These samples were graded on an ordinal scale and genotyped for variants associated with synucleinopathies. 2 key findings →
Participants: 213 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.
These samples were graded on an ordinal scale and genotyped for variants associated with synucleinopathies. 2 key findings →
Participants: 213 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In amyotrophic lateral sclerosis and neocortical Lewy body disease, co-pathologies associated with APOE ɛ4. 2 key findings →
Participants: 247 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217/Aβ42 had high accuracy to detect AD, with comparable performance across race. 2 key findings →
Design: cross-sectional Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To better understand clinical and neuropathological features of TDP-43 proteinopathies, data were analyzed from autopsied research volunteers who were followed in the National Alzheimer's Coordinating Center (NACC) data set. 4 key findings →
Design: longitudinal study Participants: 495 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) core Alzheimer disease (AD) biomarkers have shown an excellent capacity for the in vivo detection of AD. 4 key findings →
Design: case-control study Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this real-world dataset, we identified effects of multimorbidities on plasma biomarkers, especially kidney function. 2 key findings →
Design: cross-sectional Participants: 617 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are characterized by cytoplasmic protein aggregates in the brain and spinal cord that include TAR-DNA binding protein 43 (TDP-43). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal lobar degeneration (FTLD) comprises two main classes of neurodegenerative diseases characterized by neuronal/glial proteinaceous inclusions (i.e., proteinopathies) including tauopathies (i.e., FTLD-Tau) and TDP-43 proteinopathies (i.e., FTLD-TDP) while other very rare forms of FTLD are known such as FTLD with FUS pathology (FTLD-FUS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with autopsy-confirmed LBD (n = 24) and autopsy-confirmed Alzheimer disease (AD) (n = 23) and cognitively normal (n = 36) controls were studied. 4 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A growing body of evidence demonstrates an association between vascular risk factors and Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Development of validated biomarkers to detect early Alzheimer disease (AD) neuropathology is needed for therapeutic AD trials. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The term "aging-related tau astrogliopathy" (ARTAG) describes pathological accumulation of abnormally phosphorylated tau protein in astrocytes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Olfactory dysfunction is common in Alzheimer disease (AD) and other neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
All measures distinguished the dementia and control groups and all markers associated with the cognitive test scores. 4 key findings →
Participants: 84 Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a diverse group of progressive and fatal neurodegenerative diseases characterized by aberrant tau inclusions in the central nervous system. 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 →