Adults with Down syndrome (DS) are at risk for Alzheimer’s disease (AD). 4 key findings →
Design: cohort study Participants: 167 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The anterior thalamic nuclei are important for cognition, and memory in particular. 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
As a model of early fetal brain development in Down syndrome, this study examines cortical organoids generated from isogenic trisomic and disomic iPSC lines. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
An extra copy of the amyloid precursor protein gene (APP) is present in Down syndrome (DS) and APP duplication (APPdup), increasing the risk of Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation of tau tangles and Aβ plaques are prominent neuropathologies that characterize Alzheimer’s disease (AD) and Down Syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
People with Down syndrome have higher age-specific mortality rates compared to the general population as well as peers with other intellectual and developmental disabilities. 2 key findings →
Design: case-control study Participants: 137,293 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The amyloid precursor protein (APP) is heavily studied as the source of amyloid beta in Alzheimer’s disease (AD), however, the complex functions of APP remain poorly understood, as does the impact of APP dosage on neurodevelopment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adults with Down syndrome (DS) develop Alzheimer’s disease (AD) brain pathology by age 40 due to triplication of the Amyloid Precursor Protein ( APP ) gene on chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
16/100
Dysregulated expression and activity of DYRK1A, dual specificity tyrosine phosphorylation regulated kinase 1A, is a feature of several neurodevelopmental and neurodegenerative diseases, including Down syndrome, DYRK1A syndrome, autism spectrum disorders, Alzheimer’s disease, and Parkinson’s disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
16/100
Structured Abstract INTRODUCTION Adults with Down syndrome (DS) have a higher risk of developing Alzheimer’s disease (AD). 3 key findings →
Participants: 58 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer’s disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNA dysregulation is implicated in neurodegenerative disorders, including Alzheimer’s disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome (DS) develop a genetic form of Alzheimer’s disease (AD) due to an extra copy of chromosome 21, which contains the APP gene. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Down Syndrome (DS) is the most abundant genetic form of mental retardation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 534 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 10. The same 10 appear here every time.
- Neurofilament light as a blood biomarker for neurodegeneration in Down syndrome
- The striatum is an early, accurate indicator of amyloid burden using [11C]PiB in Down syndrome: Comparison of two radiotracers
- The pathological association between Down syndrome and Alzheimer disease
- Evidence for apoptosis in the fetal Down syndrome brain
- Elevated expression of beta-site amyloid precursor protein cleaving enzyme 2 in brains of patients with Down syndrome
- Neuropathological measures of increased tau phosphorylation across the Down syndrome lifespan
- Epilepsy and subsequent dementia in adults with down syndrome: a propensity score-matched cohort study using federated electronic health records
- Sleep‐like behavior and 24‐h rhythm disruption in the Tc1 mouse model of Down syndrome
- Long-term basal forebrain cholinergic-rich grafts derived from trisomy 16 mice do not develop beta-amyloid pathology and neurodegeneration but demonstrate neuroinflammatory responses
- Memory and Plasma pTau217 Refine Prognosis in 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 →