28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
A slower rate of hippocampal atrophy in normal APOE2 carriers is consistent with the lower risk of Alzheimer disease in these individuals. 5 key findings →
Design: cohort study Participants: 72 Evidence: moderate
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Patients and their study partners who were enrolled in a clinical trial supported proxy consent both for themselves and as a matter of policy. 2 key findings →
Design: randomized controlled trial Evidence: high
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This sample of the older general public generally supported a policy of surrogate consent for AD research at baseline. 1 key finding →
Design: randomized controlled trial Participants: 503 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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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. 5 key findings →
Evidence: low
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The field of aging and dementia is focusing on the characterization of the earliest stages of cognitive impairment. 1 key finding →
Evidence: low
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Synucleinopathies are neurodegenerative diseases that are associated with the misfolding and aggregation of α-synuclein, including Parkinson's disease, dementia with Lewy bodies and multiple system atrophy 1 . 4 key findings →
Evidence: low
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Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. 2 key findings →
Evidence: low
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Based on informant report, disturbed arousal and disorganized speech are specific aspects of fluctuations in dementia with Lewy bodies that reliably distinguish dementia with Lewy bodies from Alzheimer's disease and normal aging. 4 key findings →
Participants: 200 Evidence: low
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In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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MRI and CSF provide complimentary predictive information about time to conversion from amnestic mild cognitive impairment to Alzheimer disease and combination of the 2 provides better prediction than either source alone. 3 key findings →
Participants: 399 Evidence: low
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Imaging patterns of atrophy in CBS vary according to pathologic diagnosis. 4 key findings →
Design: case-control study Participants: 24 Evidence: moderate
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Of 9,033 ARIC participants with sufficient Medicare coverage data (4,980 [55.1%] female, 1993 [22.1%] Black), 671 met the definition of LOE. 2 key findings →
Design: cohort study Evidence: moderate
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Our results suggest that search strategies that use automated electronic search strategies to extract Charlson comorbidities from the clinical notes contained within the electronic medical record are feasible and reliable. 3 key findings →
Design: cohort study Participants: 1,447 Evidence: moderate
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Frontotemporal dementia (FTD) is the second most common cause of dementia in people under the age of 65 years. 2 key findings →
Evidence: low
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There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. 1 key finding →
Evidence: low
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The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. 4 key findings →
Evidence: low
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →
Participants: 53,627 Evidence: low
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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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The LBD-present group had higher QSM values in the SNc (P = 0.008) than the LBD-absent group with no differences in SNr. 5 key findings →
Design: cohort study Participants: 13 Evidence: moderate
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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. 5 key findings →
Evidence: low
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The majority of participants were female and were taking concomitant psychotropic medications (antidepressants and antipsychotics) at baseline. 3 key findings →
Design: phase-2-trial Participants: 75 Evidence: early
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This cross-sectional evaluation of the NIA-AA criteria for preclinical AD indicates that the 1-3 staging criteria coupled with stage 0 and SNAP categories classify 97% of CN subjects from a population-based sample, leaving only 3% unclassified. 2 key findings →
Design: cross-sectional Evidence: moderate
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This roughly 15-year interval where the slope of the amyloid SUVR vs time curve is greatest and roughly linear represents a large therapeutic window for secondary preventive interventions. 1 key finding →
Participants: 246 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →