Many elderly individuals remain dementia-free throughout their life. 3 key findings →
Participants: 299 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
51/100
Vascular risk factors for Alzheimer disease (AD) and vascular dementia (VaD) have been evaluated; however, few studies have compared risks by dementia subtypes and sex. 1 key finding →
Evidence: moderate
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Outer retinal degenerations, including age-related macular degeneration (AMD), are characterized by photoreceptor and retinal pigment epithelium (RPE) atrophy. 4 key findings →
Evidence: low
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The Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-Cog) is widely used in AD, but may be less responsive to change when used in people with mild cognitive impairment (MCI). 4 key findings →
Participants: 811 Evidence: low
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ADI groups differed by sex, ethnoracial background, and MMSE scores. 5 key findings →
Design: cohort study Participants: 755 Evidence: moderate
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Among 203 enrolled patients, 186 (mean [SD] age, 68.7 [5.2] years; 119 males [64.0%]) were randomized (137 to the CN-105 group, 49 to the placebo group) and underwent surgery. 5 key findings →
Design: clinical trial Evidence: high
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Inheritance of specific apolipoprotein E (apoE) alleles determines, in large part, the risk and mean age of onset of late-onset familial and sporadic Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Use of vitamin E and vitamin C supplements in combination is associated with reduced prevalence and incidence of AD. 4 key findings →
Design: cross-sectional Evidence: low
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Six standardized published measures of cognitive function were evaluated as screens of dementia in a sample of 164 (83 black, 81 white) community residents aged 65 and over selected from the Duke University EPESE (Established Populations for Epidemiologic Studies of the Elderly), a biracial cohort of 4164 residents in a five county area of piedmont North Carolina. 5 key findings →
Participants: 164 Evidence: moderate
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Prior studies report that subjects with neuropathologic evidence of AD and concomitant brain infarcts had poorer cognitive function and higher frequency of dementia than those with AD alone. 4 key findings →
Participants: 74 Evidence: low
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Mitochondrial DNA (mtDNA) variants associated with Alzheimer disease (AD) and Parkinson disease (PD) were sought by restriction endonuclease analysis in a cohort of 71 late-onset Caucasian patients. 4 key findings →
Evidence: moderate
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A genetic classification of Alzheimer disease(s) (AD) is presented. 4 key findings →
Evidence: low
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Cognitive impairment and late-life depression are associated with increased risk for subsequent dementia; however, investigations of these phenomena appear to be proceeding along separate tracks. 4 key findings →
Evidence: low
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The apolipoprotein E (apoE) type 4 allele (APOE4) is a susceptibility gene for late-onset familial and sporadic Alzheimer disease. 5 key findings →
Evidence: low
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We examined the association of mtDNA variation with Alzheimer disease (AD) risk in Caucasians (989 cases and 328 controls) testing the effect of individual haplogroups and single nucleotide polymorphisms (SNPs). 3 key findings →
Evidence: low
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49/100
Only Apolipoprotein E polymorphisms have been consistently associated with the risk of late-onset Alzheimer disease (LOAD), but they represent only a minority of the underlying genetic effect. 2 key findings →
Evidence: low
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Most older patients surviving AMI have measurable CIND. 2 key findings →
Participants: 772 Evidence: low
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There is a shortage of adequate screening instruments for dementia in poorly educated populations and non-English-speaking groups. 1 key finding →
Participants: 5,126 Evidence: low
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The brain is not only immunologically active of its own accord, but also has complex peripheral immune interactions. 5 key findings →
Evidence: low
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Three cohorts of interdisciplinary scholars (N = 53) have started and two have completed DEM-PCCT. 5 key findings →
Design: longitudinal study Participants: 53 Evidence: moderate
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There has been great interest in the prospects of using single-nucleotide polymorphisms (SNPs) in the search for complex disease genes, and several initiatives devoted to the identification and mapping of SNPs throughout the human genome are currently underway. 2 key findings →
Evidence: low
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Epidemiologic studies indicate that elderly women are at higher risk for Alzheimer disease compared to men. 3 key findings →
Evidence: low
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48/100
HIV produces a chronic viral infection of the central nervous system that elicits chronic glial activation and overexpression of glial cytokines that are also implicated in Alzheimer disease (AD) pathogenesis. 1 key finding →
Evidence: moderate
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Prevalence, 3-year incidence, and types of dementia are comparable in Black and White elderly in the Piedmont area of North Carolina. 3 key findings →
Participants: 4,136 Evidence: low
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Design identification of relevant items, pre-testing of items and refinement of administrative procedures and scoring in four successive groups of 30 subjects each, pilot testing in a group of 100 subjects comparable to those for whom the measure is intended, administration to a representative sample of 387 people aged 55 and older, and assessment of the reliability of the final measure. 2 key findings →
Participants: 30 Evidence: low
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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 29,380 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.
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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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 (3.5% 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 →