27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
As of a data cutoff of December 3, 2024, 243 participants were screened and 197 randomized in DIAN-TU-001 Tau NexGen trial (Cohort 1: 97; Cohort 2: 100). 5 key findings →
Participants: 243 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Our results elucidate the characteristics and genetic associations of p‐tau217 in a population‐based setting. 4 key findings →
Participants: 697 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A case-control GWAS was performed in the UK Biobank to identify genetic variants associated with postoperative delirium, adjusted for age, sex, genetic chip, and the first 10 principal components. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
=0.002). Early-onset CHD and genetic susceptibility are associated with a higher risk of incident dementia and a larger WMH volume. 2 key findings →
Design: cohort study Participants: 671 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Bibliometric analysis is crucial in identifying research gaps and trends and guiding future studies to address unmet needs in understanding and modeling human physiology and pathology. 1 key finding →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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Researchers conducted immunohistochemical studies on lipid changes in Alzheimer's disease brains using an antibody to apolipoprotein E. They unexpectedly discovered that apo E immunoreactivity was associated with amyloid in senile plaques, cerebral vessels, and neurofibrillary tangles, as well as in kuru plaques in Creutzfeldt-Jakob disease. 3 key findings →
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Magnetic resonance (MR) imaging studies have identified hippocampal structural alterations in the pathogenesis of schizophrenia. 4 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain imaging techniques have the potential to characterize neurobiological changes that precede the onset of cognitive impairment in persons at risk for Alzheimer's disease. 2 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid imaging studies of presymptomatic familial Alzheimer's disease have revealed the striatum and thalamus to be the earliest sites of amyloid deposition. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroplasticity may have a core role in the pathophysiology of major depressive disorder (MDD), a concept supported by experimental studies that found that excessive cortisol secretion and/or excessive production of inflammatory cytokines impairs neuronal plasticity and neurogenesis in the hippocampus. 3 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD). 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
The s allele variant of the serotonin transporter gene (5-HTT) has recently been observed to moderate the relationship of stress to depression and anxiety. 5 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Different patterns of regional brain atrophy were found among patients of different APOE genotypes. 1 key finding →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that different subcortical areas have different vulnerabilities to ischemia in CADASIL. 4 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The effects of acute sleep deprivation on β-amyloid (Aβ) clearance in the human brain have not been documented. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution is a serious environmental problem. 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a genetically complex and heterogeneous disorder. 2 key findings →
Participants: 2,700 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified many risk loci for Alzheimer's disease (AD) 1,2 , but how these loci confer AD risk is unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygenic Risk Scores (PRS) for AD offer unique possibilities for reliable identification of individuals at high and low risk of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Within this region, we defined a 42-SNP haplotype that was associated with significantly increased risk of ALS (p=7·47×10(-33) when people with familial ALS were compared with controls, odds ratio 21·0, 95% CI 11·2-39·1) and which overlapped with an association locus recently reported for frontotemporal dementia. 1 key finding →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are overlapping, fatal neurodegenerative disorders in which the molecular and pathogenic basis remains poorly understood. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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.
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 →