Carriers had higher plasma p-tau217 levels than non-carriers. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Heritability estimates were 16% for Aβ42/40, 42% for NfL, and 60% for GFAP. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The study population consisted of 194 patients (123 AD and 71 non-AD). 5 key findings →
Participants: 194 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau at threonine-181 (P-tau181) demonstrates promise as an accessible blood-based biomarker specific to Alzheimer's Disease (AD), with levels recently demonstrating high predictive accuracy for AD-relevant pathology. 2 key findings →
Participants: 1,153 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated associations between apolipoprotein E (APOE) alleles and motor manifestations in Alzheimer's dementia (AD) capitalizing on National Alzheimer's Coordinating Center data: the baseline evaluations of older adults (≥60 years) with a diagnosis of AD were analyzed. 3 key findings →
Participants: 389 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 37 SuperAgers (73% female, mean [standard deviation] 82.7 [2.8] years old) and 35 controls (54% female, 83.7 [4.3] years old) were included. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal subfield atrophy is a prime structural change in the brain, associated with cognitive aging and neurodegenerative diseases such as Alzheimer's disease. 3 key findings →
Participants: 1,086 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical genetic diagnosis was achieved in 7 of 50 (14%) of the patients, with a further 8 patients (16%) found to have established risk factors which may have contributed to their EOD. 5 key findings →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
A total of 1,350 publications with 59,818 citations were identified. 5 key findings →
Participants: 1,350 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
We performed a genome-wide association study (GWAS) of human extreme longevity (EL), defined as surviving past the 99th survival percentile, by aggregating data from four centenarian studies. 4 key findings →
Participants: 2,304 Evidence: low
Full summary, score breakdown and related studies → Original source
OptPRS predicted AD dementia and Aβ positivity, independent of apolipoprotein E (APOE). 5 key findings →
Participants: 1,634 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Two ABCA7 missense variants (rs3764647 and rs3752239) demonstrated significant association with AD risk. 4 key findings →
Participants: 319 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Thirteen pathway clusters were identified, and eight pathway-specific PRSs were significantly associated with AD diagnosis. 5 key findings →
Participants: 1,411 Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenic relevance in Alzheimer's disease (AD) presents a decrease of cerebrospinal fluid amyloid-ß42 (Aß42) burden and an increase in cerebrospinal fluid total tau (T-tau) levels. 3 key findings →
Participants: 843 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using the data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we performed a genome-wide association study (GWAS) between 565,373 single nucleotide polymorphisms (SNPs) and 16 key AD biomarkers from 1,576 subjects at four visits. 5 key findings →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, several studies have investigated the association between the rare mutation of triggering receptor expressed on myeloid cells 2 (TREM2) gene (rs75932628-T) and the risk of late-onset Alzheimer's disease (LOAD), but they did not draw the same conclusion. 5 key findings →
Participants: 786 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
We identified 7 functional variants in APP/PSENs in 8 patients, including 1 APP mutation (p. Val715Met), 3 PSEN1 mutations (p. Phe177Ser; p. Arg377Met; p. Ile416Thr), and 3 PSEN2 mutations (p. Glu24Lys; p. Gly34Ser; p. Met239Thr). 5 key findings →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source
Transcriptomics and polygenic risk analysis position resilience as an intermediate AD state. 5 key findings →
Participants: 631 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease. 1 key finding →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
[18F]Flortaucipir BPND images showed overall highest binding in the symptomatic carriers. 5 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Compared to APOE ε4 non-carriers, APOE ε4 carriers had lower rsFC in temporal DMN, but only in non-Hispanic Whites. 3 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source
This study demonstrated that APOE4 carrier status was associated with lower MoCA-INA scores in this small VaD cohort. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Alzheimer’s Disease Sequencing Project (ADSP) performed whole genome sequencing (WGS) of 584 subjects from 111 multiplex families at three sequencing centers. 1 key finding →
Participants: 584 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Variation in human lifespan is 20 to 30% heritable in twins but few genetic variants have been identified. 3 key findings →
Participants: 75,244 Evidence: low
Full summary, score breakdown and related studies → Original source
Among 455,306 UK Biobank participants, 37 carried one copy of the APOE Christchurch variant (allele frequency 0.004%). 4 key findings →
Design: cohort Participants: 455,306 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Prediction of individual clinical outcome in MCI by means of genetic assessment and (18)F-FDG PET
- Apolipoprotein E ϵ4 and cerebral hemorrhage associated with amyloid angiopathy
- Alzheimer's disease amyloid-beta peptide modulates apolipoprotein E isoform specific receptor binding
- Integrative system biology analyses of CRISPR-edited iPSC-derived neurons and human brains reveal deficiencies of presynaptic signaling in FTLD and PSP
- Apolipoprotein E in lipoprotein metabolism, health and cardiovascular disease
- Investigation of c9orf72 in 4 neurodegenerative disorders
- Non-genetic risk and protective factors and biomarkers for neurological disorders: a meta-umbrella systematic review of umbrella reviews
- APOE-epsilon4 count predicts age when prevalence of AD increases, then declines: the Cache County Study
- Coding mutations in SORL1 and Alzheimer disease
- APOE4 Causes Widespread Molecular and Cellular Alterations Associated with Alzheimer's Disease Phenotypes in Human iPSC-Derived Brain Cell Types
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →