There is loss of the microarray-derived candidate, LR11, in neurons of AD brains. 5 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
There is loss of the microarray-derived candidate, LR11, in neurons of AD brains. 5 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
All women undergo the menopause transition (MT), a neuro-endocrinological process that impacts aging trajectories of multiple organ systems including brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Interleukin-1 (IL-1) is markedly overexpressed in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, amyloid deposits along the brain vasculature lead to a condition known as cerebral amyloid angiopathy (CAA), which impairs blood-brain barrier (BBB) function and accelerates cognitive degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of amyloid β (Aβ) plaques, tau tangles, inflammation, and loss of cognitive function. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Deciphering the functional interactions of cells in tissues remains a major challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent genome wide association studies have implicated bridging integrator 1 (BIN1) as a late-onset Alzheimer's disease (AD) susceptibility gene. 3 key findings →
Participants: 71 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive, neurodegenerative disorder that is characterized by neurodegeneration, cognitive impairment, and an eventual inability to perform daily tasks. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, pathologically characterized by senile plaques and neurofibrillary tangles (NFTs), resulting in neurodegeneration. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Obesity promotes diverse pathologies, including atherosclerosis and dementia, which frequently involve vascular defects and endothelial cell (EC) dysfunction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Advances in single-cell RNA sequencing (scRNA-seq) techniques have accelerated functional interpretation of disease-associated variants discovered from genome-wide association studies (GWASs). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified the PICALM (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic susceptibility locus after APOE and BIN1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological hallmarks of Parkinson's disease (PD) are the progressive loss of dopaminergic neurons in the substantia nigra and the formation of Lewy bodies (LBs) in remaining neurons. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWASs) have discovered numerous risk genes for Alzheimer's disease (AD), but how these genes confer AD risk is challenging to decipher. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The root cause of non-inherited Alzheimer's disease (AD) remains unknown despite hundreds of research studies performed to attempt to solve this problem. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prevalence of somatic insulinopathies, like metabolic syndrome (MetS), obesity, and type 2 diabetes mellitus (T2DM), is higher in Alzheimer's disease (AD), autism spectrum disorder (ASD), and obsessive-compulsive disorder (OCD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is ample pathological and biological evidence for endo-lysosomal dysfunction in Alzheimer's disease (AD) and emerging genetic studies repeatedly implicate endo-lysosomal genes as associated with increased AD risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The chances to develop Alzheimer's disease (AD) result from a combination of genetic and non-genetic risk factors 1 , the latter likely being mediated by epigenetic mechanisms 2 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIV-1-infected opiate abusers often exhibit an accelerated form of HIV-1-associated dementia and enhanced neurological dysfunction. 3 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex and multifactorial neurodegenerative disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings provided evidence supporting a positive relationship between mononucleosis and AD, indicating a causal link between EBV infection and AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
African descent populations have a lower Alzheimer disease risk from ApoE ε4 compared to other populations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several studies have reported an association of Alzheimer's disease (AD) with polymorphic markers in SORL1. 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
Our study provides new insights into the etiology and underlying genetic architecture of AD. 2 key findings →
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events