27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among cognitively unimpaired participants with a family history of dementia, changes in cognition and brain MRI outcomes from baseline to year 3 did not differ significantly between those who followed the MIND diet and those who followed the control diet with mild caloric restriction. 5 key findings →
Design: RCT Participants: 604 Evidence: null result
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The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). 1 key finding →
Design: meta-analysis Evidence: high
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Further studies are warranted to develop and refine the specific MIND diet for different populations. 4 key findings →
Design: meta-analysis Participants: 224,049 Evidence: moderate
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After a median of 4.7 years of follow-up, the rate of cardiovascular disease was 10.7 events per 1000 person-years in the aspirin group and 11.3 events per 1000 person-years in the placebo group (hazard ratio, 0.95; 95% confidence interval [CI], 0.83 to 1.08). 4 key findings →
Participants: 19,114 Evidence: low
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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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In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified. 4 key findings →
Design: meta-analysis Participants: 2,784 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
There was no evidence that aspirin was effective in reducing risk of dementia, MCI, or cognitive decline. 2 key findings →
Participants: 19,114 Evidence: high
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Of 19 114 randomized participants, 16 855 (88.2%) had longitudinal gait and cognitive data for inclusion in this study (mean [SD] age, 75.0 [4.4] years; 9435 women [56.0%], 7558 participants [44.8%] with 12 or more years of education). 5 key findings →
Design: cohort study Participants: 7,558 Evidence: high
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Older adults with higher triglyceride levels within the normal to high-normal range had a lower dementia risk and slower cognitive decline over time compared with individuals with lower triglyceride levels. 5 key findings →
Design: randomized controlled trial Participants: 13,976 Evidence: high
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A healthy lifestyle as a composite score is associated with a substantially lower risk of Alzheimer's dementia. 5 key findings →
Design: meta-analysis Participants: 1,845 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
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Using cross-population GWAS meta-analyses, we identify novel LOAD susceptibility loci in/near LRRC4C and LHX5-AS1, both with known roles in neuronal development, as well as several novel population-unique loci. 1 key finding →
Design: meta-analysis Participants: 409,589 Evidence: high
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Dementia has been increasingly more recognized to be a common feature in patients with Parkinson's disease (PD), especially in old age. 4 key findings →
Design: systematic review Evidence: high
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Among older adults at risk of cognitive decline and dementia, a structured, higher-intensity intervention had a statistically significant greater benefit on global cognition compared with an unstructured, self-guided intervention. 5 key findings →
Participants: 1,056 Evidence: high
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MCR is common in older adults, and is a strong and early risk factor for cognitive decline. 3 key findings →
Design: cohort study Participants: 26,802 Evidence: moderate
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These data suggest a revision of the original ADAPT hypothesis that NSAIDs reduce AD risk, as follows: NSAIDs have an adverse effect in later stages of AD pathogenesis, whereas asymptomatic individuals treated with conventional NSAIDs such as naproxen experience reduced AD incidence, but only after 2 to 3 years. 5 key findings →
Participants: 54 Evidence: high
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The majority of community-dwelling older persons have brain pathology. 2 key findings →
Design: cohort study Participants: 80 Evidence: moderate
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Analysis confirmed the association of APOE with earlier AAO (P = 3.3 × 10(-96)), with associations in CR1 (rs6701713, P = 7.2 × 10(-4)), BIN1 (rs7561528, P = 4.8 × 10(-4)), and PICALM (rs561655, P = 2.2 × 10(-3)) reaching statistical significance (P Conclusions and relevance We confirmed an association of APOE (OMIM 107741) variants with AAO among affected participants with LOAD and observed novel associations of CR1 (OMIM 120620), BIN1 (OMIM 601248), and PICALM (OMIM 603025) with AAO. 3 key findings →
Design: meta-analysis Participants: 9,162 Evidence: high
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A larger number of deaths are attributable to AD dementia in the United States each year than the number (<84,000 in 2010) reported on death certificates. 1 key finding →
Design: cohort study Participants: 2,566 Evidence: moderate
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Sleep fragmentation in older adults is associated with incident AD and the rate of cognitive decline. 5 key findings →
Design: cohort study Participants: 97 Evidence: moderate
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The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis. 3 key findings →
Design: meta-analysis Participants: 3,154 Evidence: high
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After correcting for multiple comparisons using the Bonferroni procedure, we observed a statistically significant interaction between APOE-ε4 and sex on CSF total tau (β = 0.41; 95% CI, 0.27-0.55; P Conclusions and relevance We provide robust evidence of a stronger association between APOE-ε4 and CSF tau levels among women compared with men across multiple independent data sets. 5 key findings →
Design: cohort study Participants: 1,798 Evidence: moderate
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Recruitment ended in December 2014 with 16,703 Australian and 2,411 U.S. participants, a median age of 74 (range 65-98) years and 56% women. 1 key finding →
Evidence: high
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As none of the studies exceeded a duration of 6 months, the recommendations given are for the short-term management of the different non-motor symptoms. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The lack of strong association between brain beta-amyloid deposition and cognitive impairment has been a challenge for the Alzheimer's disease (AD) field. 4 key findings →
Design: meta-analysis Participants: 678 Evidence: high
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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 →