New-onset epilepsy seems to occur early in the course of dementia in DS patients. 4 key findings →
Participants: 220 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
New-onset epilepsy seems to occur early in the course of dementia in DS patients. 4 key findings →
Participants: 220 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Adults with Down syndrome (DS) have an exceptionally high frequency of Alzheimer disease (AD) with a wide variability in onset, from 40 to 70 years of age. 2 key findings →
Participants: 232 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. 1 key finding →
Design: cross-sectional Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 49.17) had a higher incidence of psychotic disorder (p = .028) compared to non-progressors and progressors. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The gene encoding the beta-amyloid precursor protein has been assigned to human chromosome 21, as has a gene responsible for at least some cases of familial Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome is caused by over-expression of genes located within a segment of chromosome 21, termed the Down locus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Adults with DS may have unique neuro- and cardio- protective factors that deserve future investigation. 4 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To study the use of a dementia screening tool in our clinic cohort of adults with Down syndrome. 1 key finding →
Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The Alzheimer amyloid protein precursor (APP) has previously been localized to human chromosome 21q11.2-q21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Neuritic pathology is a major neuroanatomical correlate of dementia in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The majority of the participants met criteria for obesity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a neurodegenerative disorder characterized by global cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Free full text
Studies in the neurotypical population have demonstrated that personal social networks can mitigate cognitive decline and the development of Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
There was a significant interaction between OSA and diagnosis for within- and between-DMN FC (p-values<0.05). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We observed higher within‐ and between‐DMN FC in the CS‐OSA compared to the CI‐OSA group; however, this difference was not observed between the CS‐nonOSA and CI‐nonOSA groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with Down syndrome carry high risk of developing Alzheimer’s disease and efforts to include this population in clinical trials remain limited. 4 key findings →
Design: longitudinal study Participants: 237 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Since its first description in 1906 by Dr. Alois Alzheimer, Alzheimer’s disease (AD) has been the most common type of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
By age 40 years over 90% of adults with Down syndrome (DS) have Alzheimer’s disease (AD) pathology and most progress to dementia. 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,045 records (3.3% of the library) are not peer-reviewed — 966 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
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