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Research

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

Find studies

Showing 51–75 of 664 studies in Down syndrome and Alzheimer's (page 3 of 27) · 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.

Longitudinal Dynamics of the Blood Proteome Within the Alzheimer Spectrum in Down Syndrome

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology 2026-09-01

In DS, longitudinal characterization of all previously identified proteins revealed distinct trajectories over time and an association of baseline levels with future cognitive decline. 5 key findings →

Design: cross-sectional Participants: 59 Evidence: moderate

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

The Down Alzheimer Barcelona Neuroimaging Initiative (DABNI): Ten Years of Progress in Understanding Alzheimer's in Down Syndrome

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Alzheimer s & Dementia 2025-12-01

The DABNI cohort included 1,135 participants with a mean age of 42.82 years (SD = 11.56), 46.3% of whom are female. 5 key findings →

Design: longitudinal study Participants: 1,135 Evidence: moderate

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

Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurobiology of Disease 1996-02-01

Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein.

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

Evidence for a membrane defect in Alzheimer disease brain

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-03-01

To determine whether neurodegeneration in Alzheimer disease brain is associated with degradation of structural cell membrane molecules, we measured tissue levels of the major membrane phospholipids and their metabolites in three cortical areas from postmortem brains of Alzheimer disease patients and matched controls. 5 key findings →

Evidence: low

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

Intraneuronal Abeta immunoreactivity is not a predictor of brain amyloidosis-beta or neurofibrillary degeneration

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Acta neuropathologica 2007-01-20

Amyloid beta (Abeta) immunoreactivity in neurons was examined in brains of 32 control subjects, 31 people with Down syndrome, and 36 patients with sporadic Alzheimer's disease to determine if intraneuronal Abeta immunoreactivity is an early manifestation of Alzheimer-type pathology leading to fibrillar plaque formation and/or neurofibrillary degeneration. 4 key findings →

Participants: 31 Evidence: low

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

Aberrant crosstalk between insulin signaling and mTOR in young Down syndrome individuals revealed by neuronal-derived extracellular vesicles

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-11-23

The alteration of the insulin-signaling/mTOR pathways represents an early event in DS brain and likely contributes to the cerebral dysfunction and intellectual disability observed in this unique population. 1 key finding →

Participants: 17 Evidence: low

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

Detection of an Alzheimer disease pattern of cerebral metabolism in Down syndrome

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Dementia (Basel, Switzerland) 1994-03-01

Correlational analysis of cerebral metabolic (rCMRglc) data obtained with positron emission tomography (PET) assesses group differences and has demonstrated reduced frontal-parietal rCMRglc interdependencies in Alzheimer's disease (AD). 2 key findings →

Design: longitudinal study Participants: 15 Evidence: moderate

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

Longitudinal trajectories of amyloid deposition, cortical thickness, and tau in Down syndrome: A deep-phenotyping case report

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2019-11-25

Until now, data on the longitudinal trajectories of amyloid accumulation, tau pathology, and brain atrophy over multiple time points remain scarce in DS. 1 key finding →

Design: longitudinal study Evidence: moderate

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

Differential Associations of Apolipoprotein E ε4 Genotype With Attentional Abilities Across the Life Span of Individuals With Down Syndrome

✓ Peer-reviewed alzhub usefulness score 50 out of 100. JAMA network open 2020-09-01

The ε4 allele of the apolipoprotein E gene (APOE ε4) is associated with an additional risk for AD. 5 key findings →

Design: cross-sectional Participants: 240 Evidence: low

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

Increased excitatory to inhibitory synaptic ratio in parietal cortex samples from individuals with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Nature communications 2021-05-10

Synaptic disturbances in excitatory to inhibitory (E/I) balance in forebrain circuits are thought to contribute to the progression of Alzheimer's disease (AD) and dementia, although direct evidence for such imbalance in humans is lacking. 3 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1996-11-01

To study the pathogenesis of central nervous system abnormalities in Down syndrome (DS), we have analyzed a new genetic model of DS, the partial trisomy 16 (Ts65Dn) mouse. 1 key finding →

Evidence: low

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

Positron emission tomography of brain β-amyloid and τ levels in adults with Down syndrome

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Archives of neurology 2011-06-01

Consistent with neuropathological findings from postmortem studies, [(18)F]FDDNP positron emission tomography shows high binding levels in Down syndrome comparable to Alzheimer disease and greater levels than in members of a control group. 3 key findings →

Design: cross-sectional Participants: 19 Evidence: low

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

The effect of acetyl-L-carnitine administration on persons with Down syndrome

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Research in developmental disabilities 2006-04-18

Since previous investigations reported improvements in cognition of patients with dementia after acetyl-L-carnitine therapy and since there is an increased risk for persons with Down syndrome to develop Alzheimer disease, this study was designed to investigate the effect of acetyl-L-carnitine administration on neurological, intellectual, and social functions in adults with Down syndrome. 2 key findings →

Participants: 40 Evidence: low

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

Plasma NT1-tau and Aβ42correlate with age and cognitive function in two large Down syndrome cohorts

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2023-03-10

Structured Abstract Introduction People with Down syndrome (DS) often develop Alzheimer disease (AD). 4 key findings →

Design: cross-sectional Participants: 85 Evidence: moderate

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

Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1989-10-01

Interleukin 1, an immune response-generated cytokine that stimulates astrocyte proliferation and reactivity (astrogliosis), was present in up to 30 times as many glial cells in tissue sections of brain from patients with Down syndrome and Alzheimer disease compared with age-matched control subjects. 3 key findings →

Evidence: low

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

Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons: Converging Insights From Alternative Hypotheses

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Frontiers in neuroscience 2019-05-07

We place these findings in the context of the selective, but by no means unique, involvement of BFCNs and their trophic dependence on NGF signaling and speculate as to how pathogenesis in these neurons is initiated, amplified and ultimately results in their dysfunction and death. 2 key findings →

Evidence: low

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

Vascular fibrosis and calcification in the hippocampus in aging, Alzheimer disease, and Down syndrome

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2001-11-28

Study of the hippocampal formation of 82 subjects, including 25 control subjects from 33 to 83 years of age, 34 subjects with Alzheimer disease (AD) from 65 to 89 years of age, and 23 subjects with Down syndrome (DS) from 33 to 72 years of age, revealed hippocampal vasculopathy with fibrosis and calcification (VFC) in 40% of control, 59% of AD, and 4% of DS subjects. 5 key findings →

Participants: 82 Evidence: moderate

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

Emerging Putative Associations between Non-Coding RNAs and Protein-Coding Genes in Neuropathic Pain: Added Value from Reusing Microarray Data

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Frontiers in neurology 2016-10-18

Regeneration of injured nerves is likely occurring in the peripheral nervous system, but not in the central nervous system. 4 key findings →

Design: meta-analysis Evidence: high

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

Association of plasma neurofilament light chain with microstructural white matter changes in Down syndrome

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2024-10-01

Early increases in plasma NfL may reflect early white matter microstructural changes prior to dementia in DS. 2 key findings →

Design: cross-sectional 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. 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