27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In the oldest old, the presence of the APOE epsilon2 allele (APOE2) was associated with a somewhat reduced risk of dementia, but paradoxically was associated with increased Alzheimer disease (AD) neuropathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Human apolipoprotein E (apoE) isoforms may differentially modulate amyloid-β (Aβ) levels. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results demonstrate that endogenous expression of E4 by stem-cell-derived forebrain excitatory neurons predisposes neurons to calcium dysregulation and ultimately cell death. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The molecular signatures of cells in the brain have been revealed in unprecedented detail, yet the ageing-associated genome-wide expression changes that may contribute to neurovascular dysfunction in neurodegenerative diseases remain elusive. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest a potential link between vascular risk and tau pathology in preclinical AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The NBV significantly correlated with all clinical scores (Rankin, NIH Stroke Scale, Barthel, structured interview for the diagnosis of Alzheimer dementia and multi-infarct dementia, Mattis dementia rating scale) at both time points independently of age and sex. 2 key findings →
Design: cross-sectional Evidence: low
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= 0.006). Univariable MR analyses indicated that education and participation reduced the risk of AD. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In their study, Chen et al 1 examined the association between apolipoprotein E (APOE) genotype and longitudinal cognitive trajectories among middle-aged and older East Asian adults participating in the Healthy Aging Longitudinal Study of Taiwan (HALST).Although sporadic late-onset Alzheimer disease (AD) is polygenic, APOE remains the strongest genetic determinant of AD risk, with carriers of the APOE ε4 allele having increased odds of developing AD dementia in a dose-dependent manner compared with APOE ε3 homozygotes. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
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< 0.001). This study suggests 2 molecular pathways underlying CAA, with a larger effect size for the pathway including SFRP1 and APOE protein and C-terminally truncated Aβ before position 40. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several genetic risk factors for Alzheimer's disease implicate genes involved in lipid metabolism and many of these lipid genes are highly expressed in glial cells 1 . 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Understanding the tissue-specific genetic controls of protein levels is essential to uncover mechanisms of post-transcriptional gene regulation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases are a growing burden, and there is an urgent need for better biomarkers for diagnosis, prognosis, and treatment efficacy. 5 key findings →
Participants: 197 Evidence: low
Full summary, score breakdown and related studies → Original source
Robust and accessible biomarkers that can capture the heterogeneity of Alzheimer's disease and its diverse pathological processes are urgently needed. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
The pleiotropic nature of the apolipoprotein E (APOE) gene is associated with complex diseases in different populations. 2 key findings →
Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source
FUS-enhanced delivery of AAV resulted in a 12.6% knockdown of APOE ε4 gene expression in the targeted hippocampus, accompanied by an over 20% decrease in apoE4 protein levels and significant reductions in astrocyte and microglia levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Biofluid markers of phosphorylated tau181 (p-tau181) are increasingly popular for the detection of early Alzheimer's pathologic changes. 3 key findings →
Participants: 727 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified 115 pathology-confirmed rpAD cases and 193 clinical rpAD cases, 80% and 69% were of non-Hispanic European ancestry. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Language impairment is common in prodromal stages of Alzheimer's disease (AD) and progresses over time. 4 key findings →
Participants: 1,560 Evidence: low
Full summary, score breakdown and related studies → Original source
Eighty-six rare missense or loss-of-function (LoF) variants completely segregated in 17.5% of families, but in 91 (22.1%) families Apolipoprotein E (APOE)-𝜀4 was the only variant segregating. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Augmenting traditional genome-wide association studies (GWAS) with advanced machine learning algorithms can allow the detection of novel signals in available cohorts. 3 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes is an established risk factor for dementia. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Five loci showed genome-wide significant association with CSF profiles, two were novel (rs145791381 [inflammation] and GRIN2D [synaptic functioning]) and three were previously described (APOE, TMEM106B, and CHI3L1). 5 key findings →
Participants: 205 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome wide association studies (GWAS) of human diseases have generally identified many loci associated with risk with relatively small effect sizes. 2 key findings →
Participants: 1,865 Evidence: low
Full summary, score breakdown and related studies → Original source
The existence of human hippocampal neurogenesis has long been disputed1-12 and its relevance in cognition remains unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau. 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 →