This represents the largest U.S.-based, multi-site, biomarker initiative of AD in DS. 1 key finding →
Design: longitudinal study Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This represents the largest U.S.-based, multi-site, biomarker initiative of AD in DS. 1 key finding →
Design: longitudinal study Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is a genetic form of Alzheimer's disease (AD) that offers crucial insights into AD pathogenesis. 2 key findings →
Design: cohort study Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 132 Evidence: moderate
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At baseline, there were 436 asymptomatic individuals, 69 patients with prodromal AD, and 127 with AD dementia. 2 key findings →
Design: cohort study Participants: 632 Evidence: moderate
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There were 132 720 unique adults with Down syndrome from 2011 to 2019: 79 578 (53.2%) were male, 17 090 (11.7%) were non-Hispanic Black, 20 777 (15.7%) were Hispanic, 101 120 (68.8%) were non-Hispanic White, and 47 692 (23.3%) had ever had an Alzheimer dementia diagnosis. 3 key findings →
Design: cohort study Participants: 132 Evidence: moderate
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Currently available literature shows limited information on aging in RGNDs, with relatively many reports of young-onset dementia. 2 key findings →
Design: longitudinal study Participants: 25 Evidence: moderate
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Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [ 11 C]PiB PET imaging, which has not been replicated with [ 18 F]florbetapir (FBP). 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Older Medicare beneficiaries in California with DS, especially those with dementia, have a high level of multimorbidity including several treatable conditions. 3 key findings →
Design: cross-sectional Participants: 100 Evidence: low
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Virtually all adults with Down syndrome (DS) show the neuropathological changes of Alzheimer disease (AD) by the age of 40 years. 2 key findings →
Design: longitudinal study Evidence: moderate
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Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB. 2 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
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Aβ40 levels changed less for the simvastatin group (not statistically significant). 4 key findings →
Design: cohort study Participants: 21 Evidence: high
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Elevations in plasma Abeta(42) peptide levels are associated with earlier onset of AD and increased risk of death. 4 key findings →
Design: cohort study Participants: 204 Evidence: moderate
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials. 1 key finding →
Design: longitudinal study Participants: 328 Evidence: moderate
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Between Feb 1, 2013, and June 28, 2019 (Barcelona), and between June 1, 2009, and Dec 31, 2014 (Cambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with prodromal Alzheimer's disease, and 83 [21%] with Alzheimer's disease dementia) and 242 euploid controls.
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It is suggested that impaired executive function in Down's syndrome is due to abnormal development of the prefrontal cortex in Down's syndrome. 3 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. 1 key finding →
Evidence: low
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Down syndrome (DS), or trisomy 21, is a common disorder associated with several complex clinical phenotypes. 1 key finding →
Participants: 30 Evidence: low
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We have purified and characterized the cerebral amyloid protein that forms the plaque core in Alzheimer disease and in aged individuals with Down syndrome. 5 key findings →
Evidence: low
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This exploratory case-control study investigates the synaptic marker beta-synuclein in serum and plasma pTau181 in adults with Down syndrome (DS) with (sDS, n = 14) and without (aDS, n = 47) clinical symptoms of Alzheimer disease (AD) as well as euploid controls (n = 23). 1 key finding →
Design: case-control study Participants: 14 Evidence: moderate
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Plasma p-tau212 might have utility for theragnostics, monitoring therapy efficacy, and as a target engagement biomarker in clinical trials both in sporadic and DSAD. 1 key finding →
Participants: 245 Evidence: low
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Characterizing the timing and progression of Alzheimer's disease biomarker onset in Down syndrome (DS) and contrasting potential timing differences with neurotypical adults is needed to identify optimal Alzheimer's disease therapeutic treatment windows in DS. 2 key findings →
Design: longitudinal study Participants: 198 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
For both cohorts, the prevalence of mosaicism was 40 and Aβ 42 concentrations. 2 key findings →
Design: longitudinal study Participants: 357 Evidence: moderate
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Of 115 participants (mean age 40.0 ± 9.2 years; 43.5% female), higher interdaily stability was associated with higher DSMSE scores B = 20.6 (95% CI 5.0-36.2). 4 key findings →
Design: cross-sectional Participants: 115 Evidence: low
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One hundred brains of patients with Down's syndrome (DS) who died in institutions for chronic care were examined for clinicopathological correlation of Alzheimer's disease. 5 key findings →
Participants: 56 Evidence: low
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Establishing this clinical definition supports future research and investigation of an underlying mechanism. 1 key finding →
Design: case-control study Participants: 35 Evidence: moderate
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →