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Find studies

Showing 251–275 of 278 studies · free to read (page 11 of 12) · 30,980 in the whole library · How the 0–100 score works

Download bibliography of these 278 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 278 studies tagged down — clear

Browse by subject, author or institution

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

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.

BACH1/HO-1 axis dysregulation links Down syndrome to Alzheimer-like neurodegeneration

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Neurochemistry international 2026-07-30

Down syndrome (DS), caused by trisomy of chromosome 21, is characterized by early-onset oxidative stress, impaired neuronal development, and an increased risk of Alzheimer's disease (AD)-like neuropathology. 2 key findings →

Evidence: low

Down syndrome (DS), characterised by compromised brain development and intellectual challenges, often manifests Alzheimer's disease (AD) -like symptoms. 2 key findings →

Evidence: low

Life Stress and Dementia Risk in Adults with Down Syndrome

✓ Peer-reviewed alzhub usefulness score 30 out of 100. Innovation in Aging 2025-12-01

We found that a higher baseline sum of stress events was associated with greater risk of conversion from baseline stable cognition to mild cognitive impairment (MCI) or dementia at follow up, even when controlling for age, sex, premorbid level of intellectual disability, site, clinical latency between assessments, and the presence of anxiety or depression (odds ratio = 1.53, p = 0.021). 5 key findings →

Evidence: low

In humans, GART [phosphoribosylglycinamide formyltransferase (EC 2.1.2.2) / phosphoribosylglycinamide synthetase (EC 6.3.4.13) / phosphoribosylaminoimidazole synthetase (EC 6.3.3.1)] is a trifunctional protein which catalyzes the second, third, and fifth reactions of the ten step de novo purine synthesis (DNPS) pathway. 4 key findings →

Evidence: low

Down syndrome (DS) brains, from 19 gestational weeks to 50 years of age were studied by immunohistochemical methods with a polyclonal antibody against synthetic peptide comprising part of the Kunitz-type protease inhibitor (KPI) domain of Alzheimer disease amyloid precursor protein (APP), residues 301 to 323 of APP 770. 1 key finding →

Evidence: low

Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS). 3 key findings →

Evidence: low

No entanto, os resultados dos estudos clínicos apresentam divergências entre si, além de limitações metodológicas, pequeno tamanho amostral e variabilidade na definição dos desfechos. 5 key findings →

Evidence: low

The mortality of adults with Down syndrome as a function of age

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Mechanisms of ageing and development 1986-11-01

This study sought to test the hypothesis that adults with Down Syndrome may age faster than the general population by comparing the rate of increase in their mortality with age with that of the general population by the method originally described by Gompertz. 1 key finding →

Evidence: low

(1) GARS-AIRS-GART is an important candidate gene in studies of Down syndrome (DS)-related Alzheimer's disease (AD), due to its chromosomal localization (21q22.1) in the Down syndrome critical region, involvement in de novo purine biosynthesis, and over-expression in DS brain. 3 key findings →

Evidence: low

Down syndrome (DS), caused by trisomy of chromosome 21, exhibits significant phenotypic variability, including intellectual disability, early-onset Alzheimer disease (AD), congenital heart defects (CHDs), haematological malignancies, and immune dysregulation. 5 key findings →

Evidence: low

Down syndrome postmortem brains exhibit reduction in [ 18 F]nifene binding to α4β2* nicotinic acetylcholinergic receptors

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-15

Alzheimer’s disease (AD) pathology including amyloid beta (Aβ) plaques and tau tangles accumulate with age in Down Syndrome (DS). 4 key findings →

Evidence: low

Oligodendrocyte Enriched Brain Organoids Reveal Impaired Oligodendroglial Maturation and Altered Neural Network Activity in Down Syndrome

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-28

Individuals with Down syndrome (DS) display developmental delay, intellectual disability, premature brain ageing, and an increased risk of Alzheimer-like neurodegeneration. 4 key findings →

Evidence: low

Multi-dimensional attention framework for personalized Alzheimer’s disease progression prediction across sporadic and genetic risk cohorts

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-17

Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability. 4 key findings →

Design: longitudinal study Participants: 1,669 Evidence: moderate

A head-to-head comparison of multiple amyloid PET radiotracers for Down syndrome clinical trials

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-03-19

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

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

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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.

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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,042 records (3.4% of the library) are not peer-reviewed — 967 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