27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Further analyses to determine clinical utility are warranted. 2 key findings →
Participants: 1,890 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both CSF p-tau and NfL correlate with disease severity and rate of disease progression in PSP. 4 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid accumulation was evaluated in 236 individuals who underwent >1 amyloid PET scan. 1 key finding →
Design: longitudinal study Participants: 236 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study suggests that early tau deposition may follow multiple trajectories during preclinical AD and may involve several cortical regions. 3 key findings →
Design: cross-sectional Participants: 447 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 18 293 participants included in the parent study, scan images were available for 10 774 (59%), of which Centiloids were successfully calculated for 10 361 (96%). 1 key finding →
Design: cross-sectional Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 levels showed a significant increase across advancing AD stages, with all between-group comparisons remaining significant after false discovery rate adjustment ( p p = 0.002) and CSF p-tau181 (β = 3.2, 95% CI 1.4-5.0, p = 0.001). 5 key findings →
Design: cohort study Participants: 731 Evidence: moderate
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We constructed models for MCI and mild dementia that predict MMSE over time. 1 key finding →
Design: longitudinal study Participants: 961 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that PA may help delay cognitive decline by modulating neurodegeneration and AD-specific tau pathologies. 4 key findings →
Design: cross-sectional Participants: 1,144 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Across the cohort of 212 individuals with SCD+ (M(Age) = 69.17 years, F 42.45%), 258 individuals with MCI (M(Age) = 72.93, F 43.80%), and 195 individuals with dementia (M(Age) = 74.07, F 48.72%), no main effect of education (ß = 0.52, 95% CI -0.30 to 1.58), but a significant education-by-group interaction on CL values, was found ( p = 0.024) using linear regression modeling. 1 key finding →
Participants: 212 Evidence: high
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Obicetrapib significantly slowed AD biomarker progression over 12 months in participants with ASCVD, with the greatest effects in ApoE4 carriers. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest a benefit of MI plus omega 3 in positive blood amyloid subjects. 4 key findings →
Participants: 483 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed. 5 key findings →
Design: cohort study Participants: 807 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide significant loci were identified for all biomarkers, including DACT1-DAAM1 (pTau217), KCNJ3 (pTau181), KLHDC4 (NfL), SLC10A7 (GFAP), and PPP4R2 (composite score). 4 key findings →
Participants: 1,972 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multiple proteinopathies commonly coexist in neurodegenerative diseases, making it essential to evaluate plasma biomarker performance in these complex diseases. 2 key findings →
Participants: 253 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 was associated with concurrent Aβ in most cortical regions and tau in temporo-parietal cortices. 3 key findings →
Design: cross-sectional Participants: 333 Evidence: moderate
Full summary, score breakdown and related studies → Original source
E280A carriers had higher p-tau231 levels than non-carriers (9.0 ± 7.4 vs. 5.2 ± 3.4 pg/mL, P < 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum p-tau217 levels were increased in individuals with iRBD and cognitive impairment (CI) on testing defined as Montreal Cognitive Assessment <26 or subthreshold parkinsonism. p-Tau217 differentiated individuals with iRBD who developed PD with CI (PD-CI) or DLB from PD phenoconverters with normal cognition (area under curve [AUC] = 0.82; 95% confidence interval, 0.70-0.93) and from iRBD non-phenoconverters with normal cognition (AUC = 0.83; 95% confidence interval, 0.77-0.89). 4 key findings →
Participants: 300 Evidence: low
Full summary, score breakdown and related studies → Original source
Unlike pNfL, which was increased similarly in both clinical groups, pGFAP was increased in FTD but lower than in AD (all P < 0.01). 4 key findings →
Design: cross-sectional Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
Unlike familial Alzheimer's disease, we have been unable to accurately predict symptom onset in presymptomatic familial frontotemporal dementia (f-FTD) mutation carriers, which is a major hurdle to designing disease prevention trials. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma levels of glial fibrillary acidic protein (GFAP) and neurofilament light (NEFL) are key dementia biomarkers. 3 key findings →
Participants: 50,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GFAP was lower in NB compared to prodromal AD (p = 0.003, d = 1.463) and AD-D (p = 0.002, d = 1.695). 5 key findings →
Design: cross-sectional Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →