These data confirm that NPS are risk factors for conversion from CIND to dementia. 1 key finding →
Participants: 230 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
No associations between n-3 PUFAs and dementia or AD were found. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The mean ± SD plasma 25(OH)D concentration was 68.7 ± 19.1 nmol/L. Plasma 25(OH)D, dietary vitamin D intake, and vitamin D-synthesis GRS were not associated with any cognitive outcomes (crude and adjusted HRs and ORs were ∼1.0 for all continuous exposures). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
IV analyses suggest education is protective against risk of dementia in older adulthood. 1 key finding →
Participants: 7,981 Evidence: moderate
Full summary, score breakdown and related studies → Original source
52/100
Polygenic risk scores have identified that genetic variants without genome-wide significance still add to the genetic risk of developing Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We studied the association between mid-life smoking and late-life dementia in the Honolulu Heart Program (1965-1971) and follow-up assessment for dementia (1991-1996) of 3734 Japanese-American men (80% of survivors). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
By multiple logistic regression, the APOE-epsilon 4 allele frequency was significantly higher in the patients positive for HSV1 in brain than in the HSV1-negative AD group, the HSV1-positive non-AD group, or the HSV1-negative non-AD group (52.8% vs 10.0%, 3.6%, and 6.3%, respectively). 3 key findings →
Participants: 40 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
52/100
Using a wide range of cognitive function and dementia endpoints, we failed to find genetic evidence of an adverse PCSK9-related impact, suggesting a neutral cognitive profile. 3 key findings →
Participants: 740,000 Evidence: low
Full summary, score breakdown and related studies → Original source
In the Cardiovascular Health Cognition Study, consumption of fatty fish was associated with a reduced risk of dementia and Alzheimer disease for those without the APOE epsilon4 allele. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
51/100
Serum hypercholesterolemia may be an early risk factor for the development of AD amyloid pathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This comprehensive population genetic study in control subjects fills the void for a PARK2 reference dataset. 3 key findings →
Participants: 1,686 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ApoE on high-density lipoproteins is primarily responsible for lipid transport and cholesterol homeostasis in the central nervous system (CNS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The results of this study suggest that hyperinsulinemia and hyperglycemia caused by insulin resistance accelerate NP formation in combination with the effects of APOE epsilon4. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In generalized estimating equation models (adjusted for age, race/ethnicity, and years of education), higher cholesterol (total cholesterol and LDL-C) concentrations and history of diabetes were associated with faster cognitive decline. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Insulin resistance (IR) is the main pathological condition underlying vascular disorders, such as diabetes and cardiovascular disease, which are well established risk factors for cognitive decline and Alzheimer disease (AD). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
= 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
Type 2 diabetes is an established risk factor for dementia. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There was no difference in age acceleration between dementia cases and controls. 3 key findings →
Participants: 160 Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic factors influencing common complex conditions have proven difficult to identify, and data from numerous investigations have provided incomplete conclusions as to the identity of these genes. 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Ten-year absolute risk of all-cause dementia increased with age, APOE ɛ4 alleles, GWAS risk alleles, diabetes, low education, and smoking in both women and men. 1 key finding →
Participants: 664 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent epidemiological and clinico-pathologic data suggest overlaps between Alzheimer disease (AD) and cerebrovascular lesions that may magnify the effect of mild AD pathology and promote progression of cognitive decline or even may precede neuronal damage and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Severe CAA confers a greater risk of VLs in AD, even within strata of APOE genotype. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Vascular contributions to cognitive impairment and dementia (VCID) are a common cause of cognitive decline, yet limited therapies exist. 2 key findings →
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. 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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