Previous hypothesis-driven research has identified many risk factors linked to dementia. 4 key findings →
Participants: 344,324 Evidence: low
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27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Previous hypothesis-driven research has identified many risk factors linked to dementia. 4 key findings →
Participants: 344,324 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. 4 key findings →
Participants: 39 Evidence: moderate
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Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used agents in clinical practice. 4 key findings →
Design: meta-analysis Evidence: high
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During follow-up, 60 individuals developed dementia, of which 49 had Alzheimer's disease (AD). 4 key findings →
Participants: 1,322 Evidence: moderate
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Identifying brain regions associated with risk factors for dementia could guide mechanistic understanding of risk factors associated with Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 8,312 Evidence: low
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We hypothesize that CRP (C-reactive protein) is associated with brain structural changes and may interact with amyloid to produce vascular and degenerative damage. 4 key findings →
Design: longitudinal study Participants: 736 Evidence: moderate
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The relative performance of semi-quantitative amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) markers in diagnosing Alzheimer's disease (AD) and predicting the cognitive evolution of patients with mild cognitive impairment (MCI) is still debated. 4 key findings →
Design: cross-sectional Participants: 677 Evidence: moderate
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The positive association of choline for cognition has been reported in both animal and human studies, yet the associations of choline with the risks of incident dementia or Alzheimer's disease (AD) in humans is unclear. 4 key findings →
Participants: 3,224 Evidence: moderate
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This study aimed to investigate the longitudinal association between decreased lung function and cognitive brain health and to explore underlying biological and brain structural mechanisms. 4 key findings →
Design: longitudinal study Participants: 43 Evidence: moderate
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Progressive supranuclear palsy (PSP) is a progressive neurodegenerative disorder characterized by aggregates of the microtubule-associated protein tau (MAPT). 4 key findings →
Design: case-control study Participants: 172 Evidence: moderate
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To test whether cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) concentration is elevated in Alzheimer's disease (AD) dementia and its associations with other hallmarks of AD, we examined the CSF GAP-43 measurements of 787 participants (245 cognitively normal (CN), 415 individuals with mild cognitive impairment (MCI) and 127 individuals with AD dementia) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. 4 key findings →
Design: longitudinal study Participants: 787 Evidence: moderate
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Type 2 diabetes is associated with increased risks of cognitive dysfunction and brain abnormalities. 4 key findings →
Participants: 10,663 Evidence: low
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Models of Alzheimer's disease (AD) pathophysiology posit that amyloidosis [A] precedes and accelerates tau pathology [T] that leads to neurodegeneration [N]. 4 key findings →
Design: longitudinal study Participants: 262 Evidence: moderate
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Among all participants, 247 (11.7%) had IADL limitations at baseline, and 151 (7.1%) developed dementia during follow-up. 5 key findings →
Design: longitudinal study Participants: 2,118 Evidence: moderate
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Cerebral blood flow (CBF) velocity is decreased in patients with Alzheimer's disease. 4 key findings →
Participants: 1,716 Evidence: low
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The gap between predicted brain age using magnetic resonance imaging (MRI) and chronological age may serve as a biomarker for early-stage neurodegeneration. 4 key findings →
Design: longitudinal study Evidence: moderate
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Sleep is essential for life, including daily cognitive processes, yet the amount of sleep required for optimal brain health as we grow older is unclear. 4 key findings →
Participants: 479,420 Evidence: low
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Orthostatic hypotension (OH) is a common cause of transient cerebral hypoperfusion in the population. 4 key findings →
Participants: 6,204 Evidence: low
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Total hippocampal volume has been consistently linked to cognitive function and dementia. 4 key findings →
Participants: 5,035 Evidence: moderate
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Apolipoprotein (APOE) e4 genotype is an accepted risk factor for accelerated cognitive aging and dementia, though its neurostructural substrates are unclear. 4 key findings →
Design: cross-sectional Participants: 8,395 Evidence: moderate
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This study aimed to investigate the associations of grip strength with incidence and mortality from dementia and whether these associations differ by sociodemographic and lifestyle factors. 4 key findings →
Participants: 788 Evidence: low
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Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures. 4 key findings →
Design: cross-sectional Participants: 995 Evidence: moderate
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Medical imaging provides numerous insights into the subclinical changes that precede serious diseases such as heart disease and dementia. 4 key findings →
Design: cross-sectional Evidence: low
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Sedentary behavior (SB) is associated with cardiometabolic disease and mortality, but its association with dementia is currently unclear. 4 key findings →
Participants: 146,651 Evidence: low
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The reference standard for amyloid-PET quantification requires structural MRI (sMRI) for preprocessing in both multi-site research studies and clinical trials. 4 key findings →
Participants: 740 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →