28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We aimed to characterise the brain structure of superagers and identify demographic, lifestyle, and clinical factors associated with this phenotype. 4 key findings →
Design: longitudinal study Participants: 64 Evidence: moderate
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Our results demonstrate that different MAPT mutations give rise to distinct atrophy patterns and clinical phenotype, providing insights into the underlying disease biology and potential utility for patient stratification in therapeutic trials. 3 key findings →
Design: cohort study Evidence: moderate
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Within the training set, individuals closer to or beyond their parent's symptom onset demonstrated reduced grey matter volume and altered functional connectivity, specifically in regions known to be vulnerable in Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 138 Evidence: moderate
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Diabetes and even prediabetes are associated with accelerated brain aging, especially among men and people with poor cardiometabolic health. 4 key findings →
Participants: 31,229 Evidence: low
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There is increasing interest in the use of technology to support social health in dementia. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE4. 2 key findings →
Evidence: low
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Ageing and a sedentary lifestyle are associated with declines in muscle function and cardiorespiratory fitness, resulting in an impaired capacity to perform daily activities and maintain independent functioning. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Behavioral and psychological symptoms of dementia include agitation, depression, apathy, repetitive questioning, psychosis, aggression, sleep problems, wandering, and a variety of inappropriate behaviors. 5 key findings →
Evidence: low
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The Systolic Blood Pressure Intervention Trial will provide important information on the risks and benefits of intensive blood pressure treatment targets in a diverse sample of high-risk participants, including those with prior cardiovascular disease, chronic kidney disease, and those aged ≥75 years. 4 key findings →
Participants: 9,361 Evidence: high
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Hearing loss is associated with poor cognitive performance and incident dementia and may contribute to cognitive decline. 5 key findings →
Participants: 164,770 Evidence: low
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The possibility that history of depression is a risk factor for dementia needs to be taken seriously and explanations of the association need to be further researched. 2 key findings →
Design: meta-analysis Evidence: high
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The relationships between total serum cholesterol (TC) and dementia and between TC and cognitive decline were investigated in a systematic review of 18 prospective studies. 5 key findings →
Design: systematic review Participants: 14,331 Evidence: high
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Patients with moderate to severe AD presented with higher mean (SD) orexin levels compared with controls (154.36 [28.16] vs 131.03 [26.55]; P Conclusions and relevance Our results demonstrate that, in AD, increased cerebrospinal fluid orexin levels are related to a parallel sleep deterioration, which appears to be associated with cognitive decline. 2 key findings →
Design: case-control study Participants: 48 Evidence: moderate
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Silent brain infarcts and white matter lesions are frequently seen on magnetic resonance imaging in healthy elderly people and both are associated with an increased risk of stroke and dementia. 5 key findings →
Design: cross-sectional Participants: 1,077 Evidence: low
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Older Medicare beneficiaries in California with DS, especially those with dementia, have a high level of multimorbidity including several treatable conditions. 3 key findings →
Design: cross-sectional Participants: 100 Evidence: low
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One of the most challenging problems in modern neuroimaging is detailed characterization of neurodegeneration. 1 key finding →
Design: longitudinal study Evidence: moderate
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Frontotemporal dementia (FTD) is the second most common cause of dementia in people under the age of 65 years. 2 key findings →
Evidence: low
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TDP-43 is a predominantly nuclear RNA-binding protein that forms inclusion bodies in frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). 2 key findings →
Evidence: low
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The ordered assembly of tau protein into abnormal filamentous inclusions underlies many human neurodegenerative diseases 1 . 2 key findings →
Evidence: low
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Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown. 5 key findings →
Evidence: low
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These results help explain the "obesity paradox" as differences in dementia risk across time are consistent with physical changes in the trajectory toward disability. 4 key findings →
Participants: 2,798 Evidence: low
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We identified two variants in TARDBP, which would encode Gly290Ala and Gly298Ser forms of TDP-43, in two kindreds with familial ALS. 2 key findings →
Participants: 259 Evidence: low
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The cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43) is a common histopathological hallmark of the amyotrophic lateral sclerosis and frontotemporal dementia disease spectrum (ALS/FTD). 5 key findings →
Evidence: low
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A locus on chromosome 9p21 has been associated with both disorders, and we aimed to identify the causal gene within this region. 3 key findings →
Participants: 305 Evidence: moderate
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There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →