28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
For more than a decade, researchers have refined criteria for the diagnosis of dementia with Lewy bodies (DLB) and at the same time have recognized that cognitive impairment and dementia occur commonly in patients with Parkinson disease (PD). 1 key finding →
Evidence: low
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Tau (MAPT) drives neuronal dysfunction in Alzheimer disease (AD) and other tauopathies. 1 key finding →
Evidence: low
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Cerebrospinal fluid and positron emission tomography amyloid-β were measured at baseline in 769 persons [161 healthy controls, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease dementia, mean age 72 years (standard deviation 7 years), 47% females] and used to predict diagnosis, APOE ε4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and phosphorylated-tau levels (cross-sectionally); and hippocampal volume, fluorodeoxyglucose positron emission tomography results and Alzheimer's Disease Assessment Scale-cognitive subscale scores (longitudinally). 2 key findings →
Participants: 769 Evidence: low
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At baseline and at follow-up MCI-AD showed higher levels P-tau(231), T-tau, IP, P-tau(231)/Abeta(42/40) and T-tau/Abeta(42/40) ratios and lower Abeta(42)/Abeta(40) than MCI-MCI or NL-NL. 2 key findings →
Design: longitudinal study Participants: 86 Evidence: moderate
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In 272 participants, mean (SD) age was 70 (4.5) years, 270 were male (99.3%), and 83 (30.5%) were amyloid-PET positive. 5 key findings →
Design: cohort study Participants: 272 Evidence: moderate
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To investigate earlier pathologies preceding filamentous tau inclusions, researchers studied wild-type and P301S mutant human tau transgenic mice. 3 key findings →
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Our data indicate that the APOE ε4 allele is an important predictor of cognitive function in PD across multiple domains. 5 key findings →
Participants: 1,079 Evidence: low
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Eight single-nucleotide polymorphisms (false discovery rate P Conclusions and relevance Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression. 2 key findings →
Design: longitudinal study Evidence: moderate
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We systematically compared structural imaging patterns of advanced brain aging (ABA) in the general-population, herein defined as significant deviation from typical BA to those found in Alzheimer disease (AD). 5 key findings →
Participants: 2,705 Evidence: moderate
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Biomarker trajectory shapes by MMSE score were complex and were affected by interactions with age and APOE status. 3 key findings →
Design: cross-sectional Participants: 343 Evidence: moderate
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White matter hyperintensities (WMHs) are frequently seen on brain magnetic resonance imaging scans of older people. 1 key finding →
Evidence: low
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Niney-two PD patients developed dementia, and 48 remained cognitively normal. 2 key findings →
Evidence: low
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CBD was associated with 4 clinical syndromes: progressive nonfluent aphasia (n = 5), behavioral variant frontotemporal dementia (n = 5), executive-motor (n = 7), and posterior cortical atrophy (n = 1). 2 key findings →
Participants: 18 Evidence: low
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Elevated CSF tau levels are associated with AD pathology and can help discriminate AD from other dementing disorders. 3 key findings →
Participants: 74 Evidence: moderate
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18 F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. 3 key findings →
Participants: 33 Evidence: low
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We examined regional distribution patterns of phosphorylated 43-kDa TAR DNA-binding protein (pTDP-43) intraneuronal inclusions in frontotemporal lobar degeneration (FTLD). 1 key finding →
Participants: 39 Evidence: low
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Under Bronfenbrenner's macrosystem framework, we highlight key quantitative and qualitative studies linking S/SDOH with AD/ADRD, identify scientific gaps in the literature, and propose guidance for future research. 1 key finding →
Evidence: low
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Among elderly Medicare beneficiaries with PD, race, sex, and neighborhood SES are strong independent predictors of DBS receipt. 5 key findings →
Design: cohort study Evidence: moderate
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LBD patients with AD copathology harbor greater neocortical SYN pathology. 1 key finding →
Participants: 36 Evidence: moderate
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These six markers describe six clinicopathological stages from cognitive normalcy to mild dementia, including stages defined by increased risk of cognitive decline. 1 key finding →
Participants: 24 Evidence: moderate
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Most approaches to machine learning from electronic health data can only predict a single endpoint. 1 key finding →
Participants: 1,909 Evidence: low
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Based on previous studies, a preclinical classification for Alzheimer's disease (AD) has been proposed. 4 key findings →
Design: cross-sectional Participants: 160 Evidence: moderate
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(n = 2,392) had a mean age of 74.4 years, 60.4% were female, and 17.1% were of self-reported Black race. 5 key findings →
Design: cross-sectional Participants: 2,392 Evidence: low
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Cross-ancestry sex-stratified analyses identified several loci with evidence of interaction (p 0.05). 5 key findings →
Design: meta-analysis Participants: 25,284 Evidence: high
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There were 13,145 individuals with risk factor data between 2015 and 2018 (51.1% aged 18-44, 31.0% aged 45-64, and 17.9% aged ≥65 years; 51.5% female after survey-weighting). 5 key findings →
Design: cross-sectional Participants: 13,145 Evidence: low
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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →