31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Head injury was associated with risk of dementia (hazard ratio [HR] = 1.44, 95% confidence interval [CI] = 1.3-1.57), with evidence of dose-response (1 head injury: HR = 1.25, 95% CI = 1.13-1.39, 2+ head injuries: HR = 2.14, 95% CI = 1.86-2.46). 3 key findings →
Design: cohort study Participants: 14,376 Evidence: moderate
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Among 13,875 individuals with nonmissing VRF and outcome data with up to 30 years of follow-up (25% Black, 54% female), 179 developed PD at a mean age of 73.4 years, 94 developed PDD at a mean age of 79.2 years, and 1,791 developed dementia without PD at a mean age of 79.7 years. 5 key findings →
Design: longitudinal study Participants: 13,875 Evidence: moderate
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A substantial proportion of the relationship between education and dementia was mediated through mid-life vascular risk factors. 2 key findings →
Design: cohort Participants: 13,368 Evidence: moderate
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Stroke, dementia, and hypertension are associated with late-onset epilepsy; however, the role of other vascular and lifestyle factors remains unclear. 5 key findings →
Design: cohort study Participants: 792 Evidence: moderate
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= 0.009). Significant differences in annualized changes in these FA and MD values were found depending on the presence or absence of type 2 diabetes and smoking. 4 key findings →
Design: longitudinal study Participants: 6,471 Evidence: moderate
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More-severe diabetes (defined by higher HbA 1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. 3 key findings →
Design: cross-sectional Participants: 1,713 Evidence: low
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MarkVCID2 enrolled 1883 individuals age 73.4 ± 7.5 years, 65.0% female, 24.2% Hispanic, and 27.1% non-Hispanic Black. 5 key findings →
Design: longitudinal study Participants: 1,883 Evidence: moderate
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Diabetes status, poor glycemic control, and longer diabetes duration were associated with worse cognitive outcomes over a median follow-up of 5 years. 4 key findings →
Participants: 5,099 Evidence: low
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Intracranial atherosclerotic disease (ICAD) is an important cause of stroke and has also been recently identified as an important risk factor for all-cause dementia, but the mechanism of its association with cognitive performance is not fully understood. 4 key findings →
Design: cohort study Participants: 346 Evidence: moderate
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The plasma proteomic changes that precede the onset of dementia could yield insights into disease biology and highlight new biomarkers and avenues for intervention. 4 key findings →
Participants: 4,110 Evidence: moderate
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We analyzed data from 11,709 participants without a history of coronary heart disease or stroke who attended the baseline examination (1987-1989) of the prospective Atherosclerosis Risk in Communities (ARIC) study. 4 key findings →
Participants: 11,709 Evidence: moderate
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Our findings suggest that poor olfaction is associated with multiple AD-related and other neurodegenerative processes. 5 key findings →
Design: cross-sectional Participants: 1,545 Evidence: moderate
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Hemoglobin A 1c (HbA 1c ), a measure of average blood glucose level, is associated with the risk of dementia and cognitive impairment. 4 key findings →
Participants: 13,000 Evidence: low
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Arterial stiffness, measured by PWV, is an emerging risk factor for dementia through its repeated relationships with cognition, cSVD, and Aβ deposition. 4 key findings →
Design: cross-sectional Evidence: low
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From 2011 to 2013, 1,744 participants completed high-resolution vessel wall MRI from the population-based Atherosclerosis Risk in Communities Study by a sampling strategy that allowed weighting back to the cohort. 4 key findings →
Participants: 291 Evidence: moderate
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Genetic risk for AD does not modify the association between hypertension and dementia. 4 key findings →
Design: cohort Participants: 11,597 Evidence: moderate
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Midlife hypertension and elevated midlife but not late-life systolic BP was associated with more cognitive decline during the 20 years of the study. 5 key findings →
Evidence: moderate
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Among ACHIEVE participants in the top quartile of predicted risk, 3-year cognitive decline in the hearing intervention was 61.6% (95% confidence interval [CI]: 33.7%-94.1%) slower than the control. 5 key findings →
Participants: 2,692 Evidence: moderate
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This study tested the hypotheses that late-midlife obstructive sleep apnea (OSA) and short and long sleep duration are associated with dementia over 15 years of follow-up. 4 key findings →
Participants: 1,667 Evidence: low
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Because cardiovascular (CV) risk factors have been associated with declines in cognitive functions and late life dementia, CV risk factors should also be associated with brain atrophy. 4 key findings →
Participants: 1,812 Evidence: moderate
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& objective Evidence is limited on how estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (UACR) relate to dementia at different ages. 4 key findings →
Design: cohort study Participants: 9,967 Evidence: moderate
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(n = 2,392) had a mean age of 74.4 years, 60.4% were female, and 17.1% were of self-reported Black race. 5 key findings →
Design: cross-sectional Participants: 2,392 Evidence: low
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During follow-up, 203 cases of hospitalisation with dementia were identified. 5 key findings →
Participants: 151 Evidence: moderate
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Even before dementia becomes apparent, cognitive decline may contribute to deterioration in oral health. 4 key findings →
Design: cohort study Participants: 10,050 Evidence: moderate
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AF is associated with greater cognitive decline and increased risk of dementia, independent of ischemic stroke. 5 key findings →
Participants: 515 Evidence: low
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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 31,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
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