27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Periventricular white matter hyperintensities (WMH; PVWMH) and deep WMH (DWMH) are regional classifications of WMH and reflect proposed differences in cause. 4 key findings →
Design: meta-analysis Participants: 26,654 Evidence: high
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Healthy cognitive ageing is a societal and public health priority. 4 key findings →
Design: cohort study Participants: 22,059 Evidence: moderate
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We created global rating scoring rules for the CDR ® plus NACC FTLD to detect and track early frontotemporal lobar degeneration (FTLD) and to conduct clinical trials in FTLD. 4 key findings →
Design: longitudinal study Participants: 40 Evidence: moderate
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We tested the hypothesis that a causal relationship exists between systolic BP (SBP) and/or diastolic BP (DBP) and risk of Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Participants: 299,024 Evidence: high
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We developed models for individualized risk prediction of cognitive decline in mild cognitive impairment (MCI) using plasma biomarkers of β-amyloid (Aβ), tau and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 573 Evidence: moderate
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Midlife vascular risk burden is associated with late-life dementia. 4 key findings →
Design: cohort study Participants: 502 Evidence: moderate
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We analyzed prospectively collected data in the Original and Offspring FHS cohorts. 4 key findings →
Design: case-control study Participants: 4,906 Evidence: moderate
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Neurofilament light (NfL) is a marker of neuroaxonal injury, a prominent feature of Alzheimer's disease. 4 key findings →
Design: cross-sectional Participants: 1,149 Evidence: moderate
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Early identification of individuals at risk of developing Alzheimer's disease (AD) dementia is important for developing disease-modifying therapies. 4 key findings →
Design: cross-sectional Participants: 1,677 Evidence: moderate
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Hippocampal morphological change is one of the main hallmarks of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 261 Evidence: moderate
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Anticholinergic burden (ACB), the cumulative effect of anticholinergic medications, is associated with adverse outcomes in older people but is less studied in middle-aged populations. 4 key findings →
Design: longitudinal study Participants: 502,538 Evidence: moderate
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To better understand clinical and neuropathological features of TDP-43 proteinopathies, data were analyzed from autopsied research volunteers who were followed in the National Alzheimer's Coordinating Center (NACC) data set. 4 key findings →
Design: longitudinal study Participants: 495 Evidence: moderate
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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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Cerebral small vessel disease is a major cause of stroke and dementia, but its genetic basis is incompletely understood. 4 key findings →
Participants: 42,310 Evidence: low
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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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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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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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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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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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Plasma markers have been reported to be associated with brain amyloid burden, tau pathology, or neurodegeneration. 4 key findings →
Design: cross-sectional Participants: 183 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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The CDR® plus NACC FTLD was able to detect early symptoms in the mildly impaired participants who were rated as CDR® sum of boxes (CDR®-SB) = 0. 4 key findings →
Design: longitudinal study Evidence: moderate
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We categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. 4 key findings →
Evidence: moderate
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However, most people with dementia live in low-income and middle-income countries (LMICs), where dementia risk prediction research is almost non-existent and the ability of current models to predict dementia is unknown. 4 key findings →
Participants: 143 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 27,380 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 →