31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD. 4 key findings →
Design: cross-sectional Participants: 257 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aggregated insoluble tau is one of two defining features of Alzheimer's disease. 3 key findings →
Participants: 448 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Insoluble tau aggregates within neurofibrillary tangles are a defining neuropathological feature of Alzheimer’s disease (AD) and closely correlate with clinical symptoms. 2 key findings →
Participants: 108 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal tau positron emission tomography (PET) is a relevant outcome in clinical trials evaluating disease-modifying therapies in Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 215 Evidence: moderate
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
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
Blood biomarkers indicative of Alzheimer's disease (AD) pathology are altered in both preclinical and symptomatic stages of the disease.
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
Although all p-tau variants increased across the AD continuum, p-tau217 Lilly showed the greatest dynamic range (13-fold increase vs 1.9-5.4-fold increase for other p-tau variants for AD dementia vs non-AD). 2 key findings →
Participants: 334 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is characterized by β-amyloid plaques and tau tangles. 4 key findings →
Participants: 88 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuroimaging and biofluid tau markers hold potential for optimising such clinical trials by augmenting participant selection, providing evidence of target engagement, and monitoring treatment efficacy. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) 1 . 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers. 3 key findings →
Participants: 400 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results indicate good diagnostic and prognostic performance of the plasma p-tau217+ Janssen assay, similar to the p-tau217 Lilly assay. 2 key findings →
Participants: 25 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The advent of PET ligands that bind tau pathology has enabled the quantification and visualization of tau pathology in aging and in Alzheimer disease (AD). 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study included 560 amyloid-positive participants (BioFINDER: n = 431; mean [SD] age, 73.6 [7.0] years; 212 female [49.2%] and 219 male [51.8%]; TRIAD: n = 129; mean [SD] age, 70.4 [8.3] years; 76 female [58.9%] and 53 male [41.1%]). 5 key findings →
Design: cohort study Participants: 431 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that structural MRI can be used to identify biologically and clinically meaningful subtypes of AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We studied the promising Alzheimer biomarker plasma tau phosphorylated at threonine 231 (p-tau231) in a cohort of cardiac arrest patients who survived to intensive care to predict long-term neurological outcomes. 4 key findings →
Design: cohort study Participants: 425 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To efficiently implement plasma and cerebrospinal fluid (CSF) biomarkers for staging and prognosis of Alzheimer disease (AD), we must understand their dynamics across disease progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau. 5 key findings →
Design: longitudinal study Participants: 494 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this patient, the clinical disease symptoms progressed rapidly in life, paralleled with an annual increase of tau PET retention of 20% to 40% in many cortical regions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both visual read methods exhibited strong concordance with semiquantitative SUVRs. 5 key findings →
Design: cohort study Participants: 1,654 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Across 3 study samples, combining the functional connectome and molecular properties substantially enhanced the explanatory power compared to single modalities, providing a valuable tool to explain regional susceptibility to tau deposition in AD. 3 key findings →
Participants: 1,000 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,045 records (3.3% of the library) are not peer-reviewed — 966 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events
Last updated