27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Epidemiologic studies suggest that a Mediterranean diet, an antioxidant-rich cardioprotective dietary pattern, delays cognitive decline, but clinical trial evidence is lacking. 5 key findings →
Design: RCT Participants: 447 Evidence: moderate
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APOE ɛ4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. 5 key findings →
Design: meta-analysis Participants: 4,203 Evidence: high
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An intervention with MedDiets enhanced with either EVOO or nuts appears to improve cognition compared with a low-fat diet. 5 key findings →
Participants: 522 Evidence: high
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Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. 4 key findings →
Design: meta-analysis Participants: 3,526 Evidence: high
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AUC for amyloid and tau PET provide expert recommendations for clinical use of these technologies in the evolving landscape of diagnostics and therapeutics for Alzheimer's disease. 2 key findings →
Design: systematic-review Evidence: moderate
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A long-term intervention with an EVOO-rich MedDiet resulted in a better cognitive function in comparison with a control diet. 4 key findings →
Design: randomized controlled trial Participants: 285 Evidence: high
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A non-synonymous genetic rare variant, rs75932628-T (p.R47H), in the TREM2 gene has recently been reported to be a strong genetic risk factor for Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Participants: 32,598 Evidence: high
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Previous studies of Aβ plasma as a biomarker for Alzheimer's disease (AD) obtained conflicting results. 5 key findings →
Design: longitudinal study Participants: 715 Evidence: moderate
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Higher adherence to the MedDiet was associated with greater gut microbial diversity (p < 0.05) and distinct microbial composition (PERMANOVA, p = 0.001). 5 key findings →
Design: longitudinal study Participants: 746 Evidence: moderate
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A total of 450 111 participants were included in the study (mean [SD] age, 51.1 [9.8] years; 70.8% women) and followed up during a median (IQR) time of 14.9 (4.1) years. 5 key findings →
Design: cohort study Participants: 111 Evidence: moderate
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Ageing and a sedentary lifestyle are associated with declines in muscle function and cardiorespiratory fitness, resulting in an impaired capacity to perform daily activities and maintain independent functioning. 2 key findings →
Evidence: high
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The 6-year absolute risk was 12.0% (95% CI, 11.9% to 12.1%) in the control group (349 cases) and 9.5% (CI, 9.4% to 9.5%) in the intervention group (280 cases). 5 key findings →
Participants: 4,746 Evidence: high
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In 2018, Carlos et al. [2] reviewed 21 studies from the SUN project that focused on the association between the MDP and several incident chronic diseases, concluding that high Mediterranean diet adherence was associated with a lower incidence of all-cause mortality, cardiovascular disease, type 2 diabetes, weight gain, metabolic syndrome, depression, cognitive decline, and nephrolithiasis, and with a lower heart rate and mitigation of the effects of obesity on cardiovascular disease (CVD) and type 2 diabetes, and our results suggested that the Mediterranean diet may improve fertility. 5 key findings →
Design: cohort study Participants: 79 Evidence: moderate
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The human metabolome reflects complex metabolic states affected by genetic and environmental factors. 5 key findings →
Participants: 23,000 Evidence: low
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This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD).
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Moreover, physical activity in the elderly is associated with a decreased risk of mortality, of common chronic illnesses (i.e. cardiovascular disease or osteoarthritis) and of institutionalization as well as with a delay in functional decline. 5 key findings →
Participants: 240 Evidence: high
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With advances in knowledge disease, boundaries may change. 1 key finding →
Evidence: low
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A total of 158 participants were included, with an average age of 75.2 years (SD 7.65). 60.8% (n=96) of patients had AD, and 39.2% (n=62) had LBD. 4 key findings →
Design: cohort study Participants: 96 Evidence: moderate
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Two recent studies have reported the association of rs75932628-T in the TREM2 gene with the risk for Alzheimer's disease (AD). 1 key finding →
Evidence: moderate
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Cognitive decline is one of the most frequent and disabling nonmotor features of Parkinson's disease. 3 key findings →
Design: longitudinal study Evidence: moderate
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Levels of insulin-like growth factor I (IGF-I), a neuroprotective hormone, decrease in serum during aging, whereas amyloid-beta (Abeta), which is involved in the pathogenesis of Alzheimer disease, accumulates in the brain. 5 key findings →
Evidence: low
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α-Synuclein species contained in PD-derived LB are pathogenic and have the capacity to initiate a PD-like pathological process, including intracellular and presynaptic accumulations of pathological α-synuclein in different brain areas and slowly progressive axon-initiated dopaminergic nigrostriatal neurodegeneration. 2 key findings →
Evidence: low
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Primary sclerosing cholangitis (PSC) is an immune-mediated cholestatic liver disease for which pharmacological treatment options are currently unavailable. 4 key findings →
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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Numerous factors need to be taken into account when managing a patient with Parkinson's disease (PD) after deep brain stimulation (DBS). 5 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 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 →