27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
These two conclusions support a dynamic biomarker model in which Alzheimer's disease is characterized first by the appearance of amyloidosis and later by tauopathy, with tauopathy being the proteinopathy associated with clinical symptoms. 1 key finding →
Design: longitudinal study Participants: 1,343 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217. 5 key findings →
Design: cross-sectional Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Protection from these ADP factors may be important for aging without significant ADP. 5 key findings →
Design: cohort study Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Vascular health had quantifiably greater impact on neurodegeneration in AD regions than on amyloid deposition. 3 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our main findings were: (i) FDG-PET uptake in the bilateral anterior cingulate cortex and anterior temporal pole was associated with baseline global cognition in cognitively stable 80+ (the resilience signature); (ii) established Alzheimer's disease imaging biomarkers did not predict baseline global cognition in this subset of participants; (iii) in the full MCSA 80+ and ADNI cohorts, amyloid burden and FDG-PET in the resilience signature were the stronger predictors of baseline global cognition; (iv) sex and systemic vascular health predicted FDG-PET in the resilience signature, suggesting vascular health maintenance as a potential pathway to preserve the metabolism of these areas; and (v) the resilience signature provided significant information about global longitudinal cognitive change even when considering amyloid status in both the MCSA and ADNI cohorts. 1 key finding →
Design: longitudinal study Participants: 192 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
GFAP was associated with amyloid and tau PET in multivariable models. 4 key findings →
Design: cross-sectional Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
We observed no differences in plasma AD biomarker levels between AA and NHW participants. 5 key findings →
Participants: 267 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau PET shows higher magnitude of binding in MAPT mutation carriers who harbor mutations that are more likely to produce AD-like tau pathology (e.g., in our series, the non-exon 10 families tend to accumulate mixed 3R/4R aggregates). 2 key findings →
Design: case-control study Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau is a stronger indicator of a temporally linked response to elevated brain Aβ than of tau pathology. 4 key findings →
Participants: 1,408 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain aging is accompanied by patterns of functional and structural change. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
While plasma biomarkers for Alzheimer's disease (AD) are increasingly being evaluated for clinical diagnosis and prognosis, few population-based autopsy studies have evaluated their utility in the context of predicting neuropathological changes. 3 key findings →
Participants: 350 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although white matter hyperintensities have traditionally been viewed as a marker of vascular disease, recent pathology studies have found an association between white matter hyperintensities and Alzheimer's disease pathologies. 4 key findings →
Participants: 434 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures. 4 key findings →
Design: cross-sectional Participants: 995 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study provides a systematic framework for selection of assay-specific cutpoints for clinical use of plasma p-tau217 for determination of amyloid status. 4 key findings →
Participants: 427 Evidence: low
Full summary, score breakdown and related studies → Original source
Longitudinal patterns of clinical decline differ between LPA and PCA but are heterogeneous and related to different patterns of topographic spread. 5 key findings →
Design: case-control study Participants: 27 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The HCTS pattern represents a definable subgroup of non-AD pathophysiology (i.e., T - [N] + ) that is associated with cognitive impairment. 2 key findings →
Participants: 684 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Systemic vascular health has significant impact on brain structure and function. 3 key findings →
Participants: 390 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the cognitively unimpaired group, only higher baseline amyloid PET was a significant independent predictor of higher tau accumulation rates (P < 0.001). 5 key findings →
Participants: 203 Evidence: low
Full summary, score breakdown and related studies → Original source
This was then correlated with overall cortical flortaucipir PET and PiB PET standardized uptake value ratio (SUVr). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-related hippocampal sclerosis may account for a significant proportion of elderly participants with amnestic dementia. 4 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The two main findings of this paper are (i) the posterior default mode network fails before measurable amyloid plaques and appears to initiate a connectivity cascade that continues throughout the disease spectrum; and (ii) high connectivity between the posterior default mode network and hubs of high connectivity (many located in the frontal lobe) is associated with amyloid accumulation. 2 key findings →
Participants: 128 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that ML-PRS approaches improved upon standard PRS for prediction of AD endophenotypes, partly related to improved accounting for nonlinear effects of genetic susceptibility alleles. 3 key findings →
Participants: 1,791 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CMBs are a common vascular pathology in the elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Multiple variables affect plasma biomarkers of amyloid pathology and neurodegeneration among CU in the general population. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most patients with Alzheimer's disease present with amnestic problems; however, a substantial proportion, over-represented in young-onset cases, have atypical phenotypes including predominant visual, language, executive, behavioural, or motor dysfunction. 1 key finding →
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 →