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Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 226–250 of 543 studies · tagged Down Syndrome (page 10 of 22) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 13,259 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Enhancing protein O-GlcNAcylation in down syndrome mice mitigates memory dysfunctions through the rescue of mitochondrial bioenergetics, stress responses and pathological markers

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Redox biology 2025-07-16

Disturbances of the single sugar modification of proteins, O-GlcNAc, have been identified as a potential connection between disrupted brain metabolism and intellectual decay. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Cerebral vasoreactivity and intima-media thickness in Down syndrome: A case-control study

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Journal of the neurological sciences 2017-11-15

Subjects with Down Syndrome (DS) have high prevalence of cerebral vascular amyloidosis, cognitive decline and dementia. 4 key findings →

Design: longitudinal study Participants: 25 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

“Patient-specific Alzheimer-like pathology in trisomy 21 cerebral organoids reveals BACE2 as a gene-dose-sensitive AD-suppressor in human brain”

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Molecular psychiatry 2020-01-31

A population of >6 million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Oxidative stress and mitochondrial dysfunction in Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Advances in experimental medicine and biology 2012-01-01

Down syndrome (DS) or trisomy 21 is the genetic disease with highest prevalence displaying phenotypic features that both include neurologic deficiencies and a number of clinical outcomes. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Bach1 overexpression in Down syndrome correlates with the alteration of the HO-1/BVR-a system: insights for transition to Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2015-01-01

Bach1, among the genes encoded on chromosome 21, is a transcription repressor, which binds to antioxidant response elements of DNA thus inhibiting the transcription of specific genes involved in the cell stress response including heme oxygenase-1 (HO-1). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Possible compensatory events in adult Down syndrome brain prior to the development of Alzheimer disease neuropathology: targets for nonpharmacological intervention

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2007-03-01

Adults with Down syndrome (DS) develop Alzheimer disease (AD) pathology progressively with age but clinical signs of dementia are delayed by at least 10 years after the first signs of disease. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Alzheimer Abeta peptide induces chromosome mis-segregation and aneuploidy, including trisomy 21: requirement for tau and APP

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular biology of the cell 2009-12-23

Both sporadic and familial Alzheimer's disease (AD) patients exhibit increased chromosome aneuploidy, particularly trisomy 21, in neurons and other cells. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Total numbers of neurons and glial cells in cortex and basal ganglia of aged brains with Down syndrome--a stereological study

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Cerebral cortex (New York, N.Y. : 1991) 2011-03-22

The total numbers of neurons and glial cells in the neocortex and basal ganglia in adults with Down syndrome (DS) were estimated with design-based stereological methods, providing quantitative data on brains affected by delayed development and accelerated aging. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Alzheimer-related altered white matter microstructural integrity in Down syndrome: A model for sporadic AD?

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2020-11-07

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

Research attitudes in families of individuals with Down syndrome: importance for clinical trials

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Alzheimer's research & therapy 2022-11-23

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

Full summary, score breakdown and related studies → Original source Free full text

Association between presenilin-1 polymorphism and maternal meiosis II errors in Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. American journal of medical genetics 2000-08-01

Several lines of evidence suggest a shared genetic susceptibility to Down syndrome (DS) and Alzheimer disease (AD). 2 key findings →

Participants: 168 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Retromer Proteins Reduced in Down Syndrome and the Dp16 Model: Impact of APP Dose and Preclinical Studies of a γ-Secretase Modulator

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Annals of neurology 2023-04-29

Our studies point to increased APP gene dose as a compromising retromer function in DS and suggest a causal role for Aβ42 and Aβ40. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Absence of familial association between dementia of Alzheimer type and Down syndrome

✓ Peer-reviewed alzhub usefulness score 41 out of 100. American journal of medical genetics 1989-08-01

The aim of this study was to test whether there is an excess of dementia of Alzheimer type (DAT) cases in Down syndrome (DS) relatives. 1 key finding →

Design: case-control study Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

From across this tag

10 of the 536 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.

↑ Change the filters

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 27,780 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.

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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.

1,034 records (3.7% 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 →

Newest studies, as a dated timeline →    Atom feed