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
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We used within-group locally estimated scatterplot smoothing models to compare the trajectory of biomarker changes with age in females versus males, as well as by apolipoprotein ɛ4 carriership. 5 key findings →
Design: cross-sectional Participants: 628 Evidence: low
Full summary, score breakdown and related studies → Original source
NF-L is a biomarker for neurodegeneration in DS with potential for use in future clinical trials to prevent or delay dementia. 2 key findings →
Design: cross-sectional Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
ChT was increased in people with DS (pwDS) compared to Ctrl. 5 key findings →
Design: cross-sectional Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
We comprehensively estimated the risk of multiple morbidity across the lifespan in people with Down syndrome compared with the general population and controls with other forms of intellectual disability. 4 key findings →
Participants: 204 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Further detailed investigations into the development and treatment of comorbidities across the lifespan are needed for a successful longitudinal approach to healthcare in people with Down syndrome. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the United States, estimates indicate there are between 250,000 and 400,000 individuals with Down syndrome (DS), and nearly all will develop Alzheimer's disease (AD) pathology starting in their 30s. With the current lifespan being 55 to 60 years, approximately 70% will develop dementia, and if their life expectancy continues to increase, the number of individuals developing AD will concomitantly increase. 4 key findings →
Participants: 400,000 Evidence: low
Full summary, score breakdown and related studies → Original source
At present, there may be over 210,000 people with Down syndrome (DS) over the age of 55 in the United States (US) who have significant needs for augmented services due to circumstances related to ordinary and/or pathological aging. 1 key finding →
Participants: 210,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Polynomial regressions indicated an 0.23 kg/m2 decrease in BMI per year beginning at age 36.5 years, which occurs alongside the period during which Aβ and tau increase and memory and mental status decline. 3 key findings →
Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome (DS) are more likely to experience earlier onset of multiple facets of physiological aging. 3 key findings →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
While post mortem studies have identified the major cell types and functional systems affected in Alzheimer's disease (AD) the initial sites and molecular characteristics of pathology are still unclear. 1 key finding →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological and experimental studies suggest that a disease-aggravating neuroinflammatory process is present at preclinical stages of Alzheimer's disease. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
This study was designed to provide information on the prevalence and nature of psychiatric disorders in 497 individuals with Down syndrome. 1 key finding →
Participants: 497 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), trisomy of human chromosome 21 (HSA21), is characterized by lifelong cognitive impairments and the development of the neuropathological hallmarks of Alzheimer's disease (AD). 4 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Trisomy 21 (T21) gives rise to Down syndrome (DS), the most commonly occurring chromosomal abnormality in humans. 2 key findings →
Participants: 400 Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Down syndrome, caused by trisomy of chromosome 21, is the single most common risk factor for early-onset Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Children with Down syndrome (DS) experience congenital and functional medical issues that predispose them to obstructive sleep apnea (OSA). 4 key findings →
Participants: 177 Evidence: low
Full summary, score breakdown and related studies → Original source
The form and distribution of senile plaques (SP) and neurofibrillary tangles (NFT) has been examined in the brains of 13 patients with Down's syndrome (DS), aged less than or equal to 50 years, using immunocytochemical and silver staining procedures. 5 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Overexpression of the amyloid precursor protein (APP) gene on chromosome 21 in Down syndrome (DS) has been linked to increased brain amyloid levels and early-onset Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
β-Amyloid precursor protein (APP) and its cleaved products are strongly implicated in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
PIB binding in DS, first appearing in striatum, began around age 40 and was strongly associated with dementia and cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a leading cause of morbidity and mortality among the elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
The sequencing of chromosome 21 and the use of models of Down's syndrome in mice have allowed us to relate genes and sets of genes to the neuropathogenesis of this syndrome, and to better understand its phenotype. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Down's syndrome (DS) or trisomy 21 is the most common genetic cause of mental retardation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
7 of the 80 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 7. The same 7 appear here every time.
- Prevalence of epilepsy and young-onset dementia in adults with intellectual disability: Contrasting Down syndrome and autism diagnoses
- Serum interleukin-6 levels correlate with the severity of dementia in Down syndrome and in Alzheimer's disease
- App gene dosage modulates endosomal abnormalities of Alzheimer's disease in a segmental trisomy 16 mouse model of down syndrome
- Hypomethylation of the amyloid precursor protein gene in the brain of an Alzheimer's disease patient
- Dendritic spine pathology and thrombospondin-1 deficits in Down syndrome
- Down syndrome and Alzheimer's disease: a link between development and aging
- Perinatal choline supplementation improves cognitive functioning and emotion regulation in the Ts65Dn mouse model of Down syndrome
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →