BIN1 is a genetic risk factor of late-onset Alzheimer disease (AD), which was identified in multiple genome-wide association studies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
I coauthored a recently published research article describing a variable length, poly-T polymorphism in the TOMM40 gene, adjacent to apolipoprotein E (APOE) on chromosome 19, that accounts for the age at onset distribution for a complex disease, late-onset Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of β-amyloid (Aβ) in the brain is a key event in Alzheimer disease pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (APOE) is the only confirmed susceptibility gene for late-onset Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) risk is modified by both genetic and environmental risk factors, which are believed to interact to cooperatively modify pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD), the most common dementing syndrome in the United States, is currently established by the presence of amyloid-β and tau protein biomarkers in the setting of clinical cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Machine learning enables scalable quantification of neuropathology, offering deeper phenotyping of Alzheimer's disease (AD). 4 key findings →
Participants: 273 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings highlight normative modelling's utility in revealing the complex interplay among sex, age, and AD risk in shaping brain structure and cognition in later life. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
43/100
None of the genetically proxied functional network features were significantly associated with neurodegenerative outcomes (adjusted P value >0.05), despite sufficient calculated power. 5 key findings →
Participants: 47 Evidence: low
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Interaction of the amino- and carboxyl-terminal domains in apolipoprotein (apo) E, referred to as domain interaction, is predicted to be more pronounced in apoE4 than in apoE3 and to underlie the association of apoE4 with Alzheimer and cardiovascular diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This joint Position Paper, developed by the Italian Expert Panel on Alzheimer convened by the Italian Society of Neurology with participation from multiple scientific societies, outlines strategic guidelines for reorganizing the patient journey in the era of anti-amyloid monoclonal antibodies for Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
AD risk was associated with shorter TL (β = -0.48, P < 2 × 10–16). 5 key findings →
Participants: 6,973 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of the 75 LOAD associated loci, 52 had at least one variant in the top1% of |nSL| in two populations from the 1000 Genomes data. 5 key findings →
Participants: 2,504 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher total meat consumption (red meat: 51%, poultry: 20%, processed meat: 29%), was associated with a better cognitive trajectory only in the APOE34/44 stratum (β per 1 z-unit increase: 0.011; CI: 0.004 to 0.018 versus -0.003; CI: -0.008 to 0.003; P for interaction = 0.002). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Over 15 years of follow-up (UKB), moderate or high CVH versus low CVH was associated with a lower risk of MCI (hazard ratio 0.82 [95% CI 0.71, 0.95], P < 0.05) but not with risk of all-cause dementia (0.97 [0.84, 1.11], P = 0.63). 4 key findings →
Participants: 41,374 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neprilysin (NEP) degrades amyloid-beta (Abeta) and is thought to contribute to its clearance from the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is one of the major causes of disability in later life, and ischemic heart disease is a leading cause of morbidity and mortality. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Senile dementia with tangles is a sporadic subset of very late onset dementia with preponderance in females over age 80 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We tested association of nine late-onset Alzheimer's disease (LOAD) risk variants from genome-wide association studies (GWAS) with memory and progression to mild cognitive impairment (MCI) or LOAD (MCI/LOAD) in older Caucasians, cognitively normal at baseline and longitudinally evaluated at Mayo Clinic Rochester and Jacksonville (n>2000). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vitamin D and vitamin D receptor (VDR) have been postulated as environmental and genetic factors in neurodegeneration disorders including multiple sclerosis (MS), Alzheimer disease (AD), and recently Parkinson disease (PD). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Previous data demonstrate that bexarotene (Bex), retinoid X receptor (RXR) agonist, reduces soluble and insoluble amyloid-β (Aβ) in Alzheimer disease (AD)-transgenic mice either by increasing the levels of mouse apolipoprotein E (apoE) or increasing ABCA1/ABCG1-induced apoE lipoprotein association/lipidation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Attention deficit is one of the core symptoms of the attention-deficit/hyperactivity disorder (ADHD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
NAD(P)H quinone oxidoreductase 1 (NQO1) is a multi-functional protein that catalyses the reduction of quinones (and other molecules), thus playing roles in xenobiotic detoxification and redox balance, and also has roles in stabilising apoptosis regulators such as p53. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 28,580 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.
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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →