Adults with Down syndrome (DS) develop Alzheimer's disease (AD) neuropathology by 40 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Adults with Down syndrome (DS) develop Alzheimer's disease (AD) neuropathology by 40 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrovascular pathology is a significant mediator in Alzheimer's disease (AD) in the general population. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that quantification of WM changes in DS could provide a promising and clinically relevant biomarker for AD clinical onset and progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This is one of the first formal studies to evaluate research attitudes among relatives of individuals with DS and shows the feasibility of using this approach to answer important questions that will guide trialists developing treatments for AD in DS. 1 key finding →
Evidence: moderate
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There are increasing calls for sharing individual biomarker results with participants in dementia research. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
People with Down syndrome (DS) have increased risk of Alzheimer disease (AD), presumably conferred through genetic predispositions arising from trisomy 21. 2 key findings →
Evidence: low
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BackgroundLifetime incidence of Alzheimer's disease (AD) in Down syndrome (DS) exceeds 90%. 2 key findings →
Participants: 18 Evidence: low
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This study explored digital health literacy skills, self-efficacy in utilizing digital health resources, and self-efficacy in managing personal health among caregivers of individuals with Alzheimer's disease and related dementias (ADRD). 2 key findings →
Evidence: low
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AI/AN patients at the end-of-life were more likely to be hospitalized and less likely to use hospice compared with their NHW counterparts. 4 key findings →
Participants: 6,975 Evidence: low
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Down syndrome (DS) provides a model for studying important aspects of Alzheimer disease (AD). 2 key findings →
Evidence: low
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Individuals with Down syndrome (DS) have high levels of oxidative stress throughout the lifespan. 1 key finding →
Evidence: low
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The amyloid beta protein and the amyloid beta-protein precursor (APP) are major constituents of senile plaques and cerebrovascular deposits in patients with Alzheimer disease and Down syndrome. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is characterized by the accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated tau, which together lead to neurodegeneration and cognitive decline. 4 key findings →
Design: clinical trial Evidence: low
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Recruitment strategies are tailored in collaboration with community organizations to align with each language group's preferences, including adjusting the blood draw and interview sequence and hosting group blood draws where participants completed the procedure together, fostering a sense of community and reducing anxiety. 5 key findings →
Participants: 252 Evidence: low
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We highlight a general overview and methodology of TNS. 5 key findings →
Evidence: low
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A total of 11 dyads participated in the study. 5 key findings →
Evidence: low
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• APOE4 carriers exhibit cerebrovascular dysfunction. • Endothelial progenitor cells (EPC) represent cell populations involved in facilitating vascular repair. • In APOE4 carriers, EPC colony count is associated with cerebral small vessel disease. • EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in APOE4 carriers prior to the development of cognitive decline. 4 key findings →
Participants: 109 Evidence: low
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This study provides new insights into the regional binding distribution of a first-generation and a second-generation Tau tracer in limbic and neocortical regions in adults with DS, as well as regional differences in Tau binding in adult with DS vs. those with AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Reduced spine densities and age-dependent accumulation of amyloid β and tau pathology are shared features of Down syndrome (DS) and Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mammogram utilization was 16% higher (Prevalence Ratio [PR] 1.16; 95% CI: 1.05, 1.29) among Medicare Advantage enrollees with dementia, compared to their counterparts in fee-for-service Medicare. 5 key findings →
Design: cross-sectional Evidence: low
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The majority of the participants met criteria for obesity. 2 key findings →
Evidence: low
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Our study suggests that exposure to O3 is associated with the higher risk of dementia in American Indians. 4 key findings →
Participants: 14,910 Evidence: low
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This study supports the need for formal reliability and validity studies of TM preparatory to the consideration of this modality for use in clinical trials for AD. 1 key finding →
Participants: 90 Evidence: low
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In the last decade, a number of important research advances in different fields have allowed Down syndrome (DS) research to flourish, creating a time of both unparalleled opportunity and considerable challenge. 1 key finding →
Evidence: low
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An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events