27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Diabetes and even prediabetes are associated with accelerated brain aging, especially among men and people with poor cardiometabolic health. 4 key findings →
Participants: 31,229 Evidence: low
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Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE4. 2 key findings →
Evidence: low
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Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. 1 key finding →
Evidence: moderate
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Cognitive impairment is one of the earliest, most common, and most disabling non-motor symptoms in Parkinson's disease (PD). 4 key findings →
Design: cohort study Participants: 360 Evidence: moderate
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Total numbers of global DALYs grew 6·1% (95% UI 4·0-8·1), from 2·64 billion (2·46-2·86) in 2010 to 2·80 billion (2·57-3·08) in 2023, but age-standardised DALY rates, which account for population growth and ageing, decreased by 12·6% (11·0-14·1), revealing large long-term health improvements. 5 key findings →
Evidence: low
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Thirty-five patients with probable DLB, 37 patients with MCI-LB, and 100 individuals without cognitive impairment were included. 5 key findings →
Design: case-control study Participants: 72 Evidence: moderate
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Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →
Participants: 49 Evidence: low
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Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer's disease (AD) in Caucasians. 2 key findings →
Design: meta-analysis Evidence: high
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Over a mean follow-up of 8.4 years (range, Conclusions and relevance This cohort study of older adults found that adherence to a dietary pattern with lower inflammatory potential was associated with lower dementia risk among individuals with AD pathology and broader neurobiological risk. 3 key findings →
Design: cohort Participants: 1,865 Evidence: early
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Alzheimer disease pathologic changes are common in DLB and are associated with the clinical phenotype. β-Amyloid is associated with cognitive impairment, and tau pathology is associated with lower frequency of clinical features of DLB. 5 key findings →
Participants: 417 Evidence: moderate
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Research into dementia prevention is of paramount importance if the dementia epidemic is to be halted. 5 key findings →
Evidence: high
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This study indicates no benefits for memantine in the long-term treatment and prophylaxis of clinically significant neuropsychiatric symptoms. 5 key findings →
Participants: 199 Evidence: high
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Alzheimer's disease is the most common cause of dementia in elderly people. 5 key findings →
Evidence: high
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Considering predementia stages, the number of persons with AD is much larger than conveyed in available literature. 1 key finding →
Evidence: low
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Having multiple CMBs or concomitant CMBs and retinopathy is associated with a profile of vascular cognitive impairment. 5 key findings →
Design: cross-sectional Participants: 3,906 Evidence: low
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The hippocampus is involved at the onset of the neuropathological pathways leading to Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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The predictive validity of mild cognitive impairment (MCI) for identifying future Alzheimer disease (AD) cases is improved in the presence of anxiety symptoms. 1 key finding →
Participants: 185 Evidence: low
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The models could aid clinicians in the interpretation of CSF biomarker and hippocampal volume results in individuals with MCI, and help research and clinical settings to prepare for a future of precision medicine in Alzheimer's disease. 1 key finding →
Participants: 883 Evidence: moderate
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The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) 1 . 4 key findings →
Design: longitudinal study Evidence: moderate
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Poor social health is likely associated with cognitive decline and risk of dementia; however, studies show inconsistent results. 4 key findings →
Participants: 4,514 Evidence: low
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We aimed to investigate whether the increased risk of dementia among individuals with diabetes can be offset by a broad combination of healthy lifestyle factors. 4 key findings →
Participants: 167,946 Evidence: moderate
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Per 1-m/s increase in ePWV was associated with an adjusted hazard ratio (HR) (95% confidence interval [CI]) of 1.51(1.30-1.75) for dementia and 1.58(1.33-1.89) for Alzheimer's disease (AD), and with an MMSE score decline (adjusted β-coefficient = -0.36; 95% CI = -0.52 to -0.21). 5 key findings →
Design: longitudinal study Participants: 1,857 Evidence: moderate
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In multi-adjusted models, higher adherence to the EAT-Lancet diet was associated with higher total mean cortical thickness, and thicker cortex in Alzheimer's disease-signature regions, while a higher adherence to the MeDi was associated with better cognitive performance. 5 key findings →
Design: cohort study Participants: 615 Evidence: moderate
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Plasma β-synuclein demonstrated discriminative properties for Aβ PET positive and negative subjects. 3 key findings →
Design: longitudinal study Participants: 51 Evidence: moderate
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A population-based longitudinal study in Sweden, the Kungsholmen Project A random sample of 370 nondemented persons, aged 75 years and older and not treated with B(12) and folate, was followed for 3 years to detect incident AD cases. 1 key finding →
Design: longitudinal study Evidence: moderate
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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 →