28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
From 2011 to 2013, 1,744 participants completed high-resolution vessel wall MRI from the population-based Atherosclerosis Risk in Communities Study by a sampling strategy that allowed weighting back to the cohort. 4 key findings →
Participants: 291 Evidence: moderate
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After cohort matching, 48% of participants were women (n = 74 464), 61% were white (n = 93 442), and 31% (n = 48 056) were Medicare Advantage insured, with a mean (SD) age of 64 (10) years. 5 key findings →
Design: cohort study Participants: 154 Evidence: moderate
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The analytic sample included 1 054 926 beneficiaries, including 219 942 (mean [SD] age, 75.3 [6.3] years; 54.6% female) who developed new complex conditions in 2019 and 834 984 (mean [SD] age, 73.8 [5.6] years; 56.7% female) who did not develop a new complex condition in 2019. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In addition to outperforming existing plasma biomarkers, the dSST predicted mid-life dementia risk over a 20-year follow-up across two independent cohorts with different ethnic backgrounds (areas under the curve [AUCs]: dSST 0.68-0.70, dSST+age 0.75-0.81). 4 key findings →
Design: longitudinal study Participants: 11,277 Evidence: moderate
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NPS were highly prevalent (≥90%) in early and late bvFTD. 5 key findings →
Design: longitudinal study Participants: 354 Evidence: moderate
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We identified 1143 dementia-free individuals with acute stroke during follow-up: 1061 (92.8%) ischemic, 82 (7.2%) hemorrhagic, 49.9% female, and 30.8% Black. 5 key findings →
Design: cohort study Evidence: moderate
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The COVID-19 pandemic forced adult day services (ADS) to close and abruptly end in-person services to clients. 5 key findings →
Design: randomized controlled trial Participants: 19 Evidence: high
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In 2006, the worldwide prevalence of Alzheimer's disease was 26.6 million. 5 key findings →
Participants: 85 Evidence: low
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Here, we present new criteria aimed to optimize early, sensitive, and specific clinical diagnosis of PSP on the basis of currently available evidence. © 2017 International Parkinson and Movement Disorder Society.
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These results suggest that, to optimize observing a treatment effect, clinical trials enrolling cognitively normal individuals should selectively recruit participants with abnormal levels of both amyloid and tau (ie, stage 2) because this group would be expected to show the greatest cognitive decline over time if untreated. 3 key findings →
Design: cohort study Evidence: moderate
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The CSDD, and particularly its mood subscale, appears to be more sensitive than the HDRS, it's subscales or the NPI-M, for comparing drug to placebo in treating major depression in AD patients. 3 key findings →
Evidence: high
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Patient treatment with sertraline was not associated with significantly greater reductions in caregiver distress than placebo treatment. 5 key findings →
Participants: 131 Evidence: high
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The new criteria for AD are presented in three documents. 2 key findings →
Evidence: low
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Behavioral symptoms such as repetitive speech, wandering, and sleep disturbances are a core clinical feature of Alzheimer disease and related dementias. 2 key findings →
Evidence: low
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We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Three themes emerged from 29 included studies: self-care needs and behaviors of ICGs, barriers to performing self-care, and enablers of self-care. 1 key finding →
Design: systematic review Evidence: high
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The number of older adults with dementia in the US and globally is projected to increase as a result of population aging and growth. 5 key findings →
Design: cross-sectional Participants: 16 Evidence: low
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Midlife hypertension and elevated midlife but not late-life systolic BP was associated with more cognitive decline during the 20 years of the study. 5 key findings →
Evidence: moderate
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The APOE ε4 genetic variant is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and is increasingly being implicated in other neurodegenerative diseases. 3 key findings →
Evidence: low
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The GGGGCC (G4C2) repeat expansion in a noncoding region of C9orf72 is the most common cause of sporadic and familial forms of amyotrophic lateral sclerosis and frontotemporal dementia. 1 key finding →
Evidence: low
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MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 4 key findings →
Evidence: low
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The fornix is a predominant outflow tract of the hippocampus and may be an important indicator of AD progression. 2 key findings →
Design: cross-sectional Participants: 75 Evidence: moderate
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The authors used mixed-effects growth models to examine longitudinal change in neuropsychological performance over a 4-year period among 197 individuals who were either normal or had mild cognitive impairment (MCI) at baseline. 4 key findings →
Design: longitudinal study Participants: 33 Evidence: moderate
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Several families with an early-onset form of familial Alzheimer's disease have been found to harbour mutations at a specific codon (717) of the gene for the beta-amyloid precursor protein (APP) on chromosome 21. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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 28,180 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 →