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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–18 of 18 studies in Down syndrome and Alzheimer's published 2009 · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

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

Other subjects

Authors

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

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

What “Down syndrome and Alzheimer's” covers

Down syndrome and Alzheimer's — Alzheimer's in adults with Down syndrome: how it is detected, tracked and treated in this group.

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.

The genetic architecture of Down syndrome phenotypes revealed by high-resolution analysis of human segmental trisomies

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-07-13

Down syndrome (DS), or trisomy 21, is a common disorder associated with several complex clinical phenotypes. 1 key finding →

Participants: 30 Evidence: low

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

Transactive response DNA-binding protein 43 burden in familial Alzheimer disease and Down syndrome

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Archives of neurology 2009-12-01

Transactive response DNA-binding protein 43 pathology occurs in FAD and DS, similar to that observed in sporadic Alzheimer disease. 2 key findings →

Participants: 42 Evidence: low

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

Differential processing of amyloid-beta precursor protein directs human embryonic stem cell proliferation and differentiation into neuronal precursor cells

✓ Peer-reviewed alzhub usefulness score 42 out of 100. The Journal of biological chemistry 2009-06-19

The amyloid-beta precursor protein (AbetaPP) is a ubiquitously expressed transmembrane protein whose cleavage product, the amyloid-beta (Abeta) protein, is deposited in amyloid plaques in neurodegenerative conditions such as Alzheimer disease, Down syndrome, and head injury. 3 key findings →

Evidence: low

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

A fibril-specific, conformation-dependent antibody recognizes a subset of Abeta plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Acta neuropathologica 2009-04-10

Beta-amyloid (Abeta) is thought to be a key contributor to the pathogenesis of Alzheimer disease (AD) in the general population and in adults with Down syndrome (DS). 3 key findings →

Evidence: low

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

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

Down syndrome--recent progress and future prospects

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Human molecular genetics 2009-04-01

Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is associated with a number of deleterious phenotypes, including learning disability, heart defects, early-onset Alzheimer's disease and childhood leukaemia. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Cerebral amyloidosis: postmortem detection with human 7.0-T MR imaging system

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Radiology 2009-09-29

The finding of postmortem susceptibility-weighted changes in the cerebral cortex of patients with cerebral amyloidosis with a human 7.0-T MR imaging system opens up the possibility of obtaining in vivo radiologic evidence of cerebral amyloid beta deposition. 1 key finding →

Evidence: low

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

Alzheimer's-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-12-28

An additional copy of the beta-amyloid precursor protein (APP) gene causes early-onset Alzheimer's disease (AD) in trisomy 21 (DS). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Decreased brain-derived neurotrophic factor depends on amyloid aggregation state in transgenic mouse models of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2009-07-01

Downregulation of brain-derived neurotrophic factor (BDNF) in the cortex occurs early in the progression of Alzheimer's disease (AD). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Function and regulation of Dyrk1A: towards understanding Down syndrome

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cellular and molecular life sciences : CMLS 2009-08-14

Down syndrome (DS) is associated with a variety of symptoms, such as incapacitating mental retardation and neurodegeneration (i.e., Alzheimer's disease), that prevent patients from leading fully independent lives. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Characterization of a mouse model overexpressing beta-site APP-cleaving enzyme 2 reveals a new role for BACE2

✓ Peer-reviewed alzhub usefulness score 34 out of 100. Genes, brain, and behavior 2009-09-22

BACE2 is homologous to BACE1, a beta-secretase that is involved in the amyloidogenic pathway of amyloid precursor protein (APP), and maps to the Down syndrome critical region of chromosome 21. 1 key finding →

Evidence: low

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

Okadaic acid induces apoptosis in Down syndrome fibroblasts

✓ Peer-reviewed alzhub usefulness score 32 out of 100. Toxicology in vitro : an international journal published in association with BIBRA 2009-12-13

Down's syndrome (DS) is characterized by several pathological aspects leading to an increased susceptibility to cardiovascular diseases, infections, leukemia, endocrine alterations. 1 key finding →

Evidence: low

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

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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 →

Newest studies, as a dated timeline →    Atom feed