27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Although sleep, physical activity and sedentary behavior have been found to be associated with dementia risk, findings are inconsistent and their joint relationship remains unclear. 4 key findings →
Participants: 431,924 Evidence: low
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Analyses were performed within the Rotterdam Study (baseline 1997), a prospective, population-based cohort. 4 key findings →
Participants: 9,446 Evidence: moderate
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Many people with mild cognitive impairment (MCI) suffer from concomitant depression or anxiety. 4 key findings →
Design: cross-sectional Participants: 4,168 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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We aimed to evaluate the link between severe hypoglycaemia and domain-specific cognitive decline, smaller brain volumes and dementia in adults with type 2 diabetes, which so far has been relatively poorly characterised. 4 key findings →
Design: cross-sectional Participants: 580 Evidence: low
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The temporal relationship of cognitive deficit and functional impairment in Alzheimer's disease (AD) is not well characterized. 4 key findings →
Design: clinical trial Evidence: low
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To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer's disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer's Disease Neuroimaging Initiative (ADNI). 4 key findings →
Design: longitudinal study Participants: 1,184 Evidence: moderate
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Setting and participants A total of 316,669 participants [mean (SD) age, 56.3 (8.1) years] without prior cardiovascular disease or dementia from the UK Biobank study at baseline survey (2006-2010) were enrolled. 4 key findings →
Design: cohort study Participants: 316,669 Evidence: moderate
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Poor social health is likely associated with cognitive decline and risk of dementia; however, studies show inconsistent results. 4 key findings →
Participants: 4,514 Evidence: low
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We aimed to investigate whether the increased risk of dementia among individuals with diabetes can be offset by a broad combination of healthy lifestyle factors. 4 key findings →
Participants: 167,946 Evidence: moderate
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Given the potential therapeutic effect of vascular disease control timing to reduce dementia risk, we investigated the age-related influences of vascular risk factor burden on brain structure throughout the lifespan. 4 key findings →
Design: cross-sectional Participants: 2,887 Evidence: moderate
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We included 730 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants without dementia (282 cognitively normal, 448 mild cognitive impairment) with baseline [ 18 F]florbetapir PET and CSF Aβ 42 available. 4 key findings →
Design: longitudinal study Participants: 318 Evidence: moderate
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Several clinical trials are planned for familial forms of frontotemporal lobar degeneration (f-FTLD). 4 key findings →
Design: case-control study Participants: 100 Evidence: moderate
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From 2000 to 2002, we assessed parental history of dementia in participants without dementia of the Rotterdam Study. 4 key findings →
Participants: 2,087 Evidence: moderate
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A high adherence to the Mediterranean-Dietary Approaches to Stop Hypertension Diet Intervention for Neurodegenerative Delay (MIND) has been associated with better cognition and a lower risk of dementia in some but not all studies. 4 key findings →
Participants: 120,661 Evidence: low
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The relationship between mild behavioral impairment (MBI) and Alzheimer's disease (AD) is intricate and still not well investigated. 4 key findings →
Design: longitudinal study Participants: 1,129 Evidence: moderate
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Median follow-up was 7.5 years (interquartile range: 7.0 to 9.0 years), during this time 387 participants (0.8 %) were diagnosed with dementia. 5 key findings →
Design: cohort study Participants: 47,371 Evidence: moderate
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This study included 10 333 FHS 5 key findings →
Design: cohort study Participants: 886 Evidence: moderate
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Increasing frailty is associated with incident AD and the rate of cognitive decline in older persons. 5 key findings →
Design: longitudinal study Participants: 823 Evidence: moderate
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Most prognostic studies on Parkinson disease have been hospital based or have applied register-based case-finding methods. 4 key findings →
Design: cohort study Participants: 6,969 Evidence: moderate
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Amyloid deposition and neurofibrillary degeneration in Alzheimer's disease specifically affect discrete neuronal systems, but the underlying mechanisms that render some brain regions more vulnerable to Alzheimer's disease pathology than others remain largely unknown. 4 key findings →
Participants: 76 Evidence: moderate
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Linear MR suggested that each additional hour/day of sleep was associated with 1% [95% confidence interval (CI) = 0-2%; P = 0.008] slower reaction time and 3% more errors in visual-memory test (95% CI = 0-6%; P = 0.05). 4 key findings →
Participants: 395 Evidence: moderate
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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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We identified individuals with an incident diagnosis of PD (n=1276) and controls (n=500 406) in UK Biobank. 4 key findings →
Participants: 1,276 Evidence: moderate
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Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson disease (PD), through neurotoxic effects. 4 key findings →
Design: cohort study Participants: 5,289 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →