28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
While APOEε4 is associated with increased amyloid-β burden, its association with cerebral tau pathology has been controversial. 5 key findings →
Design: cross-sectional Participants: 124 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The diagnostic performance of plasma biomarkers was poor (area under the curve [AUC] between 0·53 [95% CI 0·44-0·62] and 0·74 [0·66-0·82]) except for plasma NfL concentrations, which had an AUC of 0·88 (0·82-0·93) for the differentiation of the asymptomatic group versus the prodromal Alzheimer's disease group and 0·95 (0·92-0·98) for the asymptomatic group versus the Alzheimer's disease dementia group. 4 key findings →
Design: cross-sectional Participants: 282 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among individuals presenting with SCD at a memory clinic, those with a biomarker profile A-T+N+, A+T-N-, A+T+N-, and A+T+N+ were at increased risk of dementia, and showed steeper cognitive decline compared to A-T-N- individuals. 4 key findings →
Participants: 385 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous studies have suggested that the APOE ɛ4 allele plays a role in the risk and age at onset of dementia in DS; however, data on in vivo biomarkers remain scarce. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The mean (SD) age was 73.9 (7.35) years among the 237 ADNI participants and 70.2 (9.7) years among the 130 Avid-A05 participants. 2 key findings →
Design: cohort study Participants: 237 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 300 participants with DS and a control group of 37 non-DS siblings, mean (SD) age was 45.0 (10.1) years, and 167 (49.6%) were men. 4 key findings →
Design: cross-sectional Participants: 300 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among cognitively normal participants with positive biomarkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of those with negative biomarkers. 2 key findings →
Design: longitudinal study Participants: 720 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Sleep duration is linked to amyloid-β clearance while physical activity is associated with brain volume maintenance. 5 key findings →
Design: cross-sectional Participants: 4,322 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT. 2 key findings →
Design: longitudinal study Participants: 1,007 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Both participant and study partner CFI increased over the duration of the study indicating worsening cognitive functioning. 3 key findings →
Design: longitudinal study Participants: 1,147 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Mean (SD) follow-up was 4.8 (2.6) years. 3 key findings →
Design: cohort study Participants: 298 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 3363 adults were enrolled in SNAC-K (73.3% participation rate). 5 key findings →
Design: cohort study Participants: 3,363 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The sample included 4340 adults (mean [SD; range] age, 58.1 [1.1; 56-63] years; 2400 [55.3%] women); 630 (14.4%) were Black, 900 (20.7%) were Latinx, and 2610 (60.1%) were White. 5 key findings →
Design: cohort study Participants: 4,340 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study proposes a model that relates disease stages to Alzheimer's disease biomarkers.
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study updated a 2010 hypothetical model of major Alzheimer's disease (AD) biomarkers based on new evidence. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The observed metabolic alterations were associated with core pathological processes of AD to investigate their relation with amyloid pathology and tau-related neurodegeneration. 5 key findings →
Design: cohort study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A combination of plasma p-tau181, NfL, and GFAP, but not Aβ 1-42/1-40 , might be useful to discriminate AD, FTD, and DLB. 1 key finding →
Participants: 160 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We detected an increased concordance in the visual and quantitative (standardized uptake value ratio (SUVR) and total volume of distribution (VT)) [18F]AV45 PET measures when the CSF Aβ1-42/Aβ1-40 was applied compared to Aβ1-42 alone. 2 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline NfL was elevated in symptomatic carriers (median 52 pg/mL [IQR 24-69]) compared with presymptomatic carriers (9 pg/mL [6-13]; p<0·0001) and non-carriers (8 pg/mL [6-11]; p<0·0001), and was higher in converters than in non-converting carriers (19 pg/mL [17-28] vs 8 pg/mL [6-11]; p=0·0007; adjusted for age). 4 key findings →
Design: cohort study Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source
PF and BF were significantly associated with increased likelihoods of dementia, Alzheimer's disease (AD), vascular dementia (VaD), and MCI. 5 key findings →
Design: cross-sectional Participants: 5,149 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher plasma p-tau levels were associated with worse cognition at baseline and over time, with the strongest effect observed with p-tau217 in cognitively impaired individuals (β = -0.49, p < 0.001). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
T-tau, NfL, GFAP, and YKL-40 discriminated between diagnostic groups (receiver operating curve: 0.647-0.873). 5 key findings →
Participants: 1,193 Evidence: moderate
Full summary, score breakdown and related studies → Original source
After adjusting for age, plasma NfL level was higher in subjects with DAT (65.98±84.96 pg/mL), compared to in subjects with SCD (16.90±2.54 pg/mL) or MCI (25.53±10.42 pg/mL, p=0.004). 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 349 participants with available plasma data, 234 met inclusion criteria (31 controls, 141 in the training sample, and 62 in the validation sample). 5 key findings →
Design: cross-sectional Participants: 46 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 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 →