28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date. 4 key findings →
Design: case-control Participants: 12,221 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our study indicates that changes in PVS-related MRI parameters occur in MCI and AD, possibly due to impairment of the glymphatic system. 3 key findings →
Participants: 36 Evidence: low
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Better sleep consolidation attenuates the effect of APOE genotype on incident AD and development of neurofibrillary tangle pathology. 2 key findings →
Design: cohort study Participants: 698 Evidence: moderate
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Two multicentre genome-wide association (GWA) studies provided substantial evidence, implicating the complement receptor 1 gene (CR1) in Alzheimer disease (AD) genetic etiology. 3 key findings →
Participants: 1,883 Evidence: moderate
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Genetic risk factors of AD dementia demonstrate effects related to Aβ, as well as synergistic interactions with Aβ. 2 key findings →
Design: longitudinal study Participants: 702 Evidence: moderate
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Secondary analysis suggested that this effect may be driven primarily by individuals who are negative for the established AD genetic risk factor, apolipoprotein E (APOE) ɛ4. 5 key findings →
Design: case-control study Participants: 346 Evidence: moderate
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We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls. 1 key finding →
Participants: 2,323 Evidence: moderate
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Alzheimer's disease (AD), the most common cause of dementia, has long been associated with bacterial infections and inflammation-causing immunosenescence. 5 key findings →
Design: longitudinal study Participants: 108 Evidence: moderate
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Amyloid protein precursor (APP), presenilin-1 (PSEN1), and presenilin-2 (PSEN2) mutations cause autosomal dominant forms of early-onset Alzheimer disease (AD-EOAD). 4 key findings →
Participants: 170 Evidence: low
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Previous studies have evaluated gene expression in Alzheimer's disease (AD) brains to identify mechanistic processes, but have been limited by the size of the datasets studied. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The authors conducted a large genome-wide association study using 2,032 individuals from France with Alzheimer's disease and 5,328 controls. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E (APOE) gene is the best established genetic risk factor for Alzheimer's disease in later life, with the ε4 allele conferring higher risk. 5 key findings →
Design: cohort Participants: 9,496 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Female individuals had higher plaque burden than male individuals (unadjusted odds ratio [OR], 1.97; 95% CI, 1.67-2.29; P Conclusions and relevance The findings indicate that female sex, APOEε4, and both race and African ancestry were jointly associated with amyloid in this study population. 3 key findings →
Design: cross-sectional Participants: 2,268 Evidence: moderate
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Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. 5 key findings →
Design: cross-sectional Participants: 1,246 Evidence: low
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These factors should be investigated in longitudinal studies for their role in detecting onset of symptoms in AD. 1 key finding →
Design: longitudinal study Participants: 749 Evidence: moderate
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Median (interquartile range) CRP levels increased with mean (SD) age (43.3 [9.6] years, 0.95 mg/L [0.40-2.35 mg/L] vs 59.1 [9.6] years, 2.04 mg/L [0.93-4.75 mg/L] vs 61.6 [9.5] years, 2.21 mg/L [1.05-5.12 mg/L]; P Conclusions and relevance In this study, peripheral chronic low-grade inflammation in participants with ApoE4 was associated with shortened latency for onset of AD. 2 key findings →
Design: cohort study Evidence: moderate
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The ApoE ε4 allele is the most significant genetic risk factor for late-onset Alzheimer disease. 4 key findings →
Participants: 1,766 Evidence: low
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By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD. 3 key findings →
Evidence: low
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More research is needed to elucidate the neural mechanisms underlying these regional associations, which may involve motor and sensorimotor circuits hitherto largely neglected in the pathophysiology of AD. 1 key finding →
Design: cross-sectional Evidence: low
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Partial volume corrected and uncorrected results were generally in agreement; however, the correlation between (11)C-PBR28 and (11)C-Pittsburgh Compound B binding was seen only after partial volume correction. 2 key findings →
Design: longitudinal study Evidence: moderate
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At baseline measurements, amyloid burden does not distinguish between cognitively impaired and unimpaired subjects with PD without dementia, but our data suggest that amyloid contributes to cognitive, but not motor, decline over time. 3 key findings →
Design: cohort study Participants: 46 Evidence: moderate
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Limited evidence suggests that the APOEε4 allele may confer risk for CTE, but previous studies were small with limited scope. 5 key findings →
Design: cross-sectional Participants: 294 Evidence: low
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Strikingly gene-expression, network-based analysis and cell type deconvolution approaches revealed a consistent immune signature in the brain and blood of female AD patients that was absent in males. 5 key findings →
Design: meta-analysis Evidence: high
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This study provides initial data that demonstrate elevated antibodies to periodontal disease bacteria in subjects years before cognitive impairment and suggests that periodontal disease could potentially contribute to the risk of AD onset/progression. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
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.
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 →