28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Lower baseline amyloid beta (Aβ)42/40 ratio and higher phosphorylated tau 181 (p-tau181), glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) were associated with an increased risk of MCI and dementia; GFAP was most strongly associated. 5 key findings →
Participants: 2,467 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of 18 high-quality studies comprising 24 independent datasets and 4,736 participants were included. 5 key findings →
Design: systematic review Participants: 4,736 Evidence: high
Full summary, score breakdown and related studies → Original source
A total of 917 participants had a mean baseline age of 67.4 years (SD 12.1), 49.4% were female, and 48.6% self-identified as Black. 5 key findings →
Design: cohort study Participants: 30,239 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Participants with Elevated/High %p-tau217 exhibited accelerated cognitive decline, hippocampal atrophy, and significantly higher risks of progression to MCI (hazard ratio [HR] > 6.0) and dementia (HR > 9.9). 4 key findings →
Design: longitudinal study Participants: 1,204 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Donanemab-mediated slowing of disease progression occurred across baseline tau PET and plasma P-tau217 levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylated-tau (p-tau217) is a promising blood-based biomarker for Alzheimer's dementia (AD) in clinical settings. 3 key findings →
Design: cohort study Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 levels decreased significantly from 3 months, with the greatest decline between 3 and 6 months, followed by a plateau. 5 key findings →
Design: longitudinal study Participants: 153 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Adding MDLC to p-tau217 significantly explained longitudinal cognitive trajectory beyond p-tau217 alone. 5 key findings →
Design: longitudinal study Participants: 183 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 504 enrolled patients, 491 completed POD assessment (mean [SD] age, 68.4 [8.3] years; 385 [78.4%] male), of whom 106 (21.6%) developed POD. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this prospective cohort study, we included adults aged 40 years or older with subjective cognitive decline, mild cognitive impairment, or dementia, based on cognitive test results and clinical assessments, consecutively recruited at two memory clinics in Sweden, as part of the Swedish BioFINDER-2 study. 3 key findings →
Design: cohort Participants: 572 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
These findings demonstrate that plasma p-tau217 can reliably detect AD pathology in the preclinical stage. 4 key findings →
Design: systematic review Participants: 7,834 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Across the cohorts, each 10-year increase in BAI was associated with a 39% higher risk of incident dementia (hazard ratio [HR], 1.39 [95% CI, 1.21-1.59]; P Conclusions and relevance In this IPD meta-analysis, a higher sleep EEG-based BAI was associated with a higher risk of incident dementia. 3 key findings →
Design: meta-analysis Participants: 7,105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 showed the strongest individual association with Aβ PET status (area under the curve [AUC], 0.85). 5 key findings →
Design: cohort study Participants: 1,407 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combining plasma p-tau with Aβ42 or the Aβ42/40 ratio reduced the intermediate zone. 5 key findings →
Design: cross-sectional Participants: 326 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuropathology cases included 46 Parkinson's disease and 10 dementia with Lewy bodies, and clinical cases included 173 Parkinson's disease, and 64 controls. 5 key findings →
Design: cohort study Participants: 46 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Predicting not just if, but also when, cognitively unimpaired individuals are likely to develop onset of Alzheimer's disease (AD) symptoms would be useful to clinical trials and, eventually, clinical practice. 2 key findings →
Design: cohort Participants: 603 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the individual plasma p-tau variants, p-tau217 consistently outperformed p-tau181 and p-tau231. 4 key findings →
Design: longitudinal study Participants: 352 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Nine proteins (amyloid-beta 42 (Aβ42), beta-secretase 1 (BACE1), glial fibrillary acidic protein (GFAP), pTau181, pTau231, pTau217, t0tal tau (MAPT), neurofilament light (NfL) and acetylcholinesterase (AChE)) robustly differed between carriers and non-carriers cross-sectionally. 5 key findings →
Design: cohort study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 2766 participants (mean [SD] age, 69.9 [3.8] years; 486 [17.9%] Black, 196 [7.1%] Hispanic, and 2007 [73.9%] White), 1311 developed the combined end point of MCI or dementia (849 participants with MCI and 752 participants with dementia). 5 key findings →
Design: cohort Participants: 2,766 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings add to growing evidence that women have a differential tau response to Aβ that may emerge at the point of p-tau secretion. 5 key findings →
Design: cohort Participants: 1,292 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation. 2 key findings →
Design: cohort Participants: 1,028 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Detection of Alzheimer's disease (AD) before the development of clinical symptoms is critical for enabling the use of new treatments. 2 key findings →
Participants: 551 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MES-defined cognitive impairment (≤-2 standard deviation [SD] deviation after adjustment for demographics) was identified in 12.4% of participants. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In participants who progressed to amyloid-positive MCI, plasma p-tau181/Aβ42 and GFAP diverged from stable controls earliest (about 13 and 12 years before symptom onset, respectively), followed by Aβ42/Aβ40, p-tau181, and NfL, all of which became abnormal before symptom onset. 4 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. 5 key findings →
Design: cohort Participants: 2,684 Evidence: high
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 →