-targeting drugs and identifies memantine and cholinesterase inhibitors as established treatments. The ‘Combination therapy with memantine and cholinesterase inhibitors’ section describes trials combining existing drugs, but does not say that ongoing trials combine novel disease-modifying or symptomatic treatments with them. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A thorough review of the US government database identified clinical trials of biologics and small molecule drugs for 14 agents in Phase I, 34 in Phase II, and 11 in Phase III that might be completed by 2028.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > Abstract
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“The hydrophobic C-terminus of Aβ42 facilitates its aggregation and the formation of senile plaques.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Mutations in presenilin-1 (PS1) can promote Aβ accumulation through increased production and impaired autophagy functions.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“This hypothesis suggests that a reduction in the synthesis and release of ACh impairs its physiological functions, which are critical for learning, memory, and other cognitive processes.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 57
- Probably not a substantial claim. 38
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Similar to other BACE-1 inhibitors, CNP520 (umibecestat (labeled as 11, Figure 5)) has been shown to reduce the burden of amyloid-beta plaques in preclinical animals; it is presently undergoing testing phases [157,166,167].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.1. Oral Immunotherapies or Small Molecules Containing DMTs
What the sources say
- Not checked yetcites [157] Piton, 2018, Alzheimer’s Disease: Advances in Drug Development, J. Alzheimer’s Dis. source
- Not checked yetcites [166] Machauer, 2021, Discovery of Umibecestat (CNP520): A Potent, Selective, and Efficacious β-Secretase (BACE1) Inhibitor for the Prevention of Alzheimer’s Disease, J. Med. Chem. source
- Supportedcites [167] Neumann, 2018, The BACE -1 inhibitor CNP 520 for prevention trials in Alzheimer’s disease, EMBO Mol. Med. source
The section on APP-transgenic mice reports that CNP520 reduced cortical amyloid-beta plaque area compared with vehicle treatment. The Introduction states that CNP520 was being tested in the Generation Program; the indexed passages provide no page numbers. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It becomes a comprehensive care paradigm when pharmacological therapies are combined with lifestyle changes, cognitive training, and psychosocial support.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [220] Strac, 2021, Personalizing the Care and Treatment of Alzheimer’s Disease: An Overview, Pharmacogenom. Pers. Med.
- Partly supportedcites [221] Passeri, E., Elkhoury, K., Morsink, M., Broersen, K., Linder, M., Tamayol, A., Malaplate-Armand, C., Yen, F.T., and Arab-Tehrany, E. (2022). Alzheimer’s Disease: Treatment Strategies and Their Limitations. Int. J. Mol. Sci., 23. sourceExperimental — accuracy not yet measured
Section 4.2 discusses non-pharmacological therapies alongside drug treatments and describes multidomain interventions involving physical activity, cognitive training, and nutrition. The paper does not identify psychosocial support as part of that combination or describe the combination as a comprehensive care paradigm. Its discussion of social contact as a risk factor in Section 2.4 is not evidence for psychosocial support as a care component. (LLM, conf=0.85)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“AD is a progressive neurodegenerative disorder and the leading cause of dementia among older adults, characterized by a gradual decline in cognitive function, memory loss, and behavioral changes, ultimately leading to complete dependence on caregivers [7].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [7] Chen, Z.-R., Huang, J.-B., Yang, S.-L., and Hong, F.-F. (2022). Role of Cholinergic Signaling in Alzheimer’s Disease. Molecules, 27. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The tau protein hypothesis focuses on the hyperphosphorylation of tau protein leading to its detachment from microtubules, resulting in the formation of neurofibrillary tangles (NFTs) which are a hallmark of AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The glutamatergic hypothesis posits that dysregulation of glutamate, the main excitatory neurotransmitter in the central nervous system, plays a critical role in the pathogenesis of AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [10] Conway, 2020, Alzheimer’s disease: Targeting the glutamatergic system, Biogerontology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“However, the relationship between FAD mutations and Aβ levels is complex, and the plaque formation in sporadic AD is influenced by a dynamic imbalance between Aβ production and clearance mechanisms [11,12].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AChE inhibitors, such as donepezil, rivastigmine, and galantamine, have been developed as treatments based on this hypothesis, although their efficacy is limited and they do not halt disease progression [7,9].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The inflammatory hypothesis suggests that chronic neuroinflammation plays a significant role in the pathogenesis of AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The microbiota–gut–brain axis hypothesis suggests a bidirectional communication system between the gut and the brain, involving metabolic, endocrine, neural, and immune pathways.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [17] Wiatrak, B., Balon, K., Jawień, P., Bednarz, D., Jęśkowiak, I., and Szeląg, A. (2022). The Role of the Microbiota-Gut-Brain Axis in the Development of Alzheimer’s Disease. Int. J. Mol. Sci., 23. source
- Not checked yetcites [18] Doifode, 2020, The impact of the microbiota-gut-brain axis on Alzheimer’s disease pathophysiology, Pharmacol. Res. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The cholinergic hypothesis posits that the degeneration of cholinergic neurons, particularly in the basal forebrain, is a central feature of AD and is closely linked to cognitive decline.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The pathophysiological process of AD is multifaceted, involving several key hypotheses: the cholinergic, glutamatergic, amyloid, tau protein, inflammatory, microbiota–gut–brain axis, oxidative stress, metal ion, and abnormal autophagy hypotheses, as shown in the summary of AD pathophysiology in Figure 1 [8].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [8] Zhang, 2024, Recent advances in Alzheimer’s disease: Mechanisms, clinical trials and new drug development strategies, Signal Transduct. Target. Ther. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“This hyperphosphorylation promotes tau aggregation into paired helical filaments and NFTs, which correlate strongly with clinical symptoms of AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Dysbiosis, or disruption of the microbiota’s composition and functionality, can occur due to factors such as dietary changes, antibiotic use, psychosocial stress, or immune irregularities, leading to a compromised intestinal epithelial barrier.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [17] Wiatrak, B., Balon, K., Jawień, P., Bednarz, D., Jęśkowiak, I., and Szeląg, A. (2022). The Role of the Microbiota-Gut-Brain Axis in the Development of Alzheimer’s Disease. Int. J. Mol. Sci., 23. source
- Not checked yetcites [18] Doifode, 2020, The impact of the microbiota-gut-brain axis on Alzheimer’s disease pathophysiology, Pharmacol. Res. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Aβ originates from the processing of the amyloid precursor protein (APP) through sequential cleavage by β-secretase and γ-secretase, resulting in various lengths of Aβ fragments, with Aβ40 and Aβ42 being predominant.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The amyloid hypothesis emphasizes that the accumulation of Aβ plaques in the brain is a central event in the pathogenesis of AD, leading to neurodegeneration and cognitive decline.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The decline in choline acetyltransferase (ChAT) activity, combined with the detrimental effects of amyloid beta (Aβ) on cholinergic signaling, leads to decreased ACh levels. Consequently, this reduction contributes to the cognitive deficits observed in AD patients.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Additionally, tau pathology is associated with neuroinflammation, as pro-inflammatory cytokines can increase tau transcription and activate inflammatory pathways that further exacerbate tau-related neurodegeneration [13,14].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Key contributors to oxidative stress in AD include mitochondrial dysfunction, which reduces the activities of essential enzymes and disrupts mitochondrial dynamics.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [19] Jurcau, 2020, Oxidative Stress in the Pathogenesis of Alzheimer’s Disease and Cerebrovascular Disease with Therapeutic Implications, CNS Neurol. Disord.—Drug Targets
- Not checked yetcites [20] Bai, 2022, Oxidative stress: The core pathogenesis and mechanism of Alzheimer’s disease, Ageing Res. Rev. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, exposure to air pollution may worsen neuroinflammation and cognitive decline [49,50].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Not checked yetcites [49] Attademo, 2020, Air Pollution as Risk Factor for Mental Disorders: In Search for a Possible Link with Alzheimer’s Disease and Schizophrenia, J. Alzheimer’s Dis. source
- Not checked yetcites [50] He, 2022, Impact of air pollution exposure on the risk of Alzheimer’s disease in China: A community-based cohort study, Environ. Res. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, sedentary lifestyles and bad dietary habits, such as consuming large amounts of carbs and saturated fats, have been connected to an increased risk [54,55,56,57].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Not checked yetcites [54] Gentreau, 2020, Refined carbohydrate-rich diet is associated with long-term risk of dementia and Alzheimer’s disease in apolipoprotein E ε4 allele carriers, Alzheimer’s Dement. source
- Not checked yetcites [55] Frausto, D.M., Forsyth, C.B., Keshavarzian, A., and Voigt, R.M. (2021). Dietary Regulation of Gut-Brain Axis in Alzheimer’s Disease: Importance of Microbiota Metabolites. Front. Neurosci., 15. source
- Not checked yetcites [56] Ellouze, I., Sheffler, J., Nagpal, R., and Arjmandi, B. (2023). Dietary Patterns and Alzheimer’s Disease: An Updated Review Linking Nutrition to Neuroscience. Nutrients, 15. source
- Not checked yetcites [57] Khemka, 2023, Role of diet and exercise in aging, Alzheimer’s disease, and other chronic diseases, Ageing Res. Rev. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“AD is categorized into three stages: mild, moderate, and severe [24,25,26,27,28].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [24] Liew, 2021, Neuropsychiatric symptoms in early stage of Alzheimer’s and non-Alzheimer’s dementia, and the risk of progression to severe dementia, Age Ageing source
- Not checked yetcites [25] Cummings, 2021, The Role of Neuropsychiatric Symptoms in Research Diagnostic Criteria for Neurodegenerative Diseases, Am. J. Geriatr. Psychiatry source
- Not checked yetcites [26] Wiels, W.A., Wittens, M.M.J., Zeeuws, D., Baeken, C., and Engelborghs, S. (2021). Neuropsychiatric Symptoms in Mild Cognitive Impairment and Dementia Due to AD: Relation with Disease Stage and Cognitive Deficits. Front. Psychiatry, 12. source
- Not checked yetcites [27] Devanand, 2022, Associations Between Neuropsychiatric Symptoms and Neuropathological Diagnoses of Alzheimer Disease and Related Dementias, JAMA Psychiatry source
- Not checked yetcites [28] Abbate, 2019, Signs and symptoms method in neuropsychology: A preliminary investigation of a standardized clinical interview for assessment of cognitive decline in dementia, Appl. Neuropsychol. Adult source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Dementia risk has been shown to rise with toxic exposure to heavy metals as lead, mercury, and aluminum [45,46,47,48].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Not checked yetcites [45] Antoniadou, 2020, Toxic Environmental Factors and their Association with the Development of Dementia: A Mini Review on Heavy Metals and Ambient Particulate Matter, Mater. Socio Medica source
- Not checked yetcites [46] Amirrad, 2017, Alzheimer’s Disease: Dawn of a New Era?, J. Pharm. Pharm. Sci. source
- Not checked yetcites [47] Islam, F., Shohag, S., Akhter, S., Islam, M.R., Sultana, S., Mitra, S., Chandran, D., Khandaker, M.U., Ashraf, G.M., and Idris, A.M. (2022). Exposure of metal toxicity in Alzheimer’s disease: An extensive review. Front. Pharmacol., 13. source
- Not checked yetcites [48] Rehman, Q., Rehman, K., and Akash, M.S.H. (2021). Heavy Metals and Neurological Disorders: From Exposure to Preventive Interventions. Emerging Contaminants and Associated Treatment Technologies, Springer International Publishing. source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The abnormal autophagy hypothesis suggests that disruptions in the autophagy process are closely linked to the pathogenesis of AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [22] Curtis, 2019, Autophagy Dysfunction in Alzheimer’s Disease: Mechanistic Insights and New Therapeutic Opportunities, Biol. Psychiatry
- Not checked yetcites [23] Hamano, 2018, The Implications of Autophagy in Alzheimer’s Disease, Curr. Alzheimer Res. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The most well-known genes are those for presenilin-1 (PSEN1), presenilin-2 (PSEN2), and amyloid precursor protein (APP). Mutations in these genes can cause early-onset familial AD, which often manifests before the age of 65 [38].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Not checked yetcites [38] Prajapati, V., Shinde, S., Shrivastav, P., and Prajapati, B.G. (2024). New biologicals and biomaterials in the therapy of Alzheimer’s disease. Alzheimer’s Disease and Advanced Drug Delivery Strategies, Academic Press. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The two main gene categories associated with AD are deterministic and risk-factor genes [29,37].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“One of the main variables that causes AD is genetics. Certain genes that are inherited have been connected to the condition as risk factors.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AD risk factors include obesity, diabetes, high blood pressure, and high cholesterol [51,52,53].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Not checked yetcites [51] Yang, 2022, Association of Healthy Lifestyles with Risk of Alzheimer Disease and Related Dementias in Low-Income Black and White Americans, Neurology source
- Not checked yetcites [52] Heneghan, 2023, Modifiable Lifestyle Activities Affect Cognition in Cognitively Healthy Middle-Aged Individuals at Risk for Late-Life Alzheimer’s Disease, J. Alzheimer’s Dis. source
- Not checked yetcites [53] Shafighi, K., Villeneuve, S., Neto, P.R., Badhwar, A., Poirier, J., Sharma, V., Medina, Y.I., Silveira, P.P., Dube, L., and Glahn, D. (2023). Social isolation is linked to classical risk factors of Alzheimer’s disease-related dementias. PLoS ONE, 18. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The most common symptoms of AD are short-term memory loss, which is followed by a progressive impairment in both implicit and explicit memory. Those who have the condition also exhibit neuropsychiatric symptoms, and with time, they lose their ability to perform basic daily duties [24,25,26,27,28].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [24] Liew, 2021, Neuropsychiatric symptoms in early stage of Alzheimer’s and non-Alzheimer’s dementia, and the risk of progression to severe dementia, Age Ageing source
- Not checked yetcites [25] Cummings, 2021, The Role of Neuropsychiatric Symptoms in Research Diagnostic Criteria for Neurodegenerative Diseases, Am. J. Geriatr. Psychiatry source
- Not checked yetcites [26] Wiels, W.A., Wittens, M.M.J., Zeeuws, D., Baeken, C., and Engelborghs, S. (2021). Neuropsychiatric Symptoms in Mild Cognitive Impairment and Dementia Due to AD: Relation with Disease Stage and Cognitive Deficits. Front. Psychiatry, 12. source
- Not checked yetcites [27] Devanand, 2022, Associations Between Neuropsychiatric Symptoms and Neuropathological Diagnoses of Alzheimer Disease and Related Dementias, JAMA Psychiatry source
- Not checked yetcites [28] Abbate, 2019, Signs and symptoms method in neuropsychology: A preliminary investigation of a standardized clinical interview for assessment of cognitive decline in dementia, Appl. Neuropsychol. Adult source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The emotional toll is high, causing worry, despair, and exhaustion in those who provide care [35,36].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [35] Vu, 2022, Impact of Alzheimer’s Disease on Caregivers in the United States, Health Psychol. Res. source
- Not checked yetcites [36] Kerwin, 2022, Alzheimer’s disease diagnosis and management: Perspectives from around the world, Alzheimer’s Dement. Diagn. Assess. Dis. Monit.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This hypothesis suggests that metal dyshomeostasis can lead to oxidative stress, which is linked to various pathological events in AD, such as amyloidosis and tauopathy.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [21] Chen, L.-L., Fan, Y.-G., Zhao, L.-X., Zhang, Q., and Wang, Z.-Y. (2022). The metal ion hypothesis of Alzheimer’s disease and the anti-neuroinflammatory effect of metal chelators. Bioorganic Chem., 131. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Patients with AD and their families, as well as the healthcare system, bear a heavy burden. Families must deal with social, economic, and emotional difficulties as the illness worsens.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.1. Pathophysiological Mechanisms and Symptoms of AD
What the sources say
- Not checked yetcites [35] Vu, 2022, Impact of Alzheimer’s Disease on Caregivers in the United States, Health Psychol. Res. source
- Not checked yetcites [36] Kerwin, 2022, Alzheimer’s disease diagnosis and management: Perspectives from around the world, Alzheimer’s Dement. Diagn. Assess. Dis. Monit.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Conversely, maintaining cardiovascular health, eating a balanced diet rich in antioxidants, and exercising frequently can all lower the incidence of AD [55,58].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 1. Introduction > 1.2. Causes and Factors of AD
What the sources say
- Not checked yetcites [55] Frausto, D.M., Forsyth, C.B., Keshavarzian, A., and Voigt, R.M. (2021). Dietary Regulation of Gut-Brain Axis in Alzheimer’s Disease: Importance of Microbiota Metabolites. Front. Neurosci., 15. source
- Not checked yetcites [58] Zhu, 2021, Dietary fatty acids and risk for Alzheimer’s disease, dementia, and mild cognitive impairment: A prospective cohort meta-analysis, Nutrition source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Amyloidogenic proteins (Aβ) and tau are two examples of heat-shock proteins (HSPs) that can both promote and inhibit the aggregation of misfolded proteins [37,101].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [101] Yang, 2019, Heat Shock Protein Inspired Nanochaperones Restore Amyloid-β Homeostasis for Preventative Therapy of Alzheimer’s Disease, Adv. Sci. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“According to the amyloid cascade hypothesis, tau protein tangles and neuroinflammation are brought on by Aβ aggregation, which in turn leads to neuronal death and cognitive decline [90,91,92].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
- Not checked yetcites [90] Rabinovici, 2023, Amyloid-Targeting Monoclonal Antibodies for Alzheimer Disease, JAMA source
- Not checked yetcites [91] Fedele, E. (2023). Anti-Amyloid Therapies for Alzheimer’s Disease and the Amyloid Cascade Hypothesis. Int. J. Mol. Sci., 24. source
- Not checked yetcites [92] Qiao, 2024, Comparative Efficacy and Safety of Monoclonal Antibodies for Cognitive Decline in Patients with Alzheimer’s Disease: A Systematic Review and Network Meta-Analysis, CNS Drugs source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Research has indicated that tau pathology has a stronger correlation with cognitive deficits than Aβ plaques, indicating that treatment benefits from targeting tau may outweigh those from concentrating only on amyloid clearance [94,95].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Inadequate operation of these systems can lead to oxidative stress, mitochondrial dysfunction, and various other pathological conditions that damage the body, cause neuronal death, and exacerbate dementia.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [101] Yang, 2019, Heat Shock Protein Inspired Nanochaperones Restore Amyloid-β Homeostasis for Preventative Therapy of Alzheimer’s Disease, Adv. Sci. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The second generation of AChEIs, donepezil (labeled as 1, Figure 5), is an indanonebenzylpiperidine derivative that is authorized for the treatment of AD in all phases. By reversibly binding to acetylcholinesterase, it slows the hydrolysis of acetylcholine, increasing the concentration of ACh at synapses [106,107].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [106] Cummings, 2021, New approaches to symptomatic treatments for Alzheimer’s disease, Mol. Neurodegener.
- Not checked yetcites [107] Eissa, 2022, Development of new Alzheimer’s disease drug candidates using donepezil as a key model, Arch. Der Pharm. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Several clinical investigations focusing on Aβ have produced contradictory findings, casting doubt on the veracity of the amyloid theory in general.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“DMTs are treatments that postpone, moderate, or even reverse the evolution of an illness by addressing its underlying cause.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics
What the sources say
- Not checked yetcites [6] Sperling, 2022, Meaningful benefits: A framework to assess disease-modifying therapies in preclinical and early Alzheimer’s disease, Alzheimer’s Res. Ther. source
- Not checked yetcites [59] Forester, 2020, Setbacks and Opportunities in Disease-Modifying Therapies in Alzheimer Disease, JAMA Psychiatry source
- Not checked yetcites [60] Morató, X., Pytel, V., Jofresa, S., Ruiz, A., and Boada, M. (2022). Symptomatic and Disease-Modifying Therapy Pipeline for Alzheimer’s Disease: Towards a Personalized Polypharmacology Patient-Centered Approach. Int. J. Mol. Sci., 23. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“It is a first-line medication for mild-to-severe AD that has a good efficacy and tolerability in improving behavioral symptoms, activities of daily living, and cognitive performance [110,112,113].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [110] Manickam, 2022, Galantamine tethered hydrogel as a novel therapeutic target for streptozotocin-induced Alzheimer’s disease in Wistar rats, Curr. Res. Pharmacol. Drug Discov. source
- Not checked yetcites [112] Kaur, 2022, Galantamine: A Review Update, J. Drug Deliv. Ther. source
- Not checked yetcites [113] Santos, 2020, Use of galantamine in the treatment of Alzheimer’s disease and strategies to optimize its biosynthesis using the in vitro culture technique, Plant Cell Tissue Organ Cult. (PCTOC) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“DMTs are intended to delay the progression of long-term conditions such as AD and ultimately improve the patient’s quality of life [60].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.1. Definition of DMT
What the sources say
- Not checked yetcites [60] Morató, X., Pytel, V., Jofresa, S., Ruiz, A., and Boada, M. (2022). Symptomatic and Disease-Modifying Therapy Pipeline for Alzheimer’s Disease: Towards a Personalized Polypharmacology Patient-Centered Approach. Int. J. Mol. Sci., 23. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Studies have shown that Aβ buildup can start 15–20 years before clinical symptoms appear, indicating that therapy effectiveness may depend on early intervention [88,89].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
- Not checked yetcites [88] Panza, 2019, A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease, Nat. Rev. Neurol. source
- Not checked yetcites [89] Shi, M., Chu, F., Zhu, F., and Zhu, J. (2022). Impact of Anti-amyloid-β Monoclonal Antibodies on the Pathology and Clinical Profile of Alzheimer’s Disease: A Focus on Aducanumab and Lecanemab. Front. Aging Neurosci., 14. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“While lowering Aβ levels can decrease cognitive deterioration, not all patients will definitely see improved clinical outcomes from this strategy, according to certain research [86,93].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 2. Disease-Modifying Therapeutics > 2.3. Mechanisms of Action
What the sources say
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Memantine is safe and well-tolerated; it is used to treat moderate-to-severe AD alone or in combination with AChEI [124,125,126].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [124] Marotta, G., Basagni, F., Rosini, M., and Minarini, A. (2020). Memantine Derivatives as Multitarget Agents in Alzheimer’s Disease. Molecules, 25. source
- Not checked yetcites [125] Turcu, 2022, Design, synthesis, and in vitro and in vivo characterization of new memantine analogs for Alzheimer’s disease, Eur. J. Med. Chem. source
- Not checked yetcites [126] Wu, 2021, Therapeutic efficacy of novel memantine nitrate MN-08 in animal models of Alzheimer’s disease, Aging Cell source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The first disease-modifying medication for AD is a recombinant monoclonal antibody called aducanumab, also known by the brand name Aduhelm. It targets amyloid beta specifically [37]. It functions by lowering the quantity of amyloid deposits or brain plaques [130,131].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [130] Rahman, 2023, Aducanumab for the treatment of Alzheimer’s disease: A systematic review, Psychogeriatrics source
- Not checked yetcites [131] Wojtunik-Kulesza, K., Rudkowska, M., and Orzeł-Sajdłowska, A. (2023). Aducanumab—Hope or Disappointment for Alzheimer’s Disease. Int. J. Mol. Sci., 24. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Compared to oral pills, transdermal patches are more pleasant and provide a smaller dosage, which leads to fewer side effects.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [119] Rompicherla, 2021, Pharmacokinetic and pharmacodynamic evaluation of nasal liposome and nanoparticle based rivastigmine formulations in acute and chronic models of Alzheimer’s disease, Naunyn-Schmiedeberg S Arch. Pharmacol. source
- Not checked yetcites [120] Guo, 2024, Rivastigmine nasal spray for the treatment of Alzheimer’s Disease: Olfactory deposition and brain delivery, Int. J. Pharm. source
- Not checked yetcites [121] Ezzat, S.M., Salem, M.A., Mahdy, N.M.E., and Ragab, M.F. (2021). Rivastigmine. Naturally Occurring Chemicals Against Alzheimer’s Disease, Elsevier. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The reduction in amyloid-beta brain plaques, a purported surrogate endpoint that indicates the “progression” of AD, and the encouraging clinical outcomes in one of the two pivotal Phase III trials were two of the factors cited for aducanumab’s expedited approval [130,134,135,136].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [130] Rahman, 2023, Aducanumab for the treatment of Alzheimer’s disease: A systematic review, Psychogeriatrics source
- Not checked yetcites [134] Dunn, 2021, Approval of Aducanumab for Alzheimer Disease—The FDA’s Perspective, JAMA Intern. Med. source
- Not checked yetcites [135] Mullard, 2023, FDA approves second anti-amyloid antibody for Alzheimer disease, Nat. Rev. Drug Discov. source
- Not checked yetcites [136] Reardon, 2023, FDA approves Alzheimer’s drug lecanemab amid safety concerns, Nature source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“CAD106, a further active Aβ immunotherapy, is presently undergoing clinical development. It involves administering multiple doses of the whole Aβ1–6 peptide linked to the ADP-Q carrier, a virus-like particle that generates high-titer anti-Aβ antibodies [140,141,153,154].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.1. Oral Immunotherapies or Small Molecules Containing DMTs
What the sources say
- Not checked yetcites [140] Bhadane, 2024, Immunotherapeutic approaches for Alzheimer’s disease: Exploring active and passive vaccine progress, Brain Res. source
- Not checked yetcites [141] Parrocha, 2022, Current peptide vaccine and immunotherapy approaches against Alzheimer’s disease, Pept. Sci. source
- Not checked yetcites [153] Riviere, 2023, Effects of the active amyloid beta immunotherapy CAD106 on PET measurements of amyloid plaque deposition in cognitively unimpaired APOE ε4 homozygotes, Alzheimer’s Dement. source
- Not checked yetcites [154] Thakur, 2023, Attempts to Develop Vaccines Against Alzheimer’s Disease: A Systematic Review of Ongoing and Completed Vaccination Trials in Humans, Cureus
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Lecanemab (LEQEMBI, brand name), a different monoclonal antibody known as humanized immunoglobulin G1 (IgG1), which specifically targets aggregated forms of amyloid beta, was also given fast approval by the FDA earlier in the year [134,135,136].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [134] Dunn, 2021, Approval of Aducanumab for Alzheimer Disease—The FDA’s Perspective, JAMA Intern. Med. source
- Not checked yetcites [135] Mullard, 2023, FDA approves second anti-amyloid antibody for Alzheimer disease, Nat. Rev. Drug Discov. source
- Not checked yetcites [136] Reardon, 2023, FDA approves Alzheimer’s drug lecanemab amid safety concerns, Nature source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It is authorized for use in mild-to-moderate Parkinson’s disease dementia and mild-to-moderate AD [116,117,118].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs
What the sources say
- Not checked yetcites [116] Ray, 2020, Rivastigmine modifies the α-secretase pathway and potentially early Alzheimer’s disease, Transl. Psychiatry source
- Not checked yetcites [117] Vicente-Zurdo, D., Rosales-Conrado, N., León-González, M.E., Brunetti, L., Piemontese, L., Pereira-Santos, A.R., Cardoso, S.M., Madrid, Y., Chaves, S., and Santos, M.A. (2022). Novel Rivastigmine Derivatives as Promising Multi-Target Compounds for Potential Treatment of Alzheimer’s Disease. Biomedicines, 10. source
- Not checked yetcites [118] Shamsi, 2020, Probing the interaction of Rivastigmine Tartrate, an important Alzheimer’s drug, with serum albumin: Attempting treatment of Alzheimer’s disease, Int. J. Biol. Macromol. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Due to problems with binding efficiency, which show up as blue discolorations in urine, methylene blue (labeled as 12, Figure 5), which was also tried in Phase II clinical trials for mild-to-moderate AD (for suppressing tau aggregation), has drawn a lot of criticism [168,169,170].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.1. Oral Immunotherapies or Small Molecules Containing DMTs
What the sources say
- Not checked yetcites [168] Soeda, 2019, Methylene Blue Inhibits Formation of Tau Fibrils but not of Granular Tau Oligomers: A Plausible Key to Understanding Failure of a Clinical Trial for Alzheimer’s Disease, J. Alzheimer’s Dis. source
- Not checked yetcites [169] Berrocal, M., Caballero-Bermejo, M., Gutierrez-Merino, C., and Mata, A.M. (2019). Methylene Blue Blocks and Reverses the Inhibitory Effect of Tau on PMCA Function. Int. J. Mol. Sci., 20. source
- Not checked yetcites [170] How, 2018, Exploring the effects of methylene blue on amyloid fibrillogenesis of lysozyme, Int. J. Biol. Macromol. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Phase II trials (90 studies, 81 medicines): these trials continue to investigate the drugs’ safety and efficacy.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [183] Cummings, 2024, Alzheimer’s disease drug development pipeline: 2024, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [184] Huang, L.-K., Kuan, Y.-C., Lin, H.-W., and Hu, C.-J. (2023). Clinical trials of new drugs for Alzheimer disease: A 2020–2023 update. J. Biomed. Sci., 30. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The tyrosine kinase inhibitor saracatinib (AZD0530 (labeled as 14, Figure 5)) is undergoing Phase II trials [174,175,176] and has been demonstrated to improve memory in transgenic mice models of AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.1. Oral Immunotherapies or Small Molecules Containing DMTs
What the sources say
- Not checked yetcites [174] Fagiani, 2020, Targeting dementias through cancer kinases inhibition, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [175] Ramos, R., and Vale, N. (2024). Dual Drug Repurposing: The Example of Saracatinib. Int. J. Mol. Sci., 25. source
- Not checked yetcites [176] Tridente, G., Jana, A., Nath, A., and Ashraf, G.M. (2023). Protein kinase inhibitors as therapeutics in neurodegenerative and psychiatric disorders. Receptor Tyrosine Kinases in Neurodegenerative and Psychiatric Disorders, Academic Press. source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In particular, a mean difference of −73.5 centiloides and −0.31 standardized uptake value ratio (SUVR) units was found between the lecanemab and placebo treatment groups.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [187] Mukhopadhyay, 2021, A Primer on the Evolution of Aducanumab: The First Antibody Approved for Treatment of Alzheimer’s Disease, J. Alzheimer’s Dis. source
- Not checked yetcites [188] Swanson, 2021, A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer’s disease with lecanemab, an anti-Aβ protofibril antibody, Alzheimer’s Res. Ther. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PDE4 inhibitors, which are oral small compounds that selectively inhibit PDE4, an enzyme involved in controlling cAMP levels, include roflumilast (15, Figure 5), which may lessen inflammation and increase neuronal survival [177,178,179,180].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.1. Oral Immunotherapies or Small Molecules Containing DMTs
What the sources say
- Not checked yetcites [177] Wang, 2020, The Phosphodiesterase-4 Inhibitor Roflumilast, a Potential Treatment for the Comorbidity of Memory Loss and Depression in Alzheimer’s Disease: A Preclinical Study in APP/PS1 Transgenic Mice, Int. J. Neuropsychopharmacol. source
- Not checked yetcites [178] Sugin, 2020, Roflumilast: A potential drug for the treatment of cognitive impairment?, Neurosci. Lett. source
- Not checked yetcites [179] Hu, 2019, Synthesis and evaluation of clioquinol-rolipram/roflumilast hybrids as multitarget-directed ligands for the treatment of Alzheimer’s disease, Eur. J. Med. Chem. source
- Not checked yetcites [180] Hasan, 2022, Roflumilast Reduces Pathological Symptoms of Sporadic Alzheimer’s Disease in Rats Produced by Intracerebroventricular Streptozotocin by Inhibiting NF-κB/BACE-1 Mediated Aβ Production in the Hippocampus and Activating the cAMP/BDNF Signalling Pathway, Neurotox. Res. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Of these trials, 41% look into disease-modifying small molecule medications, 34% look into biological agents that change disease, and the remaining trials focus on treatments that improve cognitive function or address neuropsychiatric symptoms linked to ADs [68,70,71,182,183,184].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [68] Cummings, 2022, Alzheimer’s disease drug development pipeline: 2022, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [70] Cummings, 2020, Alzheimer’s disease drug development pipeline: 2020, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [71] Cummings, 2023, Alzheimer’s disease drug development pipeline: 2023, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [182] Cummings, 2021, Alzheimer’s disease drug development pipeline: 2021, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [183] Cummings, 2024, Alzheimer’s disease drug development pipeline: 2024, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [184] Huang, L.-K., Kuan, Y.-C., Lin, H.-W., and Hu, C.-J. (2023). Clinical trials of new drugs for Alzheimer disease: A 2020–2023 update. J. Biomed. Sci., 30. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The most recent list of studies was provided by the 2024 AD drug development pipeline, which includes 164 trials (of which 127 are exploring possible treatments or medicines).”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [68] Cummings, 2022, Alzheimer’s disease drug development pipeline: 2022, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [70] Cummings, 2020, Alzheimer’s disease drug development pipeline: 2020, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [71] Cummings, 2023, Alzheimer’s disease drug development pipeline: 2023, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [182] Cummings, 2021, Alzheimer’s disease drug development pipeline: 2021, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [183] Cummings, 2024, Alzheimer’s disease drug development pipeline: 2024, Alzheimer’s Dement. Transl. Res. Clin. Interv. source
- Not checked yetcites [184] Huang, L.-K., Kuan, Y.-C., Lin, H.-W., and Hu, C.-J. (2023). Clinical trials of new drugs for Alzheimer disease: A 2020–2023 update. J. Biomed. Sci., 30. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The BBB is impermeable to 98% of small molecules and around 100% of large molecules in relevant quantities.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [193] Conrado, 2020, Challenges in Alzheimer’s Disease Drug Discovery and Development: The Role of Modeling, Simulation, and Open Data, Clin. Pharmacol. Ther. source
- Not checked yetcites [194] Abduljawad, A.A., Elawad, M.A., Elkhalifa, M.E.M., Ahmed, A., Hamdoon, A.A.E., Salim, L.H.M., Ashraf, M., Ayaz, M., Hassan, S.S.U., and Bungau, S. (2022). Alzheimer’s Disease as a Major Public Health Concern: Role of Dietary Saponins in Mitigating Neurodegenerative Disorders and Their Underlying Mechanisms. Molecules, 27. source
- Not checked yetcites [195] Ribba, B. (2023). Reinforcement learning as an innovative model-based approach: Examples from precision dosing, digital health and computational psychiatry. Front. Pharmacol., 13. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This phenomenon is most likely caused by uncertainties in AD pathophysiology, such as the lack of validated diagnostic biomarkers and the low specificity of clinical diagnosis.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Additionally, the treatment impact increased in a dose- and exposure-dependent manner; a 25% AUC therapy was probably superior to a placebo by >0.64.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [187] Mukhopadhyay, 2021, A Primer on the Evolution of Aducanumab: The First Antibody Approved for Treatment of Alzheimer’s Disease, J. Alzheimer’s Dis. source
- Not checked yetcites [188] Swanson, 2021, A randomized, double-blind, phase 2b proof-of-concept clinical trial in early Alzheimer’s disease with lecanemab, an anti-Aβ protofibril antibody, Alzheimer’s Res. Ther. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“One of the regulatory obstacles in creating DMTs for AD is the insufficient knowledge and ability of regional regulatory organizations, in addition to post-study medication administration and sustained treatment supply.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [196] Ndebele, 2014, Regulatory Challenges Associated with Conducting Multicountry Clinical Trials in Resource-Limited Settings, JAIDS J. Acquir. Immune Defic. Syndr. source
- Not checked yetcites [197] Alemayehu, 2018, Barriers for conducting clinical trials in developing countries—A systematic review, Int. J. Equity Health source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The goal of tau treatments is to prevent tau from aggregating and spreading.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [198] Sinsky, J., Pichlerova, K., and Hanes, J. (2021). Tau Protein Interaction Partners and Their Roles in Alzheimer’s Disease and Other Tauopathies. Int. J. Mol. Sci., 22. source
- Not checked yetcites [199] Alquezar, C., Arya, S., and Kao, A.W. (2021). Tau Post-translational Modifications: Dynamic Transformers of Tau Function, Degradation, and Aggregation. Front. Neurol., 11. source
- Not checked yetcites [200] Yang, J., Zhi, W., and Wang, L. (2024). Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review. Molecules, 29. source
- Not checked yetcites [201] Sigurdsson, 2018, Tau Immunotherapies for Alzheimer’s Disease and Related Tauopathies: Progress and Potential Pitfalls1, J. Alzheimer’s Dis. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“While both aducanumab and lecanemab slowed cognitive decline and reduced amyloid plaques, they were more likely to cause amyloid-related imaging abnormalities (ARIAs), which are thought to be the most significant side effect of both drugs.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [92] Qiao, 2024, Comparative Efficacy and Safety of Monoclonal Antibodies for Cognitive Decline in Patients with Alzheimer’s Disease: A Systematic Review and Network Meta-Analysis, CNS Drugs source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, there are several review levels with conflicting results and different guidelines for participant reimbursement for trial-related injuries.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 3. AD Current Treatment Drugs > 3.2. Recent DMT’s Clinical Trials
What the sources say
- Not checked yetcites [196] Ndebele, 2014, Regulatory Challenges Associated with Conducting Multicountry Clinical Trials in Resource-Limited Settings, JAIDS J. Acquir. Immune Defic. Syndr. source
- Not checked yetcites [197] Alemayehu, 2018, Barriers for conducting clinical trials in developing countries—A systematic review, Int. J. Equity Health source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Even more targeted strategies are being developed to enhance neurotransmitter activity.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“PSEN1 and PSEN2 mutations, which are closely associated with early-onset AD and impact the γ-secretase cleavage products, such as Aβ, are important genetic factors.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [213] AlMansoori, M.E., Jemimah, S., Abuhantash, F., and AlShehhi, A. (2024). Predicting early Alzheimer’s with blood biomarkers and clinical features. Sci. Rep., 14. source
- Not checked yetcites [214] Kesu, S.M.R., Sinha, N., and Ramasangu, H. (2024). Cellular Automata Framework for Dementia Classification Using Explainable AI. Eng. Proc., 68. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TREM2 agonists are being investigated as potential therapeutic agents since they reduce inflammation and encourage amyloid-beta microglial phagocytosis [202,203,204,205].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [202] Yang, 2020, TREM2 ectodomain and its soluble form in Alzheimer’s disease, J. Neuroinflamm. source
- Not checked yetcites [203] Huang, W., Huang, J., Huang, N., and Luo, Y. (2023). The role of TREM2 in Alzheimer’s disease: From the perspective of Tau. Front. Cell Dev. Biol., 11. source
- Not checked yetcites [204] Shi, Q., Gutierrez, R.A., and Bhat, M.A. (2024). Microglia, Trem2, and Neurodegeneration. Neuroscientist, 10738584241254118. source
- Not checked yetcites [205] Pocock, 2024, Microglia and TREM2, Neuropharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finding preventative drugs derived from conventional herbal remedies is one approach to treating AD.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 5. Prospects for the Future of Phytochemical Treatment of AD
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“These systems have demonstrated notable advances in diagnostic performance, particularly in radiology.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [213] AlMansoori, M.E., Jemimah, S., Abuhantash, F., and AlShehhi, A. (2024). Predicting early Alzheimer’s with blood biomarkers and clinical features. Sci. Rep., 14. source
- Not checked yetcites [216] Forloni, 2020, Alzheimer’s disease: From basic science to precision medicine approach, BMJ Neurol. Open source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“This allows for disease stratification and may even facilitate an earlier diagnosis [214,215].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [214] Kesu, S.M.R., Sinha, N., and Ramasangu, H. (2024). Cellular Automata Framework for Dementia Classification Using Explainable AI. Eng. Proc., 68. source
- Not checked yetcites [215] Arafah, A., Khatoon, S., Rasool, I., Khan, A., Rather, M.A., Abujabal, K.A., Faqih, Y.A.H., Rashid, H., Rashid, S.M., and Ahmad, S.B. (2023). The Future of Precision Medicine in the Cure of Alzheimer’s Disease. Biomedicines, 11. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Certain dysregulated proteostasis, dysregulated circadian rhythms, inflammation, oxidative stress, tau proteinopathies, and dysregulated metabolism may all be treated therapeutically with some DMTs.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 6. Conclusions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“Combination therapy is another example; it targets different pharmacologic targets (such as tau and amyloid) or targets pathways sequentially by using successive combinations.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [217] Cummings, 2019, Treatment Combinations for Alzheimer’s Disease: Current and Future Pharmacotherapy Options, J. Alzheimer’s Dis. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“New advances in synthetic biology and genomics open up new avenues for discovering and using the medicinal properties of plants.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 5. Prospects for the Future of Phytochemical Treatment of AD
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“These markers provide information about the underlying pathophysiology of AD and are crucial for detecting the disease, especially in those who have memory problems.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [214] Kesu, S.M.R., Sinha, N., and Ramasangu, H. (2024). Cellular Automata Framework for Dementia Classification Using Explainable AI. Eng. Proc., 68. source
- Not checked yetcites [215] Arafah, A., Khatoon, S., Rasool, I., Khan, A., Rather, M.A., Abujabal, K.A., Faqih, Y.A.H., Rashid, H., Rashid, S.M., and Ahmad, S.B. (2023). The Future of Precision Medicine in the Cure of Alzheimer’s Disease. Biomedicines, 11. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These AI systems are very good at finding patterns, assessing large volumes of data, and forecasting the likelihood of developing diseases.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [213] AlMansoori, M.E., Jemimah, S., Abuhantash, F., and AlShehhi, A. (2024). Predicting early Alzheimer’s with blood biomarkers and clinical features. Sci. Rep., 14. source
- Not checked yetcites [216] Forloni, 2020, Alzheimer’s disease: From basic science to precision medicine approach, BMJ Neurol. Open source
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AI systems have been approved by the US Food and Drug Administration (FDA) for enhancing medical imaging assessments, including the identification of suspicious lesions [37,213,216].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [37] Breijyeh, Z., and Karaman, R. (2020). Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules, 25. source
- Not checked yetcites [213] AlMansoori, M.E., Jemimah, S., Abuhantash, F., and AlShehhi, A. (2024). Predicting early Alzheimer’s with blood biomarkers and clinical features. Sci. Rep., 14. source
- Not checked yetcites [216] Forloni, 2020, Alzheimer’s disease: From basic science to precision medicine approach, BMJ Neurol. Open source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Another type of combination therapy is represented by multifunctional compounds, which incorporate several activities or targets into a single medication.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [217] Cummings, 2019, Treatment Combinations for Alzheimer’s Disease: Current and Future Pharmacotherapy Options, J. Alzheimer’s Dis. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The search for new leads in AD treatment could be fruitful if herbal remedies are evaluated for lead chemicals based on their physicochemical properties and predicted BBB actions.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 5. Prospects for the Future of Phytochemical Treatment of AD
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A DMT with a particular therapeutic target may be more effective than other DMTs with different targets due to the complex and all-encompassing pathogenesis of AD, particularly if the therapeutic target of the DMT being administered aligns with the most salient pathological findings of the subpopulation.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 6. Conclusions
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Pharmacodynamic agent combinations for AD may consist of DMTs, which change the course of the disease, or symptomatic medicines, which reduce the symptoms without changing the course of the disease.”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [217] Cummings, 2019, Treatment Combinations for Alzheimer’s Disease: Current and Future Pharmacotherapy Options, J. Alzheimer’s Dis. source
- Not checked yetcites [218] Horani, 2015, Anticancer Prodrugs—Three Decades of Design, World J. Pharm. Pharm. Sci.
- Not checked yetcites [219] Dudchenko, 2024, Combination Drug Therapy for the Management of Alzheimer’s Disease, Russ. J. Geriatr. Med. source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This approach is adaptable enough to be customized for every single patient, ensuring optimal treatment outcomes [220,221].”
§ Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease > 4. Future Directions and Emerging Therapies in DMT
What the sources say
- Not checked yetcites [220] Strac, 2021, Personalizing the Care and Treatment of Alzheimer’s Disease: An Overview, Pharmacogenom. Pers. Med.
- Not checked yetcites [221] Passeri, E., Elkhoury, K., Morsink, M., Broersen, K., Linder, M., Tamayol, A., Malaplate-Armand, C., Yen, F.T., and Arab-Tehrany, E. (2022). Alzheimer’s Disease: Treatment Strategies and Their Limitations. Int. J. Mol. Sci., 23. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper relies on this without support.
Only a small percentage of AD patients benefit from the two DMTs currently approved for therapy.
“Only a small percentage of AD patients benefit from the two DMTs that are currently approved for therapy.”
The paper relies on this without support.
Several natural compounds have demonstrated potential for treating AD in both in vitro and in vivo studies.
“Nevertheless, several natural compounds have demonstrated potential for treating AD in both in vitro and in vivo studies.”
The paper relies on this without support.
Humans and animals in studies differ physiologically.
“because humans and animals in studies differ physiologically”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Several drugs focus on symptom management such as cholinesterase inhibitors (ChEIs): rivastigmine, donepezil, galantamine, and tacrine work by increasing ACh levels, improving cognition and memory, though they do not alter the disease’s progression.”
From Cholinesterase Inhibitors from Plants and Their Potential in Alzheimer’s Treatment: Systematic Review (2025) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Current treatments for AD, including cholinesterase inhibitors and memantine, offer limited symptom relief, especially in the early to moderate stages, but do not halt disease progression or address the underlying neurodegeneration.”
From Cholinesterase Inhibitors from Plants and Their Potential in Alzheimer’s Treatment: Systematic Review (2025) · cites this paper as [9]
Experimental — accuracy not yet measured
Citations
Cites
1 retracted
Hasan, N., Zameer, S., Najmi, A. K., Parvez, S., & Akhtar, M. (2022) · Neurotoxicity Research · doi:10.1007/s12640-022-00482-x · Cited by 17 · cited 1×
“PDE4 inhibitors, which are oral small compounds that selectively inhibit PDE4, an enzyme involved in controlling cAMP levels, include roflumilast ( 15 , Figure 5), which may lessen inflammation and increase neuronal survival [177–180].”
BackgroundRetractedLecanemab in early Alzheimer's disease
van Dyck, C. H., Swanson, C. J., Aisen, P., Bateman, R. J., Chen, C., Gee, M., Kanekiyo, M., Li, D., Reyderman, L., Cohen, S., et al. (2023) · New England Journal of Medicine · doi:10.1056/nejmoa2212948 · Cited by 5,678 · cited 1×
“There is insufficient safety or efficacy information on starting treatment sooner or later than in the conducted studies [137–139].”
BackgroundScheltens, P., De Strooper, B., Kivipelto, M., Holstege, H., Chételat, G., Teunissen, C. E., Cummings, J., & van der Flier, W. M. (2021) · The Lancet · doi:10.1016/s0140-6736(20)32205-4 · Cited by 5,465
Comprehensive Review on Alzheimer’s Disease: Causes and Treatment
Breijyeh, Z., & Karaman, R. (2020) · Molecules · doi:10.3390/molecules25245789 · Cited by 2,789 · cited 10×
“DMTs consist of three primary components: therapy, sick-Molecules ness, and modification [37,59].”
BackgroundInfluentialSelf-citationThe Amyloid-β Pathway in Alzheimer’s Disease
Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., Villemagne, V. L., Aisen, P., Vendruscolo, M., Iwatsubo, T., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01249-0 · Cited by 1,952 · cited 1×
“However, the relationship between FAD mutations and A β levels is complex, and the plaque formation in sporadic AD is influenced by a dynamic imbalance between A β production and clearance mechanisms [11,12].”
BackgroundZhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138 · cited 1×
“…process of AD is multifaceted, involving several key hypotheses: the cholinergic, glutamatergic, amyloid, tau protein, inflammatory, microbiota–gut– brain axis, oxidative stress, metal ion, and abnormal autophagy hypotheses, as shown in the summary of AD pathophysiology in Figure 1 [8].”
BackgroundTau-targeting therapies for Alzheimer disease
Congdon, E. E., & Sigurdsson, E. M. (2018) · Nature Reviews Neurology · doi:10.1038/s41582-018-0013-z · Cited by 1,113 · cited 3×
“This change in emphasis has made room for novel treatment strategies meant to lessen the consequences of tau-related neurodegeneration [13,95].”
BackgroundClinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group
Dubois, B., Villain, N., Frisoni, G. B., Rabinovici, G. D., Sabbagh, M., Cappa, S., Bejanin, A., Bombois, S., Epelbaum, S., Teichmann, M., et al. (2021) · The Lancet Neurology · doi:10.1016/s1474-4422(21)00066-1 · Cited by 1,051
Simpson, D. S. A., & Oliver, P. L. (2020) · Antioxidants · doi:10.3390/antiox9080743 · Cited by 1,044
Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future
Zhang, Y., Chen, H., Li, R., Sterling, K., & Song, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01484-7 · Cited by 988 · cited 1×
“While lowering A β levels can decrease cognitive deterioration, not all patients will definitely see improved clinical outcomes from this strategy, according to certain research [86,93].”
Background
Research works printed but not linked: 1
- Horani, 2015, Anticancer Prodrugs—Three Decades of Design, World J. Pharm. Pharm. Sci., 4, 1751
Cited by
Sorted by citations
Antibacterial Activity and Antifungal Activity of Monomeric Alkaloids
Thawabteh, A. M., Ghanem, A. W., AbuMadi, S., Thaher, D., Jaghama, W., Karaman, R., Scrano, L., & Bufo, S. A. (2024) · Toxins · doi:10.3390/toxins16110489 · Cited by 61
Self-citationAlkhalifa, A. E., Mokhlf, A. A., Ali, H., Al-Ghraiybah, N. F., & Syropoulou, V. (2025) · Journal of Personalized Medicine · doi:10.3390/jpm15090437 · Cited by 68
“Adu-canumab was the first anti-amyloid antibody to receive regulatory approval for mild AD with confirmed amyloid pathology, followed by lecanemab and donanemab [21].”
NLRP3 inflammasome in Alzheimer’s disease: molecular mechanisms and emerging therapies
Li, Z., & Gong, C. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1583886 · Cited by 53
“The ongoing phase 3 trial TRAILBLAZER-ALZ 2 (NCT04437511) (118), phase 2 clinical trial (NCT04795466) (81) and other AD clinical trials will offer a more comprehensive strategy for AD treatment (119) (Table 1).”
ALNasser, M. N., Alboraiy, G. M., Alsowig, E. M., & Alqattan, F. M. (2025) · Brain Sciences · doi:10.3390/brainsci15020215 · Cited by 35
Targeting of PP2 A/GSK3β/PTEN Axis in Alzheimer Disease: The Mooting Evidence, Divine, and Devil
Alqahtani, S. M., Al-Kuraishy, H. M., Al-Gareeb, A. I., Abdel‐Fattah, M. M., Alsaiari, A. A., Alruwaili, M., Papadakis, M., Alexiou, A. T., & Batiha, G. E. (2025) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-025-01554-0 · Cited by 26
“Similar to other BACE‑1 inhibitors, umibecestat has been shown to reduce the burden of Aβ in preclinical animals (Weaver 2023; Thawabteh et al. 2024).”
Tirzepatide: a novel therapeutic approach for Alzheimer’s disease
Alshehri, G. H., Al-Kuraishy, H. M., Waheed, H. J., Al-Gareeb, A. I., Faheem, S. A., Alexiou, A. T., Papadakis, M., & Batiha, G. E. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01649-z · Cited by 17
Targeting Amyloid Pathology in Early Alzheimer’s: The Promise of Donanemab-Azbt
Khartabil, N., & Awaness, A. (2025) · Pharmacy · doi:10.3390/pharmacy13010023 · Cited by 16
Gao, F., Hou, Y., Wang, Y., Liu, L., Yi, X., & Xia, N. (2025) · Biosensors · doi:10.3390/bios15080480 · Cited by 15
“It consists of D-glucose-based polyoxalate G-poly(oxalate), photosensitizer BD-Se-QM, and bis[2,4,5-trichloro 6-(pentoxy-carbonyl)phenyl]ester.”
Liu, C., Chen, X., Yang, S., Wang, X., Sun, P., Wang, J., & Zhu, G. (2024) · Experimental Neurology · doi:10.1016/j.expneurol.2024.115116 · Cited by 13
Promising Natural Remedies for Alzheimer’s Disease Therapy
Thawabteh, A. M., Ghanem, A. W., AbuMadi, S., Thaher, D., Jaghama, W., Karaman, D., & Karaman, R. (2025) · Molecules · doi:10.3390/molecules30040922 · Cited by 13
“Patients complain of cognitive decline, which is made worse by oxidative stress, chronic inflammation, and synapse loss [1,2].”
InfluentialSelf-citationNew Approaches to the Treatment of Alzheimer’s Disease
Kruk-Słomka, M., Kuceł, D., Małysz, M., Machnikowska, A., Orzelska‐Górka, J., & Biała, G. (2025) · Pharmaceuticals · doi:10.3390/ph18081117 · Cited by 12
“Subsequently, at the turn of 2024 and 2025, the manufacturer of aducanumab announced its market withdrawal, attributing the decision to its limited clinical adoption, the high cost of therapy, and ongoing uncertainties regarding the drug’s clinical efficacy [12,32] (Table 1).”
InfluentialSingh, P. K., Borkar, M. R., & Doshi, G. (2025) · Molecular Diversity · doi:10.1007/s11030-025-11198-3 · Cited by 11
Bioorganic Chemistry, Toxinology, and Pharmaceutical Uses of Datura Metabolites and Derivatives
Thawabteh, A. M., Sulaiman, S. M., Alabed, I. O., Scrano, L., Karaman, D., Karaman, R., & Bufo, S. A. (2025) · Toxins · doi:10.3390/toxins17090469 · Cited by 8
“As a tertiary amine esterified to tropic acid, hyoscyamine exhibits potent antimuscarinic activity in mammalian systems, conferring both therapeutic utility and a narrow margin of safety [46–48].”
Self-citationChallenges and Opportunities of Drug Delivery for Treatment of Alzheimer’s Disease
El-Fattah, M. A. A. (2026) · AAPS PharmSciTech · doi:10.1208/s12249-025-03316-z · Cited by 9
“For possible injuries, recent guidance by National Alzheimer's Coordinating Center (NACC) recommends participant reimbursement in case of trial-related injuries [51, 123].”
Alameen, A. A. M., Al‐kuraishy, H. M., Al-Gareeb, A. I., Shokr, M. M., & Batiha, G. E. (2026) · Microvascular Research · doi:10.1016/j.mvr.2026.104947 · Cited by 6
The Bidirectional Mechanism of Uric Acid Levels on Alzheimer’s Disease: A Narrative Review
Zhao, J., Wang, X., & Li, B. (2025) · International Journal of General Medicine · doi:10.2147/ijgm.s567473 · Cited by 5
Leng, L., Liao, Z., Lu, P., Sun, Y., Weng, Q., Fan, W., Zhu, H., Wu, W., Liu, P., Liu, X., et al. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251406619 · Cited by 5
Gutiérrez, R. M. P., Gómez, J. T., Flores, J. M. M., Téllez, M. D. L. L. C., & Muñiz-Ramírez, A. (2025) · Pharmaceuticals · doi:10.3390/ph18091391 · Cited by 5
“The three FDA-approved cholinesterase inhibitors are donepezil, galantamine, and rivastigmine [13].”
Sardar, A., Hussain, R., Khan, S. A., et al. (2025) · Journal of Computational Biophysics and Chemistry · doi:10.1142/s2737416525501042 · Cited by 3
A Review on the Pathophysiology of Alzheimer’s Disease
Agarwal, U., Kapoor, G. T., & Tonk, R. K. (2025) · Current Protein and Peptide Science · doi:10.2174/0113892037416859250915091846 · Cited by 5
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Maliyakkal, N., Kumar, S., Bhowmik, R., Parmbil, S. K., Aspatwar, A., & Mathew, B. (2025) · Advanced Theory and Simulations · doi:10.1002/adts.202501347 · Cited by 3
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Enzymes and Alzheimer's Disease: Pioneering Drug Development Strategies
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“Currently, disease-modifying therapies for AD are still limited, and existing therapies provide only symptomatic relief without modifying disease progression (Thawabteh et al., 2024; Soni et al., 2025).”
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“Moreover, the majority of these therapies focus on specific molecular pathways, often missing the broader complex - ity of neurodegenerative diseases (Thawabteh et al. 2024; Zhang et al. 2024 ).”
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Case Studies and Patents in Alzheimer’s Disease Research
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Targeting the peripheral immune system for treatment of Alzheimer’s disease
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“Although AD has been studied extensively for decades, available treatments remain largely symptomatic, with existing disease-modifying therapies providing some clinical benefits but limited by safety concerns [2–4].”
Milusheva, M., Dimitrova, D. S., Saracheva, K., Gledacheva, V., Stefanova, I. D., & Nikolova, S. (2026) · Sci · doi:10.3390/sci8100289
Metadata
- Authors
- Thawabteh, A. M., Ghanem, A. W., AbuMadi, S., Thaher, D., Jaghama, W., Karaman, D., & Karaman, R.
- Affiliations
- Birzeit University (PS)
- Al-Quds University (PS)
- University of Basilicata (IT)
- Corresponding author
- Karaman, Rafik
- Venue
- Molecules
- Publisher
- MDPI AG
- Published
- 2024-10-30
- Volume
- 29
- Issue
- 21
- Pages
- 5131
- ISSN
- 1420-3049 (ISSN-L)
- PMC
- PMC11547905
- OpenAlex
- W4403924413
- Semantic Scholar
- 3b5aac7de909b8d17998af8b07fc6969ccab0114
- Cited by
- 56
- References
- 227
- Citations by year
- 2026: 24 · 2025: 30 · 2024: 2
- FWCI
- 3.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecules (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Keywords
- Alzheimer's disease, disease-modifying therapy, amyloid-beta, tau protein, neuroinflammation, anti-amyloid therapy, neuroprotective therapy, neurogenesis, cognitive decline, FDA-approved drugs, clinical trials, small molecule drugs, biologics
- MeSH terms
- Alzheimer Disease, Animals, Clinical Trials as Topic, Humans, Amyloid beta-Peptides, tau Proteins, Neuroprotective Agents
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