28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Scale of benefit is comparable with in-person training, indicating its potential as a public health intervention. 3 key findings →
Design: randomized controlled trial Participants: 2,912 Evidence: high
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We tested the hypothesis that cerebral amyloid angiopathy (CAA) is related to Alzheimer disease (AD) dementia and decline in multiple cognitive systems in old age, independent of AD plaque and tangle pathology and other common age-related neuropathologies. 4 key findings →
Design: longitudinal study Participants: 1,113 Evidence: moderate
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We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms. 2 key findings →
Design: meta-analysis Participants: 17 Evidence: high
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Whether novel risk variants of Alzheimer's disease (AD) identified through genome-wide association studies also influence magnetic resonance imaging-based intermediate phenotypes of AD in the general population is unclear. 4 key findings →
Design: meta-analysis Participants: 8,175 Evidence: high
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Personality is associated with cognitive decline in older adults, with effects comparable to established clinical and lifestyle risk factors. 5 key findings →
Design: meta-analysis Participants: 13,987 Evidence: high
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Cognitive impairment is present in approximately 30% of patients with amyotrophic lateral sclerosis (ALS) and, especially when severe, has a negative impact on survival and caregiver burden. 2 key findings →
Design: meta-analysis Participants: 1,287 Evidence: high
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If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer's disease. 3 key findings →
Design: prospective cohort Participants: 1,806 Evidence: moderate
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11 studies were identified, including 380 patients with AD, 68 with MCI and 293 healthy controls (HC). 4 key findings →
Design: meta-analysis Participants: 380 Evidence: high
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 400 Evidence: moderate
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¹⁸F-FDFG uptake by brain tissue as measured by positron emission tomography (PET) is a well-established method for assessment of brain function in people with dementia. 4 key findings →
Design: meta-analysis Participants: 14 Evidence: high
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Brain DNA methylation in multiple AD loci is associated with AD pathologies. 5 key findings →
Design: cohort study Participants: 447 Evidence: moderate
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In older women, habitual sleep duration predicts the future risk for cognitive impairments including dementia, independent of vascular risk factors. 1 key finding →
Evidence: low
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In the oldest-old, the presence of multiple pathologies is associated with increased likelihood and severity of dementia. 4 key findings →
Design: longitudinal study Participants: 183 Evidence: moderate
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Major postoperative complications and delirium are separately associated with adverse events and demonstrate a combined effect. 4 key findings →
Design: cohort study Participants: 566 Evidence: moderate
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Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. 3 key findings →
Design: longitudinal study Evidence: moderate
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Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients. 5 key findings →
Design: longitudinal study Participants: 39 Evidence: moderate
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The cumulative incidence of cognitive impairment was 8.5% at year 1, increasing to 47.4% by year 6. 2 key findings →
Design: prospective cohort Participants: 141 Evidence: moderate
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There was a significant interaction (P = 0.024) between B vitamin treatment and plasma combined ω-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) on brain atrophy rates. 5 key findings →
Participants: 83 Evidence: low
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Classification of evidence This study provides Class I evidence that for women with AD, raloxifene does not have a significant cognitive effect. 5 key findings →
Evidence: high
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The Internet course 'Mastery over Dementia' offers an effective treatment for family caregivers of people with dementia reducing symptoms of depression and anxiety. 4 key findings →
Participants: 149 Evidence: low
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Studies were significantly heterogeneous in terms of country, outcomes assessed, and the timing of post-ED outcome assessments. 5 key findings →
Design: systematic review Participants: 7,940 Evidence: high
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TREM2 encodes for triggering receptor expressed on myeloid cells 2 and has rare, coding variants that associate with risk for late-onset Alzheimer's disease (LOAD) in Caucasians of European and North-American origin. 4 key findings →
Design: case-control study Participants: 800 Evidence: moderate
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Epidemiologic evidence suggests that cognitive and physical activities are associated with better cognition in late life. 4 key findings →
Design: randomized controlled trial Evidence: high
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Within-person changes in CSF biomarkers were also compared with changes in cortical PiB binding and progression to a CDR higher than 0 at follow-up. 2 key findings →
Design: cohort study Participants: 169 Evidence: moderate
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At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. 1 key finding →
Design: longitudinal study Participants: 468 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.
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →