Diabetes mellitus (DM) and neurodegenerative diseases/disturbances are worldwide health problems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Diabetes mellitus (DM) and neurodegenerative diseases/disturbances are worldwide health problems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The direct associations identified may present potential intervention targets, while the indirect relationships suggest that other factors are influential in the pathway linking social isolation and loneliness with chronic disease and dementia. 5 key findings →
Design: cohort study Participants: 6,670 Evidence: moderate
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Growing evidence underscores the importance of cardiovascular contributions to Alzheimer's disease and related dementias (AD/ADRD). 5 key findings →
Design: narrative review Evidence: low
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Having three or more vascular risk factors (odds ratio = 1.23, 95% confidence interval [1.04-1.47]), actively smoking (odds ratio = 1.54, 95% confidence interval [1.29-1.82]), being overweight (odds ratio = 1.46, 95% confidence interval [1.22-1.74]), and having diabetes (odds ratio = 1.29, 95% confidence interval [1.09-1.53]) were associated with higher odds of subjective cognitive decline. 2 key findings →
Design: cross-sectional Evidence: low
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Hypertension is the leading modifiable risk factor for atrial fibrillation (AF) and is estimated to be present in >70% of AF patients. 1 key finding →
Evidence: low
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About 12% of caregivers (2.8 million) were socially isolated and 27% (6.3 million) were lonely. 5 key findings →
Participants: 2,174 Evidence: low
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cBF volume declined at comparable rates in iRBD-to-PD and iRBD-to-DLB converters, but atrophy was more severe at DLB phenoconversion. cBF atrophy correlated with attention, executive, and memory deficits. 5 key findings →
Design: cross-sectional Evidence: moderate
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Dementia with Lewy bodies (DLB) frequently coexists with Alzheimer's disease pathology, yet the pattern of cortical microstructural injury and its relationship with amyloid, tau, and cerebrovascular pathologies remains unclear. 3 key findings →
Participants: 57 Evidence: low
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Patients with dementia face increased risks after general anesthesia. 4 key findings →
Participants: 27 Evidence: low
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Symptomatic GRN carriers showed elevated WMHs, primarily in the frontal lobe, while no significant increase was observed in symptomatic C9orf72 or MAPT carriers. 5 key findings →
Participants: 763 Evidence: low
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Of 43 individuals enrolled, 14 were women (33%); age (mean ± SD) was 73 ± 8.5 years. 5 key findings →
Design: clinical trial Participants: 43 Evidence: high
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Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are subtypes of Lewy body dementia, and are considered two ends of a disease spectrum. 5 key findings →
Participants: 66 Evidence: low
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Sex differences for clinicopathological correlations in LBD also occur at the regional pathology level. 3 key findings →
Participants: 357 Evidence: low
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At baseline, sbvFTD showed right-predominant temporal pole involvement associated with significant right frontal atrophy. 5 key findings →
Design: longitudinal study Evidence: moderate
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Lewy body patients showed a significantly higher degree of WMSA in the external capsule cholinergic pathway despite no significant differences in global WMSA compared to controls. 4 key findings →
Participants: 82 Evidence: moderate
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UNC13A (rs12608932-CC) is associated with both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), and shortens survival in ALS. 2 key findings →
Participants: 626 Evidence: low
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= 0.005). Cox regression analysis revealed that polypharmacy was significantly associated with a reduced risk of MCI progression to dementia (hazard ratio [HR] = 0.49, 95% confidence interval [CI]: 0.31 to 0.78) after adjusting for covariates. 5 key findings →
Design: cohort study Evidence: moderate
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Mild cognitive impairment (MCI) is a clinical condition characterized by a decline in cognitive ability and progression of cognitive impairment. 3 key findings →
Participants: 239 Evidence: moderate
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Little is known about the dysbiosis of the gut microbiome in patients with mild cognitive impairment (MCI) potentially at risk for the development of Alzheimer's disease (AD). 5 key findings →
Design: cross-sectional Participants: 14 Evidence: moderate
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< 0.001). Receiver operating characteristic (ROC) analysis identified right hippocampal MD and t-tau as optimal classifiers for AD. 4 key findings →
Design: cross-sectional Evidence: low
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Key markers and mechanisms were identified for each stage: initial neurophysiological deficits in SCD with compensatory metabolomic responses, gut-brain axis dysregulation in MCI, and extensive metabolic disruption and multisystem breakdown in AD. 5 key findings →
Participants: 277 Evidence: low
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Neurophysiological activity features and tau pet provided additional information to the clinical model when acquired up to ∼4 years prior to diagnosis, but their accuracy decreased at larger intervals. 5 key findings →
Design: longitudinal study Participants: 102 Evidence: moderate
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This innovative study aims to test the feasibility of iTBS as a cognitive enhancement strategy in MCI. 3 key findings →
Participants: 20 Evidence: high
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Subgroups with slower versus faster neurodegeneration, despite similar pathological accumulation, were compared to assess associations with genetic/lifestyles. 4 key findings →
Design: longitudinal study Participants: 529 Evidence: moderate
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MDS varied significantly by age, sex, education, and language of administration even among participants with normal cognition. 5 key findings →
Participants: 25,330 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 →