31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In recent years, several high-dimensional, accurate, and effective classification methods have been proposed for the automatic discrimination of the subject between Alzheimer's disease (AD) or its prodromal phase {i.e., mild cognitive impairment (MCI)} and healthy control (HC) persons based on T1-weighted structural magnetic resonance imaging (sMRI). 4 key findings →
Participants: 326 Evidence: low
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White matter hyperintensities (WMH) are among the most common radiological abnormalities in the ageing population and an established risk factor for stroke and dementia. 4 key findings →
Evidence: low
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A total of 43,160 participants were included (mean [standard deviation] age, 64.2 [7.7] years, 53.1 % female). 5 key findings →
Design: cross-sectional Participants: 43,160 Evidence: moderate
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Ventricular enlargement and white matter lesions are frequent findings on cerebral magnetic resonance imaging scans of elderly subjects. 4 key findings →
Participants: 90 Evidence: moderate
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In this article, the authors aim to maximally utilize multimodality neuroimaging and genetic data for identifying Alzheimer's disease (AD) and its prodromal status, Mild Cognitive Impairment (MCI), from normal aging subjects. 4 key findings →
Evidence: low
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Positron emission tomography (PET) with 18 F-fluorodeoxyglucose (FDG) reveals altered cerebral metabolism in individuals with mild cognitive impairment (MCI) and Alzheimer's dementia (AD). 4 key findings →
Participants: 332 Evidence: low
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Baseline tau-PET and a composite baseline cognitive score were the strongest independent predictors of cognitive decline. 4 key findings →
Evidence: low
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Mid-life obesity is an established risk factor for Alzheimer's disease (AD) dementia, whereas late-life obesity has been proposed as a protective state. 4 key findings →
Participants: 162 Evidence: low
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Mild cognitive impairment (MCI) marks a transitional stage between healthy aging and dementia, but the understanding of MCI in the general population remains limited. 4 key findings →
Participants: 4,198 Evidence: low
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Quantitative magnetic resonance imaging and neuropsychological evaluations were performed in 1820 dementia- and stroke-free participants from the Framingham Offspring Cohort. 4 key findings →
Evidence: moderate
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Increasing evidence suggests a role of atherosclerosis in the pathogenesis of cognitive impairment and dementia. 4 key findings →
Participants: 844 Evidence: low
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In the general population, we investigated the association of a recently developed cerebral small vessel disease (CSVD) sum score with stroke, dementia, and mortality. 4 key findings →
Participants: 66 Evidence: low
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Recent interest in enlarged perivascular spaces (ePVS) in the brain, which can be visualized on MRI and appear isointense to cerebrospinal fluid on all sequence weightings, has resulted in the necessity of reliable algorithms for automated segmentation to allow for whole brain assessment of ePVS burden. 4 key findings →
Participants: 14 Evidence: moderate
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Late-life depression (LLD) is associated with development of different types of dementia. 4 key findings →
Participants: 185 Evidence: low
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Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 4 key findings →
Evidence: low
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The differential diagnosis of frontotemporal dementia (FTD) and Alzheimer's disease (AD) is difficult due to the overlaps of clinical symptoms. 4 key findings →
Participants: 47 Evidence: low
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The subject groups for model derivation comprised 80 healthy subjects (HS), 36 patients with mild cognitive impairment (MCI) who converted to AD dementia within 18 months, 85 non-converter MCI patients who did not convert within 24 months, and 67 AD dementia patients with baseline FDG PET scan were recruited from the AD Neuroimaging Initiative (ADNI) database. 4 key findings →
Participants: 36 Evidence: moderate
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Exposure to vascular risk factors has a gradual deleterious effect on brain MRI and cognitive measures. 4 key findings →
Participants: 55 Evidence: moderate
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Midlife hearing loss was associated with smaller brain volumes, accelerated decline in executive function, accelerated accrual of white matter abnormalities, and a near doubling of dementia risk, suggesting a potential causal or biomarker role for midlife hearing loss in the prevention of late‐life dementia. 4 key findings →
Participants: 1,656 Evidence: low
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During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →
Participants: 52,693 Evidence: moderate
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Our findings indicate that liver fat mediates associations between cardiometabolic factors and WMHs and that WMHs mediate the association between liver fat and cognitive performance. 5 key findings →
Participants: 32,461 Evidence: moderate
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During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →
Participants: 52,693 Evidence: moderate
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We examined differences in cerebral blood flow (CBF) measured by Arterial Spin Labeled perfusion MRI (ASL MRI) across the continuum from cognitively normal (CN) older adults to mild Alzheimer's Disease (AD) using data from the multi-site Alzheimer's Disease Neuroimaging Initiative (ADNI). 4 key findings →
Participants: 47 Evidence: low
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The analysis tools and statistical methods used in large neuroimaging research studies differ from those applied in clinical contexts, making it unclear whether these techniques can be translated to a memory clinic setting. 5 key findings →
Participants: 213 Evidence: low
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Brain structure in later life reflects both influences of intrinsic aging and those of lifestyle, environment and disease. 4 key findings →
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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events