An update on the novel and approved drugs for Alzheimer disease
Open accessAbstract
Given the severity of the condition and the increasing number of patients, developing effective therapies for Alzheimer's disease has become a significant necessity. Aggregation of Amyloid-Beta (Aβ) plaques and Tau Protein Tangles in the brain's nerve tissue are two of the most histopathological/pathophysiological symptoms. Another important element involved in the etiology of Alzheimer's disease is the reduction in acetylcholine (ACh) levels in the brain. Currently available medications for Alzheimer's disease treatment, such as cholinesterase inhibitors and an antagonist of the N-methyl-d-aspartate receptor, can temporarily reduce dementia symptoms but not stop or reverse disease development. In addition, several medicinal plants have been shown to diminish the degenerative characteristics associated with Alzheimer's disease, either in its crude form or as isolated chemicals. This review summarises the results from previous studies that reflect an array of novel therapies underway in various phases of clinical trials. Many are discontinued due to non-adherence to the designed endpoints or the surfacing of unavoidable side effects. The present piece of article focuses on the approved drugs for the treatment of Alzheimer's disease and their related mode of action as well as the promising therapies for the treatment of the said disease. Special attention has been placed on the researched herbal drugs, with the pipeline of novel therapies underway in various phases of clinical trials. The current article includes a list of approved pharmaceuticals for treating Alzheimer's disease, prospective therapies for the illness's treatment, and a pipeline of novel therapies in various stages of clinical trials. The results suggest that the drugs under clinical trials may open new pathways for the effective treatment of patients with Alzheimer's disease while improving their quality of life.
AI snapshot
Written from the paper’s full text.
TL;DR
This narrative review summarizes FDA-approved Alzheimer disease drugs—acetylcholinesterase inhibitors, memantine, and aducanumab—alongside investigational anti-amyloid, chelation, natural-product, and clinical-trial pipeline therapies. It concludes that approved drugs mainly provide symptomatic or temporary benefit, while many trial agents have failed or been discontinued, though ongoing trials may open new treatment pathways.
Key findings
- Approved therapies include donepezil and rivastigmine for mild, moderate, and severe AD; galantamine for mild to moderate AD; and memantine, an NMDA antagonist, for moderate to severe AD. Aducanumab received FDA accelerated approval on June 7, 2021 as an anti-amyloid monoclonal antibody.
- Anti-amyloid pipeline setbacks are prominent: BACE inhibitor trials with lanabecestat, verubecestat, and atabecestat were terminated due to lack of efficacy or safety concerns; γ-secretase inhibitors are no longer regarded as a suitable target because of major safety concerns.
- In active immunization, ABvac40 generated Aβ40-specific antibodies in 92% of injected participants in a phase 1 trial; GV-971 was reported in a phase 3 study to have significant cognitive benefits in mild to severe AD.
- The review states that 40 million individuals are expected to suffer from dementia globally, with this figure predicted to double every 2 decades until around 2050. Table 1 lists herbal compounds such as berberine, curcumin, epigallocatechin-3-gallate, ginsenoside Rg1, catalpol, genistein, crocin, and huperzine A, with proposed antioxidant, anti-inflammatory, anti-amyloid, or cholinesterase-inhibitory effects.
Methods
- Narrative review; no systematic search strategy, inclusion/exclusion criteria, quality appraisal, or meta-analysis is stated.
- The paper summarizes prior studies and clinical trials, including Table 1 of herbal compounds for AD treatment and Table 2 of novel drugs in various clinical-trial phases with NCT numbers and statuses.
- Main analysis is a narrative synthesis of approved drug mechanisms, potential therapeutic approaches (anti-amyloid therapy, chelation therapy, natural drugs), and novel agents in clinical trials.
Limitations
- The paper states that many AD trials are discontinued due to non-adherence to designed endpoints or unavoidable side effects, and it notes a high percentage of failed AD clinical trials; it does not state limitations of the review itself.
- Evident from the text: as a narrative review, it lacks a systematic search and risk-of-bias assessment, relies on selected cited studies, and includes incomplete table entries (for example, IIdalopirdine phase 3 lacks trial number and status).
Model-written summary. Check it against the paper before relying on it.
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- Findingnone given
An array of novel therapies is underway in various phases of clinical trials.
“An array of novel therapies is underway in various phases of clinical trials (Table 2).”
Quote in the paperNot a substantial claim - Premisecitation
In most patients, acetylcholinesterase inhibitors were noted to be well tolerated.
“In most patients, these classes of drugs were noted to be well tolerated (Tabet, 2006).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Tabet, 2006 source
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- Premisecitation
Acetylcholinesterase plays a role in the production of amyloid plaques and neurofibrillary tangles.
“In addition, the enzyme plays a role in the production of amyloid plaques and neurofibrillary tangles.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Singh et al., 2013 source
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- Premisecitation
Acetylcholinesterase inhibitors' action on the gastro-intestinal tract causes the most common side effects, which include diarrhea, nausea, and vomiting.
“AChEIs action on the gastro-intestinal tract (git) causes the most common side effects, which include diarrhea, nausea, and vomiting (Yiannopoulou et al., 2020).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Yiannopoulou et al., 2020
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- Premisecitation
Aducanumab received expedited approval by the FDA on June 7, 2021.
“On June 7, 2021, the FDA gave Aducanumab expedited approval [FDA Approved Drug Products: Aduhelm (Aducanumab-avwa) Intravenous Injection].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites FDA Approved Drug Products: Aduhelm (Aducanumab-avwa) Intravenous Injection
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- Premisecitation
Currently, symptomatic treatments for Alzheimer's disease include acetylcholinesterase inhibitors such as donepezil, rivastigmine, and metrifonate and NMDA receptor blockers such as memantine.
“Currently, symptomatic treatments for AD include acetylcholinesterase inhibitors such as donepezil, rivastigmine, and metrifonate and NMDA receptor blockers such as memantine [Reisberg et al., 2003].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Reisberg et al., 2003
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Overstimulation of NMDA receptors by glutamate can induce neuronal injury owing to excitotoxicity in some cases.
“Overstimulation of NMDA receptors by glutamate, on the other hand, can induce neuronal injury owing to excitotoxicity in some cases (Francis, 2005).”
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- Premisecitation
Acetylcholinesterase inhibitors work by blocking acetylcholinesterase, which boosts acetylcholine levels in the brains of individuals with mild to moderate Alzheimer's disease.
“These medications work by blocking the enzyme acetylcholinesterase, which is crucial for the metabolic breakdown of acetylcholine, which results in boosting its level in the brains of individuals with mild to moderate AD.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Tabet, 2006 source
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- Premisecitation
Passive and active immunization are the two key immunotherapeutic methods for promoting Aβ clearance that are presently under investigation in various phases of analyses.
“Passive and active immunization are the 2 key immunotherapeutic methods for promoting Aβ clearance that are presently under investigation in various phases of analyses (Wisniewski et al., 2015).”
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- Premisecitation
Dizziness, agitation, hallucinations, headache, and exhaustion were the most common symptoms that arose in clinical trials of memantine.
“Dizziness, agitation, hallucinations, headache, and exhaustion were the most common symptoms that arose in clinical trials.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Molinuevo et al., 2005 source
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Metal ion imbalance in the brain is among the primary triggers in the etiology of Alzheimer's disease.
“Metal ion imbalance in the brain is among the primary triggers in the etiology of AD and hence it is appropriate to tackle this said illness with a chelation therapy technique employing metal ions (Pfaender et al., 2014).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Pfaender et al., 2014 source
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- Interpretationreasoning
These findings back the idea that stopping the formation of Aβ may not be enough to avoid the disease from progressing.
“These findings back the idea that stopping the formation of Aβ may not be enough to avoid the disease from progressing.”
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γ-secretase inhibitors are no longer regarded as a suitable target for the treatment of Alzheimer's disease due to major safety concerns.
“γ secretase inhibitors are no longer regarded a suitable target for the treatment of AD due to major safety concerns (Lopez et al., 2019).”
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In the presence of Cu(II), Zn(II), and Fe(III), a bis-8-hydroxyquinoline ligand allowed a huge rise in the potential to safeguard against β-amyloid peptide precipitation compared to clioquinol in vitro.
“In the presence of Cu(II), Zn(II), and Fe(III), a bis-8-hydroxyquinoline ligand, allowed huge rise in the potential to safeguard against b-amyloid peptide precipitation compared to CQ in vitro (Deraeve et al., 2007).”
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In intermediate or advanced dementia, the duration and durability of monotherapy or combinatorial treatment with greater doses is linked to better overall functioning and therapeutic outcomes.
“In intermediate or advanced dementia, the duration and durability of monotherapy or combinatorial treatment modality with greater doses is linked to better overall functioning and therapeutic outcomes (Calvó-Perxas et al., 2017).”
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The emergence of clioquinol as an anti-Alzheimer's disease drug has been halted due to potential neurotoxicity and undesirable mutagenic contaminants.
“Consequently, the emergence of CQ as an anti-AD drug has been halted due to potential neurotoxicity and undesirable mutagenic contaminants (Budimir et al., 2011).”
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- Premisecitation
Clinical studies with BACE inhibitors such as lanabecestat, verubecestat, and atabecestat have lately been terminated due to unanticipated challenges.
“Due to unanticipated challenges, clinical studies with BACE inhibitors such as lanabecestat, verubecestat, and atabecestat have lately been terminated (Egan et al., 2019, Henley et al., 2019).”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
Clinical trials for APH-1105 and ID1201, two α-secretase modulators that stimulate the PI3K/Akt pathway, are now underway.
“Clinical trials for APH-1105 and ID1201, two -secretase modulators that stimulate the PI3K/Akt pathway, are now underway.”
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- Premisecitation
Deferiprone has a strongly positive and significant affinity for metals such as iron, copper, and zinc in its scaffold.
“It has a strongly positive and significant affinity for metals such as iron, copper, and zinc in its scaffold (Clarke et al., 1992).”
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- Premisecitation
Memantine, an approved drug for moderate to severe Alzheimer's disease, has been shown to enhance cognitive capacities and outcomes in people with Alzheimer's disease.
“Memantine, an approved drug for the treatment of moderate to severe AD, has been shown to enhance cognitive capacities and the resultant outcomes in people with AD (Reisberg et al., 2003).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Reisberg et al., 2003
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- Interpretationcitation
Suvorexant can be an effective treatment for the behavioral and psychological symptoms associated with Alzheimer's disease.
“It can therefore be said that Suvorexant can be an effective treatment for the behavioral and psychological symptoms associated with AD (Herring et al., 2019).”
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EVP-6124 has a central role in regulating the release of various neurotransmitters.
“EVP-6124, an antagonist of 5-HT3 receptor and a agonist of 7 nicotinic acetylcholine receptor a has a central role in regulating the release of various neurotransmitters (Ahmed et al., 2019).”
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- Premisecitation
A phase 3 study of azeliragon in individuals with Alzheimer's disease and poor glucose tolerance started in 2019 and is expected to be completed in 2023.
“In the year 2018, two phase 3 clinical trials involving azeliragon for patients with mild AD were initiated and its the study (phase 3) in individuals with AD and poor glucose tolerance started in the year 2019 which is expected to be completed in 2023 (Galimberti et al., 2017).”
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Aripiprazole (spelled Apiprazole in the text) works to stabilize the dopamine system.
“Apiprazole works to stabilize the dopamine system (DSSs).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Coleman et al., 2017 source
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- Premisecitation
Bapineuzumab was the first monoclonal antibody to target Aβ in Alzheimer's disease using a passive immunotherapy technique.
“Bapineuzumab was the first monoclonal antibody to target Aβ in AD using a passive immunotherapy technique.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Salloway et al., 2014 source
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The NILVAD trial found no difference in primary or secondary endpoint measures for nilvadipine in people with Alzheimer's disease.
“The NILVAD trial, which took place in 2013, examined the effectiveness of nilvadipine in people with AD. ADAS-Cog was the main outcome measure, but there was no difference in the primary or secondary end point measures according to a published report (Bishop et al., 2004).”
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- Premisecitation
In 2018, two phase 3 clinical trials involving azeliragon for patients with mild Alzheimer's disease were initiated.
“In the year 2018, two phase 3 clinical trials involving azeliragon for patients with mild AD were initiated and its the study (phase 3) in individuals with AD and poor glucose tolerance started in the year 2019 which is expected to be completed in 2023 (Galimberti et al., 2017).”
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Following the completion of the first two bapineuzumab studies, which revealed no treatment efficacy on either cognitive or functional outcomes, further trials were halted.
“Following the completion of the first two studies, which revealed no treatment efficacy on either cognitive or functional outcomes, further trials were halted (Salloway et al., 2014).”
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In a phase 3 trial of suvorexant in patients with mild to severe Alzheimer's disease with insomnia, the first and second objectives were fulfilled.
“The effectiveness of suvorexant in patients with mild to severe AD with insomnia was studied in a phase 3 trial. Merck pointed out that the first and second objectives of the case were fulfilled.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Herring et al., 2019 source
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- Premisecitation
In a phase 3 study starting in April 2014, GV-971 had significant cognitive benefits in patients with mild to severe Alzheimer's disease.
“The effects of GV-971 on mild to severe form of AD were tested in a phase 3 study that started in April 2014 and the results of this study highlighted the fact that GV-971 has significant cognitive benefits.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Wang et al., 2019 source
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- Premisecitation
In a phase 2b study of elenbecestat (E2609), a BACE-1 inhibitor, in amyloid-PET people with MCI, prodromal AD, or mild AD, dose-dependent reduction in CSF Aβ levels was noted.
“A phase 2b study of E2609 (elenbecestat), a BACE-1 inhibitor, in amyloid-PET people with MCI, prodromal AD, or mild AD was performed and reduced dose-dependent in CSF A levels was noted.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Murakami et al., 2019 source
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- Premisecitation
Many molecules, including lignans, flavonoids, tannins, polyphenols, triterpenes, sterols, and alkaloids, have been shown to have anti-inflammatory, anti-amyloidogenic, and anticholinesterase properties.
“Many molecules, including lignans, flavonoids, tannins, polyphenols, triterpenes, sterols, and alkaloids, have been shown to have anti-inflammatory, anti-amyloidogenic, anticholinesterase, and anti-inflammatory properties.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Olajide et al., 2017 source
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- Premisecitation
In the phase 2b study of elenbecestat, there was no significant change in AD Composite Score or CDR-SB score.
“There is no significant change in AD. Composite Score or CDR-SB score (Murakami et al., 2019).”
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Aripiprazole helps to improve the reduction of neurite-induced neuropathy.
“It helps to improve the reduction of neurite-induced neuropathy.”
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- Premisecitation
In Alzheimer's disease-related psychosis, aripiprazole has the potential to remove the neurotoxicity induced by Aβ.
“In AD-related psychosis, this treatment has the potential to remove the neurotoxicity induced by Aβ (Coleman et al., 2017).”
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PremisecitationAβ peptides with A38, A40, and A42 are generated after sequential breakdown of amyloid precursor protein (APP) by β- and γ-secretase.
“After the sequential breakdown of the big precursor protein amyloid precursor protein (APP) by the β- and γ-e -secretase, Aβ peptides with A38, A40, and A42 being the most prevalent forms are generated (Yiannopoulou et al., 2013).”
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PremisecitationThe mitochondrial dysfunction hypothesis for Alzheimer's disease pathogenesis posits that amyloidosis, cell cycle re-entry, and tau phosphorylation are all caused by mitochondrial failure in the Alzheimer's disease brain.
“the mitochondrial dysfunction hypothesis for AD pathogenesis posits that amyloidosis, cell cycle re-entry, and tau phosphorylation are all caused by mitochondrial failure in the AD brain (Swerdlow et al., 2014).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Swerdlow et al., 2014 source
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PremisecitationAccording to the amyloid hypothesis, Aβ production in the brain sets off a chain of events that leads to the clinical symptoms of Alzheimer's disease.
“According to the “amyloid hypothesis,” Aβ production in the brain sets off a chain of events that leads to the clinical symptoms of AD.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Anand et al., 2017 source
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PremisecitationThe amyloid cascade theory is highly corroborated by pathology, genetics, and biochemistry; therefore, exploration of therapies has been mostly designed to target Aβ peptide or clumps in Alzheimer's disease.
“The amyloid cascade theory is highly corroborated by pathology, genetics, and biochemistry; therefore, exploration of these therapies has been mostly designed to target A peptide or clumps in AD (Hardy and Selkoe., 2002).”
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PremisecitationThe predominant route of elimination for donepezil and galantamine is hepatic metabolism, whereas for rivastigmine it is both hepatic and intestinal metabolism.
“The predominant route of elimination for donepezil and galantamine is reported to be hepatic metabolism, whereas those for rivastigmine is both hepatic and intestinal metabolism.”
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PremisecitationAducanumab treatment lowers amyloid-β according to animal reports, while human trials revealed no substantial improvements in amyloid-40 and amyloid-42.
“Acurenumab treatment lowers amyloid-, according to reports from animals and while human trials revealed no substantial improvements in amyloid-40 and amyloid-42 (Ferrero et al., 2016).”
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PremisecitationIntraperitoneal injection of aducanumab into Tg2576 mice demonstrated parenchymal plaques and facilitated their clearance without generating microhemorrhages.
“Intraperitoneal injection of aducanumab into Tg2576 mice was reported to demonstrate parenchymal plaques and facilitate in their clearance without generating microhemorrhages (Dunstan et al., 2011).”
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PremisecitationLocal inflammation, oxidation, excess glutamate, and tau hyperphosphorylation are components of the amyloid cascade.
“Local inflammation, oxidation, production of excess glutamate known as exitootoxicity, and tau hyperphosphorylation are all components of the cascade [Anand et al., 2017].”
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PremisecitationThe FDA has approved donepezil and rivastigmine for mild, moderate, and severe Alzheimer's disease, respectively, while galantamine has been approved for mild and moderate Alzheimer's disease.
“The FDA has approved donepezil and rivastigmine for mild, moderate, and severe AD, respectively, while galantamine has been approved for mild and moderate AD (Rountree et al., 2013).”
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PremisecitationThe formation of amyloid oligomers is primarily responsible for neurotoxicity and commences the amyloid cascade.
“The formation of amyloid oligomers is primarily responsible for neurotoxicity and commences the amyloid cascade.”
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PremisecitationAll BACE inhibitor treatments reduced cerebrospinal fluid Aβ42 in a dose-dependent manner, but without providing any cognitive or functional benefits, and several were inadequately tolerated and ineffective in subjects with prodromal Alzheimer's disease.
“All the treatments reduced cerebrospinal fluid (CSF) Aβ42 in a dose-dependent manner, but without providing any cognitive or functional benefits, and several of them were inadequately tolerated and ineffective in subjects with prodromal AD.”
Quote in the paperSubstantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationGalantamine has a t1/2 of 6 to 8 hours, donepezil has a 70-hour elimination half-life, and rivastigmine has a short elimination half-life but a prolonged duration of effect.
“Galantamine has a t1/2 of 6 to 8 h, while donepezil has a 70-hour elimination half-life. Rivastigmine has a short elimination half-life, but it has a prolonged duration of effect (Atri 2019).”
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PremisecitationA phase 2 research using UB-311, a synthetic peptide utilized as an Aβ vaccine, is now underway in individuals with mild or moderate Alzheimer's disease; it produced a total response rate in phase 1, with swelling at the injection site and agitation as the most common side effects, and patients with mild Alzheimer's disease had a slower rate of cognitive decline.
“A phase 2 research using UB-311, a synthetic peptide utilized as an Aβ vaccine, is now underway in individuals who are experiencing mild or moderate episodes of AD. It produced a total response rate in AD patients during the phase 1 of clinical trial. Swelling at the injection site and agitation were the most common side effects. Patients with mild AD had a slower rate of cognitive decline (Hull”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Hull et al., 2017 source
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PremisecitationDonepezil and galantamine block acetylcholinesterase specifically and reversibly, but rivastigmine is a pseudo-irreversible acetylcholinesterase and butyrylcholinesterase inhibitor.
“Donepezil and galantamine are known to block acetylcholinesterase specifically and reversibly, but rivastigmine is a “pseudo-irreversible” acetylcholinesterase and butyrylcholinesterase inhibitor.”
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PremisecitationKLVFF is a peptide sequence that mimics the hydrophobic center region of Aβ and eventually replaces natural polypeptides; it is resistant to proteolytic degradation and can break down oligomerics to a limited level.
“Another promising treatment is KLVFF, a peptide sequence that mimics the hydrophobic center region of the Aβ and eventually replaces natural polypeptides. The KLVFF compound, which is resistant to proteolytic degradation and can also break down oligomerics to a limited level, is the final compound, can also break down oligomerics to a minor amount. (Stark et al., 2017).”
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PremisecitationClioquinol chelates metal ions, decreasing Aβ aggregation; it can chelate metal ions from metal-Aβ species into CQ-Cu(II) or CQ-Zn(II) complexes in a 2:1 ratio, preventing metal ions from adhering to Aβ and dispersing brain aggregates in vitro.
“Metal ions can be chelated with CQ, decreasing Aβ aggregation. It also has the capability to chelate metal ions from metal–Aβ species into CQ–Cu(II) or CQ–Zn(II) complexes in a 2:1 ratio, preventing metal ions from adhering to Ab and dispersing brain aggregates in vitro [Ferrada et al., 2007].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Ferrada et al., 2007
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PremisecitationMemantine is a non-competitive NMDA receptor antagonist that counteracts the negative effects of high glutamate concentrations in the brain.
“Memantine is known to be a non-competitive NMDA receptor antagonist that counteracts the negative effects of high glutamate concentrations in the brain (Yiannopoulou et al., 2013).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Yiannopoulou et al., 2013 source
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PremisecitationElenbecestat (E2609) and umibecestat (CNP520) are two agents in different phases of clinical trials.
“Elenbecestat (E2609) and umibecestat (CNP520) are the two agents which are in different phases of clinical trials (Cummings et al., 2019).”
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PremisecitationThe lanabecestat phase 3 investigation was halted due to a lack of efficacy, and the verubecestat and atabecestat trials were halted owing to inefficacy and safety concerns, respectively.
“The lanabecestat phase 3 investigation was halted due to a lack of efficacy, and the verubecestat and atabecestat trials were halted as well owing to inefficacy and safety concerns, respectively.”
Quote in the paperSubstantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe iron chelator deferiprone (DFP, 3-hydroxy-1,2-dimethylpyridin-4(1H)-one) is known to treat thalassaemia.
“The iron chelator deferiprone (DFP, 3-hydroxy-1,2-dimethylpyridin-4(1H)-one) is known to treat thalassaemia (Telpoukhovskaia et al., 2013).”
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PremisecitationCrenezumab, gantenerumab, and solanezumab are major therapies enrolled for preclinical studies or for at-risk populations, and are also studied in prodromal and very mild Alzheimer's disease patients.
“Crenezumab, gantenerumab, and solanezumab are the major therapies that are enrolled for preclinical studies or for at-risk populations, while crenezumab, gantenerumab, and solanezumab are the drugs that are for studies in prodromal and very mild AD patients (Yang et al., 2019).”
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PremisecitationAn ideal metal chelator for Alzheimer's disease should meet essential qualities including moderate binding for metals, effective transit through biological membranes (particularly the blood-brain barrier), and thereby lower toxicity.
“A metal chelator as an ideal drug for AD should meet essential qualities including moderate binding for metals, effective transit through biological membranes (particularly the BBB) and thereby lower toxicity (Bendova et al., 2010).”
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PremisecitationClioquinol indicated promising results in a phase IIa clinical trial in Alzheimer's patients and slowing cognitive decline.
“CQ indicated promising results in a phase IIa clinical trial in Alzheimer's patients and slowing cognitive decline [Ritchie et al., 2003].”
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PremisecitationScyllo-inositol is an Aβ42 aggregation inhibitor that was studied in Alzheimer's disease subjects (ELND005); a phase 2 clinical study found no confirmation of ELND005's clinical benefit and the study was stopped due to severe toxicity concerns.
“The oral drug, scyllo-inositol is a Aβ42 aggregation inhibitor that was studied in AD subjects (ELND005). A clinical study (phase 2) in patients with AD found no confirmation of ELND005′s clinical benefit, and the study was stopped due to severe toxicity concerns (Salloway et al., 2011).”
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May combine two claims.
PremisecitationMemantine can be used in conjunction with an acetylcholinesterase inhibitor because their modes of action are complementary; the combinatorial therapy is usually beneficial to patients, with cumulative results and no rise in side effects.
“Memantine can be used in conjunction with an AChEI because their modes of action are complimentary. The said combinatorial therapy is usually beneficial to patients, with cumulative results and no rise in side effects (Kishita et al., 2020).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Kishita et al., 2020 source
Not checked in the free run.
May combine two claims.
PremisecitationAPH-1105 is an intranasal therapy for mild to moderate Alzheimer's disease, while ID1201 also activates α-secretase and is studied in subjects with mild Alzheimer's disease.
“APH-1105 is an intranasal therapy for mild to moderate AD while ID1201 also activates α -secretase and is studied in subjects with mild AD (Cho et al., 2014).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Cho et al., 2014 source
Not checked in the free run.
May combine two claims.
PremisecitationPassive antibody immunotherapy using monoclonal antibodies is the most efficient and prospective class; its chief disadvantages are cerebral microhemorrhages and vasogenic edema.
“The most efficient and prospective class is passive Ab immunotherapy using mAbs. The chief disadvantages of this class of medicines are cerebral microhemorrhages and vasogenic edema (Yiannopoulou et al., 2013).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Yiannopoulou et al., 2013 source
Not checked in the free run.
May combine two claims.
PremisecitationABvac40 is being assessed as the first active vaccine; in a phase 1 trial in Alzheimer's disease patients aged 50 to 85 years, there was no evidence of incident vasogenic edema or microhemorrhages, and antibodies specific to Aβ40 were generated in 92% who had ABvac40 injections.
“ABvac40 is being assessed as the first active vaccine. AD Patients with aged 50 to 85 years old participated in a phase one trial. There was no evidence of incident vasogenic edema or microhemorrhages. Antibodies specific to Aβ40 were generated in 92 % who had ABvac40 injections (Lopez et al., 2019).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Lopez et al., 2019 source
Not checked in the free run.
May combine two claims.
PremisecitationEtazolate (EHT0202) is an α-secretase modulator that acts as a selective GABA receptor modulator and was reported to have a safety profile with good tolerance in Alzheimer's disease patients.
“Etazolate (EHT0202) is listed as another α-secretase modulators which acts as a selective GABA receptor modulator. The agent was reported to have a safety profile with a good tolerance in AD patients (Vellas et al., 2011).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Vellas et al., 2011 source
Not checked in the free run.
May combine two claims.
PremisecitationPreliminary results from the BAN2401 studies revealed a treatment-afflicted effect of a reduction in cerebral amyloid load in Alzheimer's disease patients, together with a slowing of cognitive deterioration.
“The preliminary results from the BAN2401 studies revealed a treatment-afflicted effect of a reduction in cerebral amyloid load in AD patients, together with a slowing of cognitive deterioration (Panza et al., 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Panza et al., 2018 source
Not checked in the free run.
May combine two claims.
PremisecitationAnti-amyloid therapy acts by two major mechanisms: either by reducing Aβ42 production and Aβ-plaque burden or by promoting Aβ clearance.
“To circumvent the said condition, anti-amyloid therapy acts by two major mechanisms either by reducing of Aβ42 production and Aβ-plaque burden or by promoting Aβ clearance (Atri 2019).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Atri 2019 source
Not checked in the free run.
May combine two claims.
PremisecitationRivastigmine forms a covalent carbamoyl-AChE complex after reacting with the crucial active site serine, preventing it from catalyzing the synthesis of acetylcholine.
“The “pseudo irreversible” acetylcholinesterase activity of rivastigmine refers to the fact that it forms a covalent carbamoyl-AChE complex after reacting with the crucial active site serine, preventing it from catalyzing the synthesis of acetylcholine.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Atri 2019 source
Not checked in the free run.
May combine two claims.
PremisecitationFree radicals can be scavenged by the Zn(II)-curcumin complex and the Cu(II)-curcumin complex; the Cu(II)-curcumin complex had a better potential to scavenge free radicals compared to curcumin and the Zn(II)-curcumin combination.
“Free radicals can also be scavenged by the Zn (II)–curcumin complex and the Cu(II)–curcumin complex. Furthermore, as compared to curcumin and Zn (II)–curcumin combination, Cu(II)–curcumin complex had a better potential to scavenge free radicals. The findings could help researchers better understand the role of curcumin in the treatment of AD (Krishnankutty et al., 2003).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Krishnankutty et al., 2003
Not checked in the free run.
May combine two claims.
PremisecitationEven though deferiprone has a C log P value of 1.4, which is too negligible to cross the blood-brain barrier, its low molecular weight and suitable structure render it relatively easy to optimize, and it has been used as a lead compound in the development of multi-target directed ligands for the treatment of Alzheimer's disease.
“Even though DFP has a C log P value of 1.4, which is too negligible to cross the BBB, its low molecular weight as well as its suitable structure render it relatively easy to optimize, and it has been used as a lead compound in the development of multi-target directed ligands (MTDL) for the treatment of AD (Santos 2008).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Santos 2008 source
Not checked in the free run.
May combine two claims.
InterpretationreasoningEVP-6124 enhances cholinergic neurotransmission, which increases cognitive abilities.
“It enhances cholinergic neurotransmission, which increases cognitive abilities.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationResearchers have developed and tested a variety of therapies for Alzheimer's disease, including anti-amyloid and anti-tau interventions, neurotransmitter mutations, anti-neuroinflammation and neuroprotection interventions, cognitive enhancement, and behavioral submission.
“Researchers have developed and tested a variety of therapies, including anti-amyloid and anti-tau interventions, neurotransmitter mutations, anti- neuroinflammation and neuroprotection interventions, cognitive enhancement, and behavioral submission (Huang et al., 2020)”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Huang et al., 2020 source
Not checked in the free run.
May combine two claims.
PremisecitationGV-971 (sodium oligo-mannurarate) binds to several amyloid sites, destabilizes and prevents Aβ synthesis, and increases the elimination of Aβ.
“GV-971 (sodium oligo-mannurarate) binds to several amyloid sites, further destabilizes, and prevents Aβ synthesis, and increases the elimination of Aβ (Wang et al., 2019).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Wang et al., 2019 source
Not checked in the free run.
May combine two claims.
PremisecitationEVP-6124 is an antagonist of the 5-HT3 receptor and an agonist of the α7 nicotinic acetylcholine receptor.
“EVP-6124, an antagonist of 5-HT3 receptor and a agonist of 7 nicotinic acetylcholine receptor a has a central role in regulating the release of various neurotransmitters (Ahmed et al., 2019).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Ahmed et al., 2019 source
Not checked in the free run.
Probably not a substantial claim: may not pass S2 (checkable), S4 (based). May combine two claims.
Interpretationnone givenThe results suggest that the drugs under clinical trials may open new pathways for the effective treatment of patients with Alzheimer's disease while improving their quality of life.
“The results suggest that the drugs under clinical trials may open new pathways for the effective treatment of patients with Alzheimer's disease while improving their quality of life.”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationNilvadipine, a dihydropyridine calcium channel blocker, has the capacity to lower Aβ production and increase Aβ clearance.
“The dihydropyridine calcium channel blocker nilvadipine with a capacity of lowering Aβ production and increasing clearance Aβ was evaluated for neuroprotective and anti-inflammatory properties (Lawlor et al., 2018).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Lawlor et al., 2018 source
Not checked in the free run.
The paper relies on this without support.
Extracellular amyloid plaques and intracellular Tau neurofibrillary tangles are the most common histopathologic lesions in Alzheimer's disease.
“Extracellular amyloid plaques and intracellular Tau neurofibrillary tangles are the most common histopathologic lesions in AD.”
The paper relies on this without support.
Both cholinergic and glutamatergic neurochemical systems are involved in the genesis of Alzheimer's disease.
“There is pertinent evidence to support the fact that that both cholinergic and glutamatergic neurochemical systems are involved in the genesis of AD.”
The paper relies on this without support.
Acetylcholine concentration and function are reduced in the brains of Alzheimer's disease sufferers.
“Both concentration and function are reduced in brains of AD sufferers.”
The paper relies on this without support.
The cholinergic theory of Alzheimer's disease is supported by impairment and other presynaptic cholinergic limitations, such as loss of cholinergic neural network and diminished acetylcholinesterase activity.
“The cholinergic theory of AD is supported by this impairment and other presynaptic cholinergic limitations, such as loss of cholinergic neural network and diminished acetylcholinesterase activity.”
The paper relies on this without support.
Acetylcholinesterase action is enhanced in Alzheimer's disease patients, which contributes to higher acetylcholine breakdown and decreased acetylcholine concentrations in the brain.
“The action of acetylcholinesterase is enhanced in AD patients, which contributes to higher acetylcholine breakdown and decreased acetylcholine concentrations in the brain.”
The paper relies on this without support.
Currently available medications for Alzheimer's disease treatment, such as cholinesterase inhibitors and an antagonist of the N-methyl-d-aspartate receptor, can temporarily reduce dementia symptoms but not stop or reverse disease development.
“Currently available medications for Alzheimer's disease treatment, such as cholinesterase inhibitors and an antagonist of the N-methyl-d-aspartate receptor, can temporarily reduce dementia symptoms but not stop or reverse disease development.”
The paper relies on this without support.
Currently available treatments for Alzheimer's disease, such as cholinesterase inhibitors and the N-methyl-d-aspartate receptor antagonist, can temporarily reduce psychiatric symptoms but cannot stop or cure the progression of the disease.
“Currently available treatments for AD, such as cholinesterase inhibitors and the N-methyl-d-aspartate receptor antagonist, can temporarily reduce psychiatric symptoms but not stop or cure the progression of the disease.”
The paper relies on this without support.
Many international pharmaceutical companies have conducted numerous clinical trials of amyloid-cleansing treatments for Alzheimer's disease, but none have been successful.
“From an amyloid perspective, many international pharmaceutical companies have conducted numerous clinical trials in the treatment based on amyloid cleansing, but none have been successful.”
The paper relies on this without support.
A high percentage of Alzheimer's disease clinical trials on therapeutics have failed.
“Considering the recent knowledge of a high percentage of failed AD clinical trials on therapeutics, more recent trials appear to be bolstered by the convergence of advances in AD biomarkers, the positioning of a single primary outcome and fabrication of novel trial designs.”
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?
Current treatments for Alzheimer's disease offer limited symptom relief, especially in early to moderate stages, but do not halt disease progression or address underlying neurodegeneration.
“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 [8]
The Introduction and Clinical trials of novel drugs for AD sections say cholinesterase inhibitors and memantine provide temporary symptom relief without stopping disease progression. The stage qualifier is not supported for both drugs: the Conventional pharmacotherapy section describes cholinesterase inhibitors for mild-to-moderate AD but memantine for moderate-to-severe AD. The paper’s distinction between symptomatic and progression-targeting treatments supports the point that these drugs do not address underlying neurodegeneration. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCholinesterase inhibitors rivastigmine, donepezil, galantamine, and tacrine work by increasing acetylcholine levels, improving cognition and memory, though they do not alter disease progression.
“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 [8]
The Conventional pharmacotherapy section identifies all four drugs as acetylcholinesterase inhibitors and says this class raises brain acetylcholine levels. The Introduction describes these treatments as symptomatic and distinguishes them from therapies that slow or stop progression. Our copy does not specifically say that these four drugs improve cognition and memory, so that part of the claim remains unsupported. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Acetylcholinesterase activity is described as both diminished and enhanced
MajorThe introduction lists diminished acetylcholinesterase activity among the impairments in AD, but the pharmacotherapy section says its action is enhanced in AD patients.
“The cholinergic theory of AD is supported by this impairment and other presynaptic cholinergic limitations, such as loss of cholinergic neural network and diminished acetylcholinesterase activity.”
“The action of acetylcholinesterase is enhanced in AD patients, which contributes to higher acetylcholine breakdown and decreased acetylcholine concentrations in the brain.”
A 2004 reference is cited for findings from a 2013 trial
MinorThe paper says the NILVAD trial took place in 2013 but attributes its reported outcomes to a Bishop et al. publication dated 2004. That publication cannot report outcomes from the later trial.
“The NILVAD trial, which took place in 2013, examined the effectiveness of nilvadipine in people with AD. ADAS-Cog was the main outcome measure, but there was no difference in the primary or secondary end point measures according to a published report (Bishop et al., 2004).”
“Bishop G.M. Robinson S.R. Physiological roles of amyloid-beta and implications for its removal in Alzheimer's disease Drugs Aging 21 10 2004 621 630”
Elenbecestat trial is both terminated and expected to continue
MinorTable 2 marks the elenbecestat phase 3 trial as terminated, while the subsequent discussion says the elenbecestat trials are expected to run until December 2023.
“| Elenbecestat (E2609)/Phase 3 | NCT02956486 | “A 24-Month Study to Evaluate the Efficacy and Safety of Elenbecestat (E2609) in Participants With Early Alzheimer's Disease” | BACE inhibitor | Terminated |”
“The said trials are expected to run until December 2023.”
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Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
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Current and Future Treatments in Alzheimer Disease: An Update
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“AChEIs action on the gastro-intestinal tract (git) causes the most common side effects, which include diarrhea, nausea, and vomiting (Yiannopoulou et al., 2020).”
The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives
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“Further another theory suggests the mitochondrial dysfunction hypothesis for AD pathogenesis posits that amyloidosis, cell cycle re-entry, and tau phosphorylation are all caused by mitochondrial failure in the AD brain (Swerdlow et al., 2014).”
Alzheimer's disease drug development pipeline: 2019
Cummings, J., Lee, G., Ritter, A., Sabbagh, M., & Zhong, K. (2019) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2019.05.008 · Cited by 762 · cited 1× · see citing works
“Elenbecestat (E2609) and umibecestat (CNP520) are the two agents which are in different phases of clinical trials (Cummings et al., 2019).”
Clinical trials of new drugs for Alzheimer disease
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“Researchers have developed and tested a variety of therapies, including antiamyloid and anti-tau interventions, neurotransmitter mutations, anti- neuroinflammation and neuroprotection interventions, cognitive enhancement, and behavioral submission (Huang et al., 2020) An array of novel therapies is underway in various…”
Current and future treatments for Alzheimer's disease
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“…proposes that A b generation in the brain propagates a series of pathophysiologic events that culminate in the clinical manifestation of AD The formation of amyloid oligomers, which eventually trigger the amyloid cascade, is primarily responsible for neurotox-icity (Yiannopoulou et al., 2013).”
InfluentialAlzheimer’s Disease: Past, Present, and Future
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A phase III randomized trial of gantenerumab in prodromal Alzheimer’s disease
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A phase II trial of huperzine A in mild to moderate Alzheimer disease
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“…of skin cancer, while avagacestat was linked to a higher percentage of cognitive decline as well as adverse dose-limiting effects such as the incidence of skin cancer while tarenflurbil had little blood–brain barrier penetration (Doody et al., 2013; Coric et al., 2015; Muntimadugu et al., 2016).”
Metal ions, Alzheimer's disease and chelation therapy
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Preliminary Results of a Trial of Atabecestat in Preclinical Alzheimer’s Disease
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Nilvadipine in mild to moderate Alzheimer disease: A randomised controlled trial
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“The dihydropyridine calcium channel blocker nilvadipine with a capacity of lowering Ab production and increasing clearance Ab was evaluated for neuroprotective and anti-inflammatory properties (Lawlor et al., 2018).”
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The present and future of pharmacotherapy of Alzheimer's disease: a comprehensive review
Anand, A., Patience, A. A., Sharma, N., & Khurana, N. (2017) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2017.09.043 · Cited by 174 · cited 1× · see citing works
“Local inflam-mation, oxidation, production of excess glutamate known as exi-tootoxicity, and tau hyperphosphorylation are all components of H.A. Alhazmi and M. Albratty Saudi Pharmaceutical Journal 30 (2022) 1755–1764 the cascade [ Anand et al., 2017 ].”
Huang, M., Jiang, X., Liang, Y., Liu, Q., Chen, S., & Guo, Y. C. (2017) · Experimental Gerontology · doi:10.1016/j.exger.2017.02.004 · Cited by 171 · see citing works
Biomarker validation of a cued recall memory deficit in prodromal Alzheimer disease
Wagner, M., Wolf, S., Reischies, F. M., Daerr, M., Wolfsgruber, S., Jessen, F., Popp, J., Maier, W., Hüll, M., Frölich, L., et al. (2012) · Neurology · doi:10.1212/wnl.0b013e318245f447 · Cited by 170 · see citing works
Tchantchou, F., Lacor, P. N., Cao, Z., Lao, L., Hou, Y., Cui, C., Klein, W. L., & Luo, Y. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1189 · Cited by 163 · see citing works
Genistein ameliorates β-amyloid peptide (25–35)-induced hippocampal neuronal apoptosis
Zeng, H., Chen, Q., & Zhao, B. (2003) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2003.10.018 · Cited by 155 · cited 1× · see citing works
“Zeng et al., 2004 Crocin Crocus sativus It worked by reducing stress-related oxidative damage to the brain and other organs in the tested rat model.”
Hoi, C. P., Ho, Y. P., Baum, L., & Chow, A. H. L. (2010) · Phytotherapy Research · doi:10.1002/ptr.3178 · Cited by 154 · see citing works
Lautenschläger, M., Sendker, J., Hüwel, S., et al. (2014) · Phytomedicine · doi:10.1016/j.phymed.2014.10.009 · Cited by 139 · see citing works
BILOBALIDE AND NEUROPROTECTION
DeFeudis, F. V. (2002) · Pharmacological Research · doi:10.1016/s1043-6618(02)00233-5 · Cited by 136 · see citing works
EHT0202 in Alzheimers Disease: A 3-Month, Randomized, Placebo- Controlled, Double-Blind Study
Vellas, B., Sol, O., J. Snyder, P., Ousset, P.-J., Haddad, R., Maurin, M., Lemarie, J.-C., Desire, L., & P. Pando, M. (2011) · Current Alzheimer Research · doi:10.2174/156720511795256053 · Cited by 133 · cited 2× · see citing works
“The agent was reported to have a safety profile with a good tolerance in AD patients (Vellas et al., 2011).”
Ansari, N., & Khodagholi, F. (2013) · Current Neuropharmacology · doi:10.2174/1570159x11311040005 · Cited by 131 · cited 1× · see citing works
“Numerous studies have been conducted to look at the benefits of complete extraction of plants on AD, as well as to identify the functional factors involved in achieving the necessary therapeutic benefits (Ansari et al., 2013).”
The discovery of suvorexant, the first orexin receptor drug for insomnia
Coleman, P. J., Gotter, A. L., Herring, W. J., Winrow, C. J., & Renger, J. J. (2017) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-010716-104837 · Cited by 128 · see citing works
Memantine: targeting glutamate excitotoxicity in Alzheimer’s disease and other dementias
Molinuevo, J. L., Lladó, A., & Rami, L. (2005) · American Journal of Alzheimer's Disease & Other Dementias® · doi:10.1177/153331750502000206 · Cited by 125 · cited 1× · see citing works
“Anxiety, emesis, urinary tract infections, and increased sweating were among the less commonly reported symptoms ( Molinuevo et al., 2005 ).”
Bandegi, A. R., Rashidy‐Pour, A., Vafaei, A. A., & Ghadrdoost, B. (2014) · Europe PMC (PubMed Central) · doi:10.5681/apb.2014.073 · Cited by 121 · cited 1× · see citing works
“Bandegi et al., 2014 Trans-crocetin, was observed to pass the BBB and enter the CNS when evaluated in Caco-2 monolayer cell culture, although crocin bioavailability was likely limited after oral treatment.”
Chang, X., Rong, C., Chen, Y., Yang, C., Hu, Q., Mo, Y., Zhang, C., Gu, X., Zhang, L., He, W.-Q., et al. (2015) · Experimental Cell Research · doi:10.1016/j.yexcr.2015.04.004 · Cited by 119 · see citing works
Characterization of biometal profiles in neurological disorders
Pfaender, S., & Grabrucker, A. M. (2014) · Metallomics · doi:10.1039/c4mt00008k · Cited by 117 · see citing works
Lopez Lopez, C., Tariot, P. N., Caputo, A., Langbaum, J. B., Liu, F., Riviere, M., Langlois, C., Rouzade‐Dominguez, M., Zalesak, M., Hendrix, S., et al. (2019) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2019.02.005 · Cited by 116 · cited 2× · see citing works
“Antibodies specific to A b 40 were generated in 92 % who had ABvac40 injections (Lopez et al., 2019).”
InfluentialAbdallah, S. M., Zayed, M. A., & Mohamed, G. G. (2010) · Arabian Journal of Chemistry · doi:10.1016/j.arabjc.2010.02.006 · Cited by 112 · cited 1× · see citing works
“Magnetic and solid reflectance confirmed the geometrical structure of the formed complexes with the metal ions (Abdallah et al., 2010).”
Stabilities of 1,2-dimethyl-3-hydroxy-4-pyridinone chelates of divalent and trivalent metal ions
Clarke, E. T., & Martell, A. E. (1992) · Inorganica Chimica Acta · doi:10.1016/s0020-1693(00)80327-8 · Cited by 109 · cited 1× · see citing works
“It has a strongly positive and significant affinity for metals such as iron, copper, and zinc in its scaffold (Clarke et al., 1992).”
Bihaqi, S. W., Singh, A., & Tiwari, M. (2012) · Indian Journal of Pharmacology · doi:10.4103/0253-7613.100383 · Cited by 108 · see citing works
Pioglitazone for the treatment of Alzheimer’s disease
Galimberti, D., & Scarpini, E. (2017) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2017.1265504 · Cited by 106 · see citing works
Kishita, N., Backhouse, T., & Mioshi, E. (2020) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988719856690 · Cited by 103 · cited 1× · see citing works
“The said combinatorial therapy is usually beneficial to patients, with cumulative results and no rise in side effects (Kishita et al., 2020).”
Effectiveness of antidementia drugs in delaying Alzheimer's disease progression
Rountree, S. D., Atri, A., Lopez, O. L., & Doody, R. S. (2013) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2012.01.002 · Cited by 97 · cited 1× · see citing works
“Acetylcholinesterase inhibitors The FDA has approved donepezil and rivastigmine for mild, moderate, and severe AD, respectively, while galantamine has been approved for mild and moderate AD (Rountree et al., 2013).”
Physiological Roles of Amyloid-?? and Implications for its Removal in Alzheimer???s Disease
Bishop, G. M., & Robinson, S. R. (2004) · Drugs & Aging · doi:10.2165/00002512-200421100-00001 · Cited by 94 · cited 1× · see citing works
“ADAS-Cog was the main outcome measure, but there was no difference in the primary or secondary end point measures according to a published report (Bishop et al., 2004).”
Yang, T., Dang, Y., Ostaszewski, B., Mengel, D., Steffen, V., Rabe, C., Bittner, T., Walsh, D. M., & Selkoe, D. J. (2019) · Annals of Neurology · doi:10.1002/ana.25513 · Cited by 91 · see citing works
Chakravarthi, K., & Avadhani, R. (2013) · Journal of Natural Science Biology and Medicine · doi:10.4103/0976-9668.117025 · Cited by 87 · see citing works
Ferrada, E., Arancibia, V., Bárbara Loeb, L., Norambuena, E., Olea‐Azar, C., & Huidobro-Toro, J. P. (2007) · NeuroToxicology · doi:10.1016/j.neuro.2007.02.004 · Cited by 81 · cited 1× · see citing works
“A b species into CQ–Cu(II) or CQ–Zn(II) complexes in a 2:1 ratio, preventing metal ions from adhering to Ab and dispersing brain aggregates in vitro [Ferrada et al., 2007].”
Olajide, O. J., Yawson, E. O., Gbadamosi, I. T., Arogundade, T. T., Lambe, E., Obasi, K., Lawal, I. T., Ibrahim, A., & Ogunrinola, K. Y. (2017) · Environmental Toxicology and Pharmacology · doi:10.1016/j.etap.2017.02.010 · Cited by 79 · see citing works
Bendova, P., Mackova, E., Haskova, P., Vavrova, A., Jirkovsky, E., Sterba, M., Popelova, O., Kalinowski, D. S., Kovarikova, P., Vavrova, K., et al. (2010) · Chemical Research in Toxicology · doi:10.1021/tx100125t · Cited by 73 · cited 1× · see citing works
“A metal chelator as an ideal drug for AD should meet essential qualities including moderate binding for metals, effective transit through biological membranes (particularly the BBB) and thereby lower toxicity (Bendova et al., 2010).”
Hull, M., Sadowsky, C., Arai, H., Leterme, G. L. P., Holstein, A., Booth, K., Peng, Y., Yoshiyama, T., Suzuki, H., Ketter, N., et al. (2017) · Current Alzheimer Research · doi:10.2174/1567205014666170117101537 · Cited by 65 · cited 1× · see citing works
“Patients with mild AD had a slower rate of cognitive decline (Hull et al., 2017).”
Jeong, E. J., Hwang, L., Lee, M., Lee, K. Y., Ahn, M., & Sung, S. H. (2013) · Food and Chemical Toxicology · doi:10.1016/j.fct.2013.12.003 · Cited by 59 · see citing works
Recent developments on 3-hydroxy-4-pyridinones with respect to their clinical applications
Santos, M. A. (2008) · Coordination Chemistry Reviews · doi:10.1016/j.ccr.2008.01.033 · Cited by 54 · cited 2× · see citing works
“4, which is too negligible to cross the BBB, its low molecular weight as well as its suitable structure render it relatively easy to optimize, and it has been used as a lead compound in the development of multi-target directed ligands (MTDL) for the treatment of AD (Santos 2008).”
InfluentialBis-8-hydroxyquinoline ligands as potential anti-Alzheimer agents
Deraeve, C., Piti, M., Mazarguil, H., & Meunier, B. (2007) · New Journal of Chemistry · doi:10.1039/b616085a · Cited by 53 · see citing works
Herring, W. J., Roth, T., Krystal, A. D., & Michelson, D. (2019) · Journal of Sleep Research · doi:10.1111/jsr.12782 · Cited by 53 · see citing works
Synthesis, Characterization, and Antitumour Studies of Metal Chelates of Some Synthetic Curcuminoids
KRISHNANKUTTY, K., & John, V. T. (2003) · Synthesis and Reactivity in Inorganic and Metal-Organic Chemistry · doi:10.1081/sim-120017791 · Cited by 50 · cited 1× · see citing works
“The findings could help researchers better understand the role of curcumin in the treatment of AD (Krishnankutty et al., 2003).”
Panza, F., Seripa, D., Lozupone, M., Solfrizzi, V., Imbimbo, B. P., Barulli, M. R., Tortelli, R., Capozzo, R., Bisceglia, P., Dimitri, A., et al. (2018) · Expert Opinion on Biological Therapy · doi:10.1080/14712598.2018.1389885 · Cited by 41 · cited 1× · see citing works
“The preliminary results from the BAN2401 studies revealed a treatment-afflicted effect of a reduction in cerebral amyloid load in AD patients, together with a slowing of cognitive deterioration (Panza et al., 2018).”
Telpoukhovskaia, M. A., Patrick, B. O., Rodríguez‐Rodríguez, C., & Orvig, C. (2013) · Molecular BioSystems · doi:10.1039/c3mb25600f · Cited by 33 · cited 1× · see citing works
“Deferiprone (DFP) and its derivatives The iron chelator deferiprone (DFP, 3-hydroxy-1,2-dimethylpyr idin-4(1H)-one) is known to treat thalassaemia (Telpoukhovskaia et al., 2013).”
Catalpol provides protective effects against cerebral ischaemia/reperfusion injury in gerbils
Liu, Y., Li, P., Suo, J.-J., Sun, Y., Zhang, B., Lu, H., Zhu, H., & Zhang, G. (2014) · Journal of Pharmacy and Pharmacology · doi:10.1111/jphp.12261 · Cited by 32 · cited 1× · see citing works
“( Liu et al., 2014d ).”
Murakami, K., & Irie, K. (2019) · Molecules · doi:10.3390/molecules24112125 · Cited by 31 · see citing works
on behalf of the Registry of Dementias of Girona Study Group (ReDeGi Study Group), Calvó-Perxas, L., Turró-Garriga, O., Vilalta-Franch, J., Lozano-Gallego, M., de Eugenio, R., Márquez, F., Carmona, O., Gich, J., Manzano, A., et al. (2017) · Drugs & Aging · doi:10.1007/s40266-017-0446-x · Cited by 30 · see citing works
Ahmed, M., Malik, M., Teselink, J., Lanctôt, K. L., & Herrmann, N. (2019) · Drugs & Aging · doi:10.1007/s40266-019-00668-7 · Cited by 29 · cited 1× · see citing works
“EVP-6124, an antagonist of 5-HT3 receptor and a agonist of 7 nicotinic acetylcholine receptor a has a central role in regulating the release of various neurotransmitters (Ahmed et al., 2019).”
Liu, D., Zhang, H., GU, W., Liu, Y., & Zhang, M. (2014) · Molecular Medicine Reports · doi:10.3892/mmr.2014.1958 · Cited by 28 · see citing works
He, Q. P., Sun, J., Wang, Q., et al. (2014) · Journal of the Chinese Medical Association · doi:10.1016/j.jcma.2014.01.001 · Cited by 27 · see citing works
Amyloid binding properties of curcumin analogues in Alzheimer’s disease postmortem brain tissue
Veldman, E. R., Jia, Z., Halldin, C., & Svedberg, M. M. (2016) · Neuroscience Letters · doi:10.1016/j.neulet.2016.07.045 · Cited by 27 · cited 1× · see citing works
“…combination, Cu(II)–cur-H By lowering oxidative damage, PC12 cells were found to be protected from A b induced neurotoxicity. and tau hyperphosphorylation with a dose of 5–10 l M. Veldman et al., 2016 In an Alzheimer’s transgenic mouse model, curcumin has been reported to reverse amyloid etiology.”
Zhou, H., Liu, J., Ren, L., et al. (2014) · PubMed · Cited by 20 · see citing works
Zhou, H., Liu, J., Ren, L., Liu, W., Xing, Q., Men, L., Song, G., & Du, J. (2014) · Chinese Medical Journal · doi:10.3760/cma.j.issn.0366-6999.20132137 · Cited by 20 · see citing works
Genistein Inhibited Amyloid-β induced Inflammatory Damage in C6 Glial Cells
Zhao, X., Yuan, L., Yu, H., Xi, Y., Ma, W., Zhou, X. J., Ding, J., & Xiao, R. (2014) · Archives of Medical Research · doi:10.1016/j.arcmed.2013.12.008 · Cited by 17 · see citing works
Peptidomimetics That Inhibit and Partially Reverse the Aggregation of Aβ<sub>1–42</sub>
Stark, T., Lieblein, T., Pohland, M., Kalden, E., Freund, P., Zangl, R., Grewal, R., Heilemann, M., Eckert, G. P., Morgner, N., et al. (2017) · Biochemistry · doi:10.1021/acs.biochem.7b00223 · Cited by 17 · cited 1× · see citing works
“(Stark et al., 2017).”
Cho, W.-H., Park, J.-C., Kim, D.-H., Kim, M.-S., Lee, S.-Y., Park, H., Kang, J.-H., Yeon, S.-W., & Han, J.-S. (2014) · Neuroscience Letters · doi:10.1016/j.neulet.2014.09.036 · Cited by 13 · see citing works
Dunstan, R. W., Bussière, T., Engber, T., et al. (2011) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2011.05.2025 · Cited by 2 · see citing works
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Hossain, M. S., & Hussain, M. H. (2025) · Pharmacology Research & Perspectives · doi:10.1002/prp2.70131 · Cited by 94 · see citing works
“While there is no cure for AD, many drugs can help enhance cognitive function, reduce clinical deterioration, and relieve symptoms like memory loss [98–100].”
Nagori, K., Nakhate, K. T., Yadav, K., Ajazuddin, & Pradhan, M. (2023) · Future Pharmacology · doi:10.3390/futurepharmacol3040053 · Cited by 61 · see citing works
Alkhalifa, A. E., Mokhlf, A. A., Ali, H., Al-Ghraiybah, N. F., & Syropoulou, V. (2025) · Journal of Personalized Medicine · doi:10.3390/jpm15090437 · Cited by 63 · see citing works
“These include acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine) and the NMDA receptor antagonist memantine [19].”
Pirhaghi, M., Mamashli, F., Moosavi-Movahedi, F., Arghavani, P., Amiri, A., Davaeil, B., Mohammad-Zaheri, M., Mousavi-Jarrahi, Z., Sharma, D., Langel, Ü., et al. (2024) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.3c01167 · Cited by 46 · see citing works
Puranik, N., & Song, M. (2025) · Neurology International · doi:10.3390/neurolint17020026 · Cited by 46 · see citing works
“Pharmaceuticals that may slow down the clinical decline of AD patients and treatments that may temporarily relieve some of the disease’s related symptoms are the two types of medications approved by the US Food and Drug Administration (FDA) [71].”
Unveiling the impact of aging on BBB and Alzheimer's disease: Factors and therapeutic implications
Jha, N. K., Jha, N. K., Nuli, M. V., Gupta, S. K., Kanna, S., Gahtani, R. M., Hani, U., Singh, A. K., Abomughaid, M. M., Abomughayedh, A. M., et al. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102224 · Cited by 42 · see citing works
Newer Therapeutic Approaches in Treating Alzheimer’s Disease: A Comprehensive Review
Sree, R. R., Kalyan, M., Anand, N., Mani, S., Gorantla, V. R., Sakharkar, M. K., Song, B., & Chidambaram, S. B. (2025) · ACS Omega · doi:10.1021/acsomega.4c05527 · Cited by 45 · see citing works
Research progress of PROTACs for neurodegenerative diseases therapy
Cai, Z., Yang, Z., Li, H., & Fang, Y. (2024) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2024.107386 · Cited by 35 · see citing works
Harnessing the potential of mesenchymal stem cells–derived exosomes in degenerative diseases
Liao, H., Yang, Y., Liu, Y., Tseng, H., Huo, T., Chiou, S., & Chang, C.-H. (2024) · Regenerative Therapy · doi:10.1016/j.reth.2024.08.001 · Cited by 31 · see citing works
“The FDA has approved several medications for AD treatment, including cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) and mem-antine, an NMDA receptor modulator [109].”
BackgroundAcetylcholinesterase: Structure, dynamics, and interactions with organophosphorus compounds
Hung, L., Sanbonmatsu, K. Y., Williams, R. F., et al. (2025) · Protein Science · doi:10.1002/pro.70297 · Cited by 30 · see citing works
“Several FDA-approved drugs target AChE in a reversible manner, as a therapeutic for Alzheimer ’ s disease (Alhazmi & Albratty, 2022), including donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne), and as of July 2024, Zunveyl, which is a prodrug of galantamine (Baakman et al., 2016;…”
Class balancing diversity multimodal ensemble for Alzheimer’s disease diagnosis and early detection
Francesconi, A., di Biase, L., Cappetta, D., Rebecchi, F., Soda, P., Sicilia, R., & Guarrasi, V. (2025) · Computerized Medical Imaging and Graphics · doi:10.1016/j.compmedimag.2025.102529 · Cited by 30 · see citing works
“Thus, developing strategies for detection of AD at early stages, prior to the manifestation of clinical symptoms, is crucial for timely treatment and progression delay [6].”
ALNasser, M. N., Alboraiy, G. M., Alsowig, E. M., & Alqattan, F. M. (2025) · Brain Sciences · doi:10.3390/brainsci15020215 · Cited by 35 · see citing works
Exploring Alzheimer's disease treatment: Established therapies and novel strategies for future care
Soni, U., Singh, K., Jain, D., & Pujari, R. (2025) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2025.177520 · Cited by 26 · see citing works
Neuroprotective Effect of α-Lipoic Acid against Aβ25–35-Induced Damage in BV2 Cells
Pei, X., Hu, F., Hu, Z., Luo, F., Li, X., Xing, S., Sun, L., & Long, D. (2023) · Molecules · doi:10.3390/molecules28031168 · Cited by 26 · see citing works
“Alzheimer’s disease (AD) is the most common neurodegenerative disease and seems to be one of the major healthcare challenges of the present century [1].”
BackgroundComputational investigation of quinazoline derivatives as Keap1 inhibitors for Alzheimer's disease
Gote, S. A., Thapa, S., Dubey, S., Nargund, S. L., & Biradar, M. S. (2023) · Informatics in Medicine Unlocked · doi:10.1016/j.imu.2023.101334 · Cited by 22 · see citing works
Research Progress on the Pathogenesis, Diagnosis, and Drug Therapy of Alzheimer’s Disease
Yang, Y., & Qiu, L. (2024) · Brain Sciences · doi:10.3390/brainsci14060590 · Cited by 22 · see citing works
“…level of interaction between these hypotheses [17,18]. noninvasive neuroimaging positron invasive high distinguish been a AD or methods that can completely reverse AD, and the main , antibodies Aducanumab and Lecanemab have been approved by the FDA for marketing through clinical trials [24,25].”
BackgroundHussain, F., Tahir, A., Rehman, H. M., et al. (2025) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2025.117327 · Cited by 21 · see citing works
Gut instincts: Unveiling the connection between gut microbiota and Alzheimer's disease.
Peddinti, V., Avaghade, M. M., Suthar, S., Rout, B., Gomte, S. S., Agnihotri, T., & Jain, A. (2024) · Clinical Nutrition ESPEN · doi:10.1016/j.clnesp.2024.02.019 · Cited by 20 · see citing works
Protein aggregation and neurodegenerative disease: Structural outlook for the novel therapeutics
Arar, S. H., Haque, M. A., & Kayed, R. (2023) · Proteins Structure Function and Bioinformatics · doi:10.1002/prot.26561 · Cited by 19 · see citing works
Ribeiro, J., Lopes, I., & Gomes, A. C. (2023) · Molecules · doi:10.3390/molecules28166015 · Cited by 19 · see citing works
Zellmer, J. C., Tarantino, M. B., Kim, M. M., Lomoio, S., Maesako, M., Hajnóczky, G., & Bhattacharyya, R. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14417 · Cited by 20 · see citing works
“47,48 Rivastigmine modulates MAM stabilization by regulating the levels of MAM-anchoring mitofusin-2 (MFN2).”
Antisense therapy: a potential breakthrough in the treatment of neurodegenerative diseases
Romanò, R., & Bucci, C. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.385285 · Cited by 20 · see citing works
“Another example is AD, for which the FDA approved two categories of drugs: those that slow down the clinical decline in patients and those that may alleviate some of the symptoms (Alhazmi and Albratty, 2022).”
BackgroundBhatt, A., Bhardwaj, H., & Srivastava, P. (2024) · Neuroscience · doi:10.1016/j.neuroscience.2024.07.019 · Cited by 19 · see citing works
Ghallab, D. S., & Ghareeb, D. A. (2024) · Scientia Horticulturae · doi:10.1016/j.scienta.2024.113563 · Cited by 16 · see citing works
Drugs repurposing in the experimental models of Alzheimer’s disease
Joodi, S. A., Ibrahim, W. W., & Khattab, M. M. (2025) · Inflammopharmacology · doi:10.1007/s10787-024-01608-7 · Cited by 14 · see citing works
Alzheimer’s disease and immunotherapy
Qin, W., Pang, Y., Nie, S., Quan, M., & Jia, J. (2024) · Current Medicine · doi:10.1007/s44194-024-00035-8 · Cited by 15 · see citing works
“The third-generation agents also prompted safety concerns (Alhazmi and Albratty 2022).”
Shoukat, S., Zia, M. A., Uzair, M., Alsubki, R. A., Sajid, K., Shoukat, S., Attia, K. A., Fiaz, S., Ali, G. M., Kimiko, I., et al. (2023) · Molecular Biology Reports · doi:10.1007/s11033-023-08674-0 · Cited by 13 · see citing works
Therapeutic potential of fucoidan in central nervous system disorders: A systematic review
Yang, J., Zhao, H., & Qu, S. (2024) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2024.134397 · Cited by 13 · see citing works
Kushwaha, N., Panjwani, D., Patel, S., Ahlawat, P., Yadav, M. R., & Patel, A. (2024) · Journal of drug targeting · doi:10.1080/1061186x.2024.2417012 · Cited by 16 · see citing works
“…potential therapeutic agents. these nanoplatforms may protect therapeutic agents from degradation, enhance their blood-brain barrier permeability, and enable precise accumulation in affected brain areas [3,4]. chimeric antigen receptor therapy, first proposed in 1989, has been FDA-approved in 2017.”
Ramírez-Cruz, A., Gómez‐González, B., Baiza-Gutman, L. A., Manuel‐Apolinar, L., Mejía, S. Á., López-Cervantes, S. P., Ortega‐Camarillo, C., Cruz, M., Gómez‐Olivares, J. L., & Díaz-Flores, M. (2023) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2023.176068 · Cited by 12 · see citing works
A review of pomegranate supplementation: A promising remedial avenue for Alzheimer's disease
Ullah, A., Khan, A., Ahmed, S., Irfan, H. M., Hafiz, A. A., Jabeen, K., Alruwaili, M., Alotaibi, M., Naeem, W. A., Khan, A., et al. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e22483 · Cited by 12 · see citing works
“…(2) acetylcholinesterase inhibitors (Rivastigmine, Donepezil, Galantamine, and Tacrine); (3) glutamate inhibitors (Memantine); (4) chelating agents (Clioquinol and deferiprone); and (5) natural substances (berberine, curcumin, epigallocatechin-3-gallate, ginsenoside Rg1, genistein etc [119].”
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A Narrative Review on the Neuroprotective Potential of Brown Macroalgae in Alzheimer’s Disease
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Targeting the redox neuroinflammatory nexus: insights into Alzheimer’s and Parkinson’s diseases
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Photodynamic and Photothermal Therapies using Nanotechnology Approach in Alzheimer's Disease
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“In the US, drugs that may slow the clinical decline of AD patients, as well as treatments that may temporarily relieve some of the symptoms associated with the disease, have been approved by the Food and Drug Administration (FDA) (Table 1 ) [27].”
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Novel Pitolisant-Derived Sulfonyl Compounds for Alzheimer Disease
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“[45] AD remains the most common cause of dementia.”
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“While available treatments offer temporary symptom relief, there remains no cure for AD [2].”
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“However, these medications offer symptomatic relief without halting disease progression [16].”
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“Therapeutic interventions that promote efferocytosis in the neuronal niche can at least be applied as an adjunctive therapy to currently FDA-approved anti-amyloid medications to lessen the pile of neuronal cellular debris [192, 193].”
BackgroundNovel Emerging Targets Identification in Reducing Risk of Alzheimer’s Disease
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Current Drugs Used: Classification and Pharmacology
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“Despite these mechanisms, MEM only provides modest symptomatic benefit, may cause side effects, and does not alter disease progression (Reisberg et al., 2003; Alhazmi and Albratty, 2022).”
Kynurenic acid derivatives in treatment for Alzheimer's disease
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Advances in the treatment of Alzheimer’s disease
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“Clioquinol, a hydroxyquinoline ionophore, is a representative example of this therapeutic strategy, as it can sequester metal ions and reduce A β aggregation (Alhazmi and Albratty, 2022).”
Early-stage research and new pharmacological targets in Alzhei-mer's dementia
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“Conventional approved treatments are symptomatic agents with no effect on disease progression [1, 2], including acetylcholinesterase inhibitors (rivastigmine, donepezil, galantamine) and memantine, an N -methyl- d -aspartate receptor antagonist [2, 3, 5].”
Antioxidants and their possible benefits in neurodegeneration
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Nanocrystals: a new herald for the management of Alzheimer’s disease
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“New drugs in pipeline to manifested treat AD [40] .”
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“…the specific manifestations of dementia may vary depending on the type, common symptoms generally include gradual memory loss, impaired concentration and alertness, confusion, motor skills problems, speech disorders, and visual-spatial deficits (Alhazmi & Albratty, 2022; Rabinovici & Miller, 2010).”
Haque, A., Alenezi, K. M., Rasheed, M. S. M. A., Rahman, M. A., Anwar, S., Ahamad, S., & Gupta, D. K. (2025) · Frontiers in Medicine · doi:10.3389/fmed.2025.1529845 · Cited by 2 · see citing works
- Authors
- Alhazmi, H. A., & Albratty, M.
- Affiliations
- Jazan University (SA)
- Corresponding author
- Albratty, Mohammed
- Venue
- Saudi Pharmaceutical Journal
- Published
- 2022-12
- Volume
- 30
- Issue
- 12
- Pages
- 1755-1764
- ISSN
- 1319-0164 (ISSN-L)
- PMC
- PMC9805975
- OpenAlex
- W4304687787
- Semantic Scholar
- ecd3ae74331775e127cc9a0b44d808f840c5e8d4
- Cited by
- 122
- References
- 85
- Citations by year
- 2026: 24 · 2025: 38 · 2024: 43 · 2023: 17
- FWCI
- 3.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Saudi Pharmaceutical Journal (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, approved drugs, new drugs, amyloid plaques, acetylcholine deficiency, cholinesterase inhibitors, NMDA receptor antagonists, herbal drugs, medicinal plants, drug development pipeline, clinical trials, mechanism of action
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