Alzheimer's disease
Open accessAbstract
In this Seminar, we highlight the main developments in the field of Alzheimer's disease. The most recent data indicate that, by 2050, the prevalence of dementia will double in Europe and triple worldwide, and that estimate is 3 times higher when based on a biological (rather than clinical) definition of Alzheimer's disease. The earliest phase of Alzheimer's disease (cellular phase) happens in parallel with accumulating amyloid β, inducing the spread of tau pathology. The risk of Alzheimer's disease is 60-80% dependent on heritable factors, with more than 40 Alzheimer's disease-associated genetic risk loci already identified, of which the APOE alleles have the strongest association with the disease. Novel biomarkers include PET scans and plasma assays for amyloid β and phosphorylated tau, which show great promise for clinical and research use. Multidomain lifestyle-based prevention trials suggest cognitive benefits in participants with increased risk of dementia. Lifestyle factors do not directly affect Alzheimer's disease pathology, but can still contribute to a positive outcome in individuals with Alzheimer's disease. Promising pharmacological treatments are poised at advanced stages of clinical trials and include anti-amyloid β, anti-tau, and anti-inflammatory strategies.
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European and American associations have highlighted the importance of biomarkers in AD, which is featured by amyloid-β (Aβ) plaques (A), pathological tau (T), and neurodegeneration (N).
“Recently, both European and American associations highlighted the importance of biomarkers in AD which is featured by amyloid-β (Aβ) plaques (A), pathological tau (T), and neurodegeneration (N) [6][7][8].”
From Identification of novel diagnostic panel for mild cognitive impairment and Alzheimer’s disease: findings based on urine proteomics and machine learning (2023) · cites this paper as [8]
The Diagnostic criteria section describes the ATN research framework—amyloid (A), phosphorylated tau (T), and neurodegeneration (N)—and emphasizes the importance of biomarkers in Alzheimer’s disease. It does not establish the claim that both European and American associations highlighted their importance. It also specifies that amyloid and phosphorylated tau, rather than all three ATN categories, define Alzheimer’s disease in that framework. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMutations in MAPT are sufficient to cause dementia (frontotemporal dementia, FTD).
“Cognitive loss is much more robustly correlated with MAPT based NFTs pathology, and mutations in MAPT are sufficient to cause dementia (frontotemporal dementia, FTD) (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Tau-PET section (page not provided) says tau-PET binding topography correlates with cognitive deficits, supporting the sentence’s point about tau pathology and cognition. Our copy does not state that MAPT mutations are sufficient to cause frontotemporal dementia; searches for MAPT mutations and frontotemporal dementia found no such passage. (LLM, conf=0.83)
Experimental — accuracy not yet measuredMutations in MAPT might not cause AD because MAPT pathology does not drive the accumulation of Aβ pathology.
“Mutations in MAPT might not cause AD because MAPT pathology does not drive the accumulation of Aβ pathology (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Pathophysiology section says amyloid β induces the spread of tau pathology, and the Diagnostic criteria section describes amyloid β as a defining feature of Alzheimer’s disease. Neither passage establishes that MAPT mutations do not cause Alzheimer’s disease or that tau pathology cannot drive amyloid β accumulation. A search for MAPT found a reference to the MAPT lifestyle trial, not to mutations in the gene. (LLM, conf=0.76)
Experimental — accuracy not yet measuredCognitive loss is much more robustly correlated with MAPT based NFTs pathology.
“Cognitive loss is much more robustly correlated with MAPT based NFTs pathology, and mutations in MAPT are sufficient to cause dementia (frontotemporal dementia, FTD) (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Tau-PET passage (Introduction > Imaging biomarkers; page not provided) says that, unlike amyloid-β deposition, tau-PET binding topography correlates with cognitive deficits. This supports the comparison in the claim, but the passage concerns a tau-imaging measure rather than directly measuring MAPT-based neurofibrillary tangles. The cited sentence also attributes the claim that MAPT mutations suffice to cause frontotemporal dementia to this source; searches for MAPT and frontotemporal dementia did not find support for that claim in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThis injury is further enhanced by aging, vascular damage, metabolic conditions such as Type II Diabetes and genetic risk factors.
“This injury is further enhanced by aging, vascular damage, metabolic conditions such as Type II Diabetes and genetic risk factors (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Epidemiology section identifies advanced age and APOE ε4 as major Alzheimer’s disease risk factors and associates cardiovascular risks with dementia. The Pathophysiology discussion also places ageing and vascular changes in the disease landscape. But the paper does not establish that type 2 diabetes or these factors enhance the injury described in the claim; it cautions that vascular risks may contribute to dementia without increasing Alzheimer’s pathology. (LLM, conf=0.86)
Experimental — accuracy not yet measured
The classic model of AD is based on the Aβ cascade and proposes that aggregated Aβ stimulates inflammation, and that these two factors produce additive injury to elicit neurodegeneration in AD.
“The classic model of AD is based on the Aβ cascade and proposes that aggregated Aβ stimulates inflammation, and that these two factors produce additive injury to elicit neurodegeneration in AD (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Conclusions identify an amyloid-β cascade hypothesis, and the Pharmacological section says neuroinflammation contributes to neurodegeneration. But the Pathophysiology section places neuroinflammation upstream of or parallel to amyloid-β accumulation; it does not describe aggregated amyloid-β stimulating inflammation or the two producing additive injury. The paper also says the cascade hypothesis has been modified, rather than presenting the cited sequence as its account. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe direct connection between Aβ and MAPT pathology is poorly understood, as shown by the weak correlation between the distribution of Aβ pathology and the distribution of MAPT pathology in humans.
“The direct connection between Aβ and MAPT pathology is poorly understood, as shown by the weak correlation between the distribution of Aβ pathology and the distribution of MAPT pathology in humans (Serrano-Pozo et al., 2011; Perez-Nievas et al., 2013; Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Pathophysiology section says amyloid β induces the spread of tau pathology “via an unknown way,” supporting the claim that their direct connection is poorly understood. The Imaging biomarkers section contrasts tau-PET topography with amyloid β deposition, but does not report a weak correlation between the spatial distributions of the two pathologies in humans. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredHippocampal structural abnormalities and neuronal loss are key neuropathological hallmarks of AD, contributing to cognitive decline.
“Research studies have shown that hippocampal structural abnormalities and neuronal loss are the key neuropathological hallmarks of AD, contributing to the cognitive decline observed in the disease (Venkateshappa et al., 2012; Scheltens et al., 2021).”
From AD-Like Neuropsychiatric Dysfunction in a Mice Model Induced by a Combination of High-Fat Diet and Intraperitoneal Injection of Streptozotocin (2024) · cites this paper as Scheltens et al., 2021
The Imaging biomarkers section identifies medial temporal lobe atrophy as a validated imaging measure of neurodegeneration in Alzheimer’s disease. The Fluid biomarkers section relates synaptic pathology to cognitive decline. However, the paper identifies amyloid and tau pathology as defining characteristics; it does not establish hippocampal neuronal loss as a key neuropathological hallmark or directly link hippocampal structural changes to cognitive decline. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe efficacy of Aβ antibodies in improving cognitive function is limited.
“their efficacy in improving cognitive function is limited (2, 3)”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [2]
The Pharmacological section says Aβ monoclonal antibodies may slow disease progression, but clinical-trial ambiguities remain and no such treatment had yet been approved. It does not establish how effective the antibodies are at improving cognitive function specifically, so the claim is more definite than the source supports. (LLM, conf=0.78)
Experimental — accuracy not yet measuredCNS diseases include neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease, as well as traumatic brain injuries and spinal cord injuries.
“The diseases encompass various severe conditions, including neurodegenerative disorders like Alzheimer’s disease (AD) [3, 4] and Parkinson’s disease (PD) [5, 6], as well as traumatic brain injuries (TBI) [7] and spinal cord injuries (SCI) [8].”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [3]
Cognitive loss is only weakly correlated with the accumulation of Aβ.
“Mutations in amyloid precursor protein (APP) cause AD, however cognitive loss is only weakly correlated with the accumulation of Aβ (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
Mutations in APP cause AD.
“Mutations in amyloid precursor protein (APP) cause AD, however cognitive loss is only weakly correlated with the accumulation of Aβ (Scheltens et al., 2021).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Scheltens et al., 2021
The Genetics section describes an APP mutation associated with prolonged cognitive health, but does not state that APP mutations cause Alzheimer’s disease. A search for causative APP mutations found discussion of clinical mutations in presenilins, not APP; the protective APP variant does not rule out other APP mutations being causative. (LLM, conf=0.72)
Experimental — accuracy not yet measuredNeuroinflammation, oxidative stress, autophagy, glymphatic dysfunction, blood vessel alteration, blood-brain barrier leakage, and gut microbiome abnormality all contribute to the cellular pathology underlying Alzheimer's disease.
“This is associated with other processes such as neuroinflammation, oxidative stress, autophagy, dysfunction of the glymphatic system, alteration in blood vessels, leakage of the blood‐brain barrier, and abnormality in the gut microbiome, all contributing to the cellular pathology underlying Alzheimer's disease 138 .”
From Mental health care for older adults: recent advances and new directions in clinical practice and research (2022) · cites this paper as [138]
Two important genes linked to AD risk are APOE and TREM2.
“Two important genes linked to AD risk are APOE and TREM2. 122”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [122]
The E4 allele of APOE increases the risk of developing late-onset AD.
“The E4 allele of APOE increases the risk of developing late-onset AD.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [196]
Genetics is one of the main variables that causes AD, with certain inherited genes connected to the condition as risk factors.
“One of the main variables that causes AD is genetics. Certain genes that are inherited have been connected to the condition as risk factors.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [29]
The two main gene categories associated with AD are deterministic and risk-factor genes.
“The two main gene categories associated with AD are deterministic and risk-factor genes [29,37].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [29]
Alzheimer's disease is characterized by the presence of amyloid β protein plaques, phosphorylated tau-containing neurofibrillary tangles, and neurodegeneration.
“Alzheimer’s disease (AD) is characterized by the presence of amyloid β (Aβ) protein plaques, phosphorylated tau (p-tau)–containing neurofibrillary tangles, and neurodegeneration [1].”
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An Update on Dual Orexin Receptor Antagonists and Their Potential Role in Insomnia Therapeutics
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- Authors
- Scheltens, P., De Strooper, B., Kivipelto, M., Holstege, H., Chételat, G., Teunissen, C. E., Cummings, J., & van der Flier, W. M.
- Affiliations
- Amsterdam University Medical Centers (NL)
- Karolinska University Hospital (SE)
- Cleveland Clinic (US)
- Corresponding author
- Scheltens, Philip
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2021-04
- Volume
- 397
- Issue
- 10284
- Pages
- 1577-1590
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC8354300
- OpenAlex
- W4206046172
- Cited by
- 5,465
- References
- 155
- Citations by year
- 2026: 1183 · 2025: 1629 · 2024: 1297 · 2023: 825 · 2022: 416 · 2021: 111
- FWCI
- 89.85
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion)
- PubMed Central (acceptedVersion)
- Lirias (KU Leuven) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- DZNE Pub (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Biogen (P20GM109025)
- Weston Brain Institute
- EU Joint Programme – Neurodegenerative Disease Research
- Fondation Vaincre Alzheimer
- Health~Holland
- European Commission (EU-FP7)
- Institut National de la Santé et de la Recherche Médicale
- ZonMw (733051102)
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (EU-FP7)
- Association France Alzheimer
- Hjärnfonden
- Knut och Alice Wallenbergs Stiftelse
- Alzheimerfonden
- Stichting Dioraphte
- Alzheimer Nederland
- Vlaamse regering
- FONDATION ALZHEIMER
- Région Normandie
- Janssen Prevention Center
- GIESKES-STRIJBIS FONDS
- Medical Research Council
- Center for Innovative Medicine
- National Institute on Aging (R01AG053798, P20AG068053, P30AG072980)
- National Institute of General Medical Sciences (P20GM109025)
- National Institute of Neurological Disorders and Stroke (U01NS093334)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, dementia prevalence, amyloid-beta, tau pathology, apolipoprotein E, biomarkers, amyloid PET, phosphorylated tau, anti-amyloid therapy, anti-tau therapy, anti-inflammatory therapy, dementia risk
- MeSH terms
- Alzheimer Disease, Humans
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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