Among 1431 participants, the mean (SD) age was 71.2 (8.8) years; 751 (52.5%) were male. 2 key findings →
Design: cohort study Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among 1431 participants, the mean (SD) age was 71.2 (8.8) years; 751 (52.5%) were male. 2 key findings →
Design: cohort study Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Whilst cerebrospinal fluid (CSF) and positron emission tomography (PET) biomarkers for amyloid-β (Aβ) and tau pathologies are accurate for the diagnosis of Alzheimer's disease (AD), their broad implementation in clinical and trial settings are restricted by high cost and limited accessibility. 3 key findings →
Design: longitudinal study Participants: 1,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 6514 participants (mean age, 69.5 years; 50.5% female), median follow-up time ranged from 1.5 to 4.0 years. 5 key findings →
Design: longitudinal study Participants: 6,514 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
AUC for amyloid and tau PET provide expert recommendations for clinical use of these technologies in the evolving landscape of diagnostics and therapeutics for Alzheimer's disease. 2 key findings →
Design: systematic-review Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma tau partly reflects AD pathology, but the overlap between normal aging and AD is large, especially in patients without dementia. 3 key findings →
Design: longitudinal study Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
In the discovery cohort, the mean (SD) age was 70.9 (8.5) years, 191 (58%) were male, the mean (SD) MMSE score was 27.1 (1.9), and 110 individuals with MCI (33%) converted to dementia (71 to AD dementia). 4 key findings →
Design: cohort study Participants: 110 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Levels of plasma p-tau217 increased significantly in Aβ+ participants before showing significant deceleration (χ2 = 21.7; P Conclusions and relevance This study found that tau PET is valuable for both prognostic and real-time tracking of disease progression. 2 key findings →
Design: cohort Participants: 1,707 Evidence: moderate
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A total of 716 individuals were included in the analysis: 413 cognitively unimpaired (CU) participants (58.6% female; mean age = 70.6 years, SD = 7.9) and 303 cognitively impaired (CI) participants (54.7% female; mean age = 73.2 years, SD = 7.4). 5 key findings →
Design: longitudinal study Participants: 716 Evidence: moderate
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Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20 Evidence: low
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Higher educational level (standardized β = 0.23, P Conclusions and relevance Results of this study suggest that women and young patients with AD have relative preservation of brain structure when exposed to neocortical pathological tau. 3 key findings →
Design: cross-sectional Participants: 260 Evidence: moderate
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Of 386 participants, 199 (52%) were female, and the mean (SD) age was 68 (8) years. 3 key findings →
Design: cohort study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 and p-tau181 were correlated (r=0·90, p diff =0·31) and in pathology-confirmed Alzheimer's disease (n=15, mean age 73 years [SD 12]) versus pathologically confirmed FTLD (n=68, mean age 67 years [SD 8]; AUC=0·96 [0·92-1·00] for p-tau217, AUC=0·91 [0·82-1·00] for p-tau181; p diff =0·22). 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings indicate that tau accumulates even in amyloid-negative healthy OA and this process can be measured with in vivo tau-PET. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
With the potential development of new disease-modifying Alzheimer's disease (AD) therapies, simple, widely available screening tests are needed to identify which individuals, who are experiencing symptoms of cognitive or behavioral decline, should be further evaluated for initiation of treatment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Identifying a clinical distinction between the invariably lethal prion disease Creutzfeldt-Jakob disease (CJD) and nonprion rapidly progressive dementias is important and sometimes difficult; thus, reliable tools for diagnosis are in great demand. 4 key findings →
Design: cohort study Participants: 30 Evidence: moderate
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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
Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum. 5 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The spread of protein aggregates during disease progression is a common theme underlying many neurodegenerative diseases. 3 key findings →
Evidence: low
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
Biomarkers to determine underlying frontotemporal lobar degeneration (FTLD) tau or TAR DNA-binding protein (TDP) pathology during life are needed to advance clinical trials targeting specific FTD pathologies. 3 key findings →
Participants: 513 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We recommend a new term, "primary age-related tauopathy" (PART), to describe a pathology that is commonly observed in the brains of aged individuals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease, post-mortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with Brodmann area 35, and the entorhinal cortex. 5 key findings →
Participants: 215 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Researchers used a tau PET agent to examine tau retention patterns in cognitively normal older people and compared them with young controls and Alzheimer's disease patients. 3 key findings →
Evidence: low
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 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 →