Diabetes increased the risk of conversion to dementia. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Diabetes increased the risk of conversion to dementia. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Low levels of vitamin D were associated with substantial cognitive decline in the elderly population studied over a 6-year period, which raises important new possibilities for treatment and prevention. 5 key findings →
Participants: 858 Evidence: low
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A cohort of 4 522 160 US veterans (4 243 462 [93.8%] male; median [interquartile range] age, 64.1 [55.7-75.5] years; 3 702 942 [82.0%] white, 667 550 [14.8%] black, and 145 593 [3.2%] other race) was followed up for a median (interquartile range) of 10.0 (6.8-10.2) years. 5 key findings →
Design: cohort study Evidence: moderate
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Cognitive exercise training in healthy older individuals produces strong and persistent protective effects on longitudinal neuropsychological performance. 3 key findings →
Design: longitudinal study Participants: 54 Evidence: high
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Nineteen studies met our inclusion criteria and quality assessments. 3 key findings →
Design: systematic review Evidence: high
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Depressive symptoms may increase the risk of progressing from mild cognitive impairment (MCI) to dementia. 2 key findings →
Design: randomized controlled trial Evidence: high
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Impaired glucose regulation is a defining characteristic of type 2 diabetes mellitus (T2DM) pathology and has been linked to increased risk of cognitive impairment and dementia. 4 key findings →
Evidence: high
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The measured benefits in clinical trials for the treatment of mixed dementia are best described as statistically significant differences in cognitive test scores and clinician and caregiver impressions of change. 1 key finding →
Evidence: low
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Greater understanding of the risk factors and mechanisms of incident dementia in stroke survivors is needed for prevention and management. 3 key findings →
Design: longitudinal study Participants: 355 Evidence: moderate
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Our results support the notion that antihypertensive treatment has beneficial effects on cognitive decline and prevention of dementia, and indicate that these effects may differ between drug classes with ARBs possibly being the most effective. 5 key findings →
Design: systematic review Participants: 15 Evidence: high
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Whether the cognitive benefits of physical exercise can improve the overall well-being of this group remains unknown. 2 key findings →
Design: randomized controlled trial Participants: 120 Evidence: high
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Our data from a population-based study support the hypothesis that estrogen-replacement therapy is associated with a reduced prevalence of Alzheimer's disease in postmenopausal women. 4 key findings →
Evidence: low
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We observed a complex series of relationships between social-environment variables and cognitive decline and dementia. 3 key findings →
Design: longitudinal study Participants: 2,854 Evidence: moderate
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In total, 1,234 articles were identified from the search; 21 articles met inclusion criteria. 5 key findings →
Design: systematic review Evidence: high
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Intake of coffee alone or in combination with tea was associated with lower risk of poststroke dementia. 3 key findings →
Design: cohort study Participants: 365,682 Evidence: moderate
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This is relevant as the number of old people (a) living alone and (b) suffering from dementia is expected to increase rapidly in the next decades. 2 key findings →
Design: longitudinal study Participants: 201 Evidence: moderate
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Increasing evidence indicates that physical activity and exercise training may delay or prevent the onset of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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APOE ε4 carriage and older age were predictors of longitudinal Aβ accumulation within the Aβ- group but not the Aβ+ group. 5 key findings →
Design: longitudinal study Participants: 325 Evidence: moderate
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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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Longitudinal clinical-pathological studies have increasingly recognized the importance of mixed pathologies (the coexistence of one or more neurodegenerative and cerebrovascular disease pathologies) as important factors in the development of Alzheimer's disease (AD) and other forms of dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
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The acceleration of incidence rates for AD and dementia slows down with the increase in age, although we find no evidence of a rate decline. 2 key findings →
Design: meta-analysis Evidence: high
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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
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PSCI is common after stroke, especially in the first year, and ranges from mild to severe. 1 key finding →
Design: cohort study Evidence: high
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a multi-center study assessing neuroimaging in diagnosis and longitudinal monitoring. 4 key findings →
Design: longitudinal study Participants: 339 Evidence: moderate
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Alzheimer's disease is a common and devastating disease for which there is no readily available biomarker to aid diagnosis or to monitor disease progression. 1 key finding →
Design: case-control study Participants: 50 Evidence: moderate
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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 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.
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 →