The study encompassed 284 cases with dementia and 1080 controls. 1 key finding →
Design: case-control study Evidence: moderate
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Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma amyloid-β (Aβ) peptide levels have been examined as a low-cost accessible marker for risk of incident Alzheimer's disease (AD) and dementia, but results have varied between studies. 4 key findings →
Participants: 2,189 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
68/100
Subjective cognitive decline (SCD) is recognized to be in the Alzheimer disease (AD) cognitive continuum. 4 key findings →
Design: cohort study Participants: 3,585 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From the 868 Framingham Heart Study participants who returned for a second PSG, this cohort included 346 participants with a mean age of 69 years (range, 60-87 years); 179 (52%) were female. 4 key findings →
Design: cohort Participants: 346 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
These results from the largest longitudinal cohort registry of patients with CAA-ri support the transient and potentially relapsing inflammatory nature of the clinical-radiologic acute manifestations of the disease and the effectiveness of slow oral tapering off after IV corticosteroid pulse therapy in preventing recurrences. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Fasting lipid fractions (triglycerides [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuous variables, and results are reported per SD increase of each lipid fraction. 5 key findings →
Design: cohort study Participants: 9,294 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Atrial fibrillation, hypertension, and angina were associated with a greater rate of decline and may represent modifiable risk factors for secondary prevention in Alzheimer disease. 3 key findings →
Design: longitudinal study Participants: 135 Evidence: moderate
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Accumulating data suggest that cerebrovascular disease contributes to Alzheimer's disease pathophysiology and progression toward dementia. 5 key findings →
Design: cohort study Participants: 1,722 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of the 7342 total sample, 4348 participants (60.3%) were women. 5 key findings →
Design: cohort study Participants: 7,342 Evidence: moderate
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Elevated blood pressure during midlife, persistence of elevated blood pressure into late life, and, among nonhypertensives, a steep decline in blood pressure during mid- to late life were associated with an increased dementia risk in a community-based cohort. 5 key findings →
Participants: 1,440 Evidence: moderate
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Dementia risk may be attenuated by physical activity (PA); however, the specific activity levels optimal for dementia prevention are unclear. 4 key findings →
Design: cohort study Participants: 1,604 Evidence: moderate
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Among eligible participants (n = 705,061), 264,294 individuals (37.5% of eligible participants) initiated any statin during 2001-2010 ("initiators"), of whom 249,613 (94.4%) were matched with 255,937 unique noninitiators to create the analytic sample (322,358 unique participants; mean age at baseline = 67.4 years; 55.1% female). 3 key findings →
Design: cohort Participants: 322,358 Evidence: high
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Higher concentrations of serum biomarkers were associated with the development of clinical AD; especially, the time-specific associations were notable: t-tau 8 to 16 years, and Nf-L and GFAP 4 to 8 years prior to clinical AD. 3 key findings →
Design: longitudinal study Participants: 1,327 Evidence: moderate
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Blood biomarkers showed significant longitudinal changes corresponding to cognitive decline, clinical AD, and structural MRI characteristics. 5 key findings →
Design: longitudinal study Participants: 1,327 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 158 participants who accurately recalled their Alzheimer disease risk assessment 6 weeks after risk disclosure, 75 (47.5%) believed their Alzheimer disease risk was more than 5% points different from the Alzheimer disease risk estimate they were given. 2 key findings →
Design: randomized controlled trial Participants: 158 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein. 1 key finding →
Participants: 85 Evidence: moderate
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Among older Medicare beneficiaries, incident AF is common and has remained relatively stable for more than a decade. 3 key findings →
Design: cohort study Participants: 433,123 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We estimated the remaining lifetime risks of developing Alzheimer's disease (AD) and dementia from all causes, based on data from longitudinal population studies. 5 key findings →
Design: longitudinal study Participants: 198 Evidence: moderate
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66/100
Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. 1 key finding →
Participants: 515 Evidence: low
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There were 132 720 unique adults with Down syndrome from 2011 to 2019: 79 578 (53.2%) were male, 17 090 (11.7%) were non-Hispanic Black, 20 777 (15.7%) were Hispanic, 101 120 (68.8%) were non-Hispanic White, and 47 692 (23.3%) had ever had an Alzheimer dementia diagnosis. 3 key findings →
Design: cohort study Participants: 132 Evidence: moderate
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Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →
Evidence: low
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We analyzed prospectively collected data in the Original and Offspring FHS cohorts. 4 key findings →
Design: case-control study Participants: 4,906 Evidence: moderate
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Circulating homocysteine levels (tHcy), a product of the folate one carbon metabolism pathway (FOCM) through the demethylation of methionine, are heritable and are associated with an increased risk of common diseases such as stroke, cardiovascular disease (CVD), cancer and dementia. 4 key findings →
Design: meta-analysis Participants: 2,710 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
66/100
Researchers conducted a large, two-stage meta-analysis of genome-wide association studies in individuals of European ancestry.
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →