28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Study-level data from 14 studies, 2,310,330 individuals, and 102,174 dementia case patients were included. 3 key findings →
Design: meta-analysis Participants: 2,310,330 Evidence: high
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Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. 5 key findings →
Design: meta-analysis Participants: 94,437 Evidence: high
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These findings suggest that a hearing intervention might reduce cognitive change over 3 years in populations of older adults at increased risk for cognitive decline but not in populations at decreased risk for cognitive decline. 5 key findings →
Design: randomized controlled trial Participants: 858 Evidence: high
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We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. 4 key findings →
Design: case-control study Participants: 85,133 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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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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Random-effects models revealed small but statistically significant effects with better psychological well-being in African American caregivers compared with white caregivers in both population-based (d = -0.22) and convenience sample studies (d = -0.21). 2 key findings →
Design: meta-analysis Participants: 159 Evidence: high
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Vitamin E had no benefit in patients with mild cognitive impairment. 5 key findings →
Participants: 769 Evidence: low
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Estrogen replacement therapy for 1 year did not slow disease progression nor did it improve global, cognitive, or functional outcomes in women with mild to moderate AD. 3 key findings →
Participants: 42 Evidence: high
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Cognitive reserve (CR) may reduce the risk of dementia. 5 key findings →
Design: meta-analysis Evidence: moderate
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Physical exercise has been shown to increase brain volume and improve cognition in randomized trials of non-demented elderly. 2 key findings →
Evidence: high
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Evidence: low
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Higher baseline body mass index (BMI) and slower declining BMI in late life are associated with a reduced risk of dementia, suggesting that low BMI or a faster decline in BMI in late life may be preclinical indicators of an underlying dementing illness, especially for those who were initially overweight or obese. 3 key findings →
Design: cohort study Evidence: moderate
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Study objectives To determine the effect of self-reported clinical diagnosis of obstructive sleep apnea (OSA) on longitudinal changes in brain amyloid PET and CSF biomarkers (Aβ42, T-tau, and P-tau) in cognitively normal (NL), mild cognitive impairment (MCI), and Alzheimer's disease (AD) elderly. 2 key findings →
Design: longitudinal study Participants: 516 Evidence: moderate
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The intervention group showed less discomfort (-1.06; 95% confidence interval [CI] = -1.88 to -0.23) and fewer sentinel events (-0.40; 95% CI = -0.64 to -0.16), specifically pneumonia (-0.08; 95% CI = -0.14, -0.02). 5 key findings →
Design: randomized controlled trial Participants: 116 Evidence: high
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Each additional copy of the apolipoprotein E4 (APOE4) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2 homozygotes have a particularly low risk. 2 key findings →
Evidence: low
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In patients with moderately severe impairment from Alzheimer's disease, treatment with selegiline or alpha-tocopherol slows the progression of disease.
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Adults were more likely than children to screen positive for a single autoantibody (4.0% vs. 2.6%) but less likely for multiple autoantibodies (0.83% vs. 2.8%; P < 0.001). 5 key findings →
Participants: 135,914 Evidence: low
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Clinical characteristics and demographics were similar between groups. 5 key findings →
Design: randomized controlled trial Participants: 89 Evidence: high
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Neuronal inclusions of poly(GA), a protein unconventionally translated from G4C2 repeat expansions in C9ORF72, are abundant in patients with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) caused by this mutation. 4 key findings →
Evidence: low
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Among ACHIEVE participants in the top quartile of predicted risk, 3-year cognitive decline in the hearing intervention was 61.6% (95% confidence interval [CI]: 33.7%-94.1%) slower than the control. 5 key findings →
Participants: 2,692 Evidence: moderate
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Alzheimer's disease is the most common dementia and is pathologically characterized by deposition of amyloid-beta peptide (Abeta) into beta-amyloid plaques, neuronal injury and low-level, chronic activation of brain immunity. 4 key findings →
Evidence: low
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MCI diagnosis frequencies are substantively affected by the stringency of the criteria, but the relative rankings of MCI subtype diagnoses are fairly consistent regardless of the stringency of the criteria. 5 key findings →
Design: longitudinal study Participants: 373 Evidence: moderate
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Since increased BBB permeability is found in tauopathies without Aß pathology, like PSP, we suspected that tau accumulation alone could not only be sufficient, but even more important than Aß for BBB damage. 4 key findings →
Design: longitudinal study Evidence: moderate
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Medial temporal lobe atrophy (MTA) scores 1) distinguish probable Alzheimer disease (AD) and amnestic mild cognitive impairment (MCI) subjects from nonamnestic MCI and no cognitive impairment (NCI) subjects, 2) help predict diagnosis at baseline, and 3) predict transition from NCI to MCI and from MCI to probable AD. 1 key finding →
Participants: 117 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.
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 →