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Research

30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 151–175 of 236 studies · free to read · tagged Down Syndrome (page 7 of 10) · 30,580 in the whole library · How the 0–100 score works

Download bibliography of these 236 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; 16,054 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.

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

Quantification of modified amyloid beta peptides in Alzheimer disease and Down syndrome brains

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of neuropathology and experimental neurology 1998-11-01

To gain insights into the different forms of modified amyloid beta peptides (A beta) in the Alzheimer disease (AD) and Down syndrome (DS) brain, we used two-site ELISAs with antibodies specific for isomerized (i.e. A beta with L-isoaspartate at positions 1 and 7) and pyroglutamate-modified (i.e. A beta beginning with pyroglutamate at position 3) forms of A beta to quantitate the levels of these different A beta peptides in formic acid extracts of AD and DS frontal cortex. 1 key finding →

Evidence: low

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

Positron emission tomography and neuropathologic estimates of fibrillar amyloid-β in a patient with Down syndrome and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Archives of neurology 2011-11-01

Florbetapir PET can be used to detect increased cerebral-to-cerebellar fibrillar Aβ burden in a Down syndrome patient with Alzheimer disease, even in the presence of frequent amyloid angiopathy and diffuse plaques in the cerebellum. 3 key findings →

Evidence: low

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

Alzheimer-Like Pattern of Hypometabolism Emerges with Elevated Amyloid-β Burden in Down Syndrome

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01

In adults with DS, early amyloid-β accumulation in the striatum is divergent from sporadic AD; however, despite the early striatal amyloid-β, glucose hypometabolism was confined to the typical AD-associated regions, which occurs similarly in autosomal dominant AD. 1 key finding →

Evidence: low

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

Beyond amyloid: Immune, cerebrovascular, and metabolic contributions to Alzheimer disease in people with Down syndrome

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neuron 2022-04-25

People with Down syndrome (DS) have increased risk of Alzheimer disease (AD), presumably conferred through genetic predispositions arising from trisomy 21. 2 key findings →

Evidence: low

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

Poor Sleep as a Precursor to Cognitive Decline in Down Syndrome : A Hypothesis

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer's disease & Parkinsonism 2013-08-01

We propose that sleep disruption is a lever arm that influences how cognition emerges in development and then declines in response to Alzheimer disease in people with Down syndrome. 3 key findings →

Evidence: low

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

Adaptation of a Protocol for Disclosure of Amyloid PET Results for Adults with Down Syndrome and Their Caregivers

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Alzheimer s & Dementia 2025-12-01

Adults with DS are often supported by family caregiver(s), who face challenges including lack of awareness of the increased risk of developing AD, difficulty in obtaining a timely diagnosis, limited resources for psychosocial support, and lack of access to clinical trials. 5 key findings →

Design: longitudinal study Evidence: moderate

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

An investigation of the molecular mechanisms engaged before and after the development of Alzheimer disease neuropathology in Down syndrome: a proteomics approach

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Free radical biology & medicine 2014-08-20

Down syndrome (DS) is one of the most common causes of intellectual disability, owing to trisomy of all or part of chromosome 21. 3 key findings →

Evidence: low

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

Large-scale organoid study suggests effects of trisomy 21 on early fetal neurodevelopment are more subtle than variability between isogenic lines and experiments

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in neuroscience 2023-02-03

This study examines cortical organoids generated from a panel of isogenic trisomic and disomic iPSC lines (subclones) as a model of early fetal brain development in Down syndrome (DS). 3 key findings →

Evidence: low

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

Adaptation of the Clinical Dementia Rating Scale for adults with Down syndrome

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of neurodevelopmental disorders 2019-12-16

The modified questionnaire and interview instruments capture a range of impairment in DS adults, including subthreshold symptomatology, and the instruments provide complementary information relevant to the ascertainment of dementia in DS. 2 key findings →

Evidence: low

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

Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Antioxidants (Basel, Switzerland) 2026-04-21

Down syndrome (DS), caused by trisomy 21, is the most prevalent genetic condition associated with accelerated aging and near-universal development of early-onset Alzheimer's disease (AD). 1 key finding →

Evidence: low

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

VAMP-2 Is a Surrogate Cerebrospinal Fluid Marker of Alzheimer-related Cognitive Impairment in Adults With Down Syndrome

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer's research & therapy 2021-03-23

There is an urgent need for objective markers of Alzheimer’s disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression and assess response to disease-modifying therapies. 4 key findings →

Participants: 80 Evidence: moderate

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

Relationship between tau and SV2A in the neurotypical population and translation to the Down syndrome population

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-12-01

Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →

Participants: 94 Evidence: moderate

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

Relationship between tau and SV2A in the neurotypical population and translation to the Down syndrome population

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Alzheimer s & Dementia 2025-12-01

Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →

Participants: 94 Evidence: moderate

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

Regional binding of tau and amyloid PET tracers in Down syndrome autopsy brain tissue

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Molecular neurodegeneration 2020-11-23

This study provides new insights into the regional binding distribution of a first-generation and a second-generation Tau tracer in limbic and neocortical regions in adults with DS, as well as regional differences in Tau binding in adult with DS vs. those with AD. 5 key findings →

Evidence: low

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

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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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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