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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 376–400 of 664 studies in Down syndrome and Alzheimer's (page 16 of 27) · 28,180 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.

Other subjects

Authors

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

Institutions

From OpenAlex; 13,658 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.

Genetics of β-Amyloid Precursor Protein in Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Cold Spring Harbor perspectives in medicine 2017-06-01

Alzheimer's disease (AD) is characterized neuropathologically by neuronal cell loss, extracellular neuritic plaques composed of β-amyloid (Aβ), and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Lysosomal Dysfunction in Down Syndrome Is APP-Dependent and Mediated by APP-βCTF (C99)

✓ Peer-reviewed alzhub usefulness score 38 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2019-05-01

Direct measurements of lysosomal pH uncovered a significant elevation (0.6 units) as a basis for slowed LC3 turnover and the inactivation of cathepsin D and other lysosomal hydrolases known to be unstable or less active when lysosomal pH is persistently elevated. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Dysfunction of autophagy and endosomal-lysosomal pathways: Roles in pathogenesis of Down syndrome and Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Free radical biology & medicine 2017-10-06

Individuals with Down syndrome (DS) have an increased risk of early-onset Alzheimer's Disease (AD), largely owing to a triplication of the APP gene, located on chromosome 21. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

The promoter activity of the gene encoding Alzheimer beta-amyloid precursor protein (APP) is regulated by two blocks of upstream sequences

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Brain research. Molecular brain research 1991-02-01

Transcriptional regulation of the gene encoding the amyloid precursor protein (APP) may play an important role in the formation of the amyloid depositions observed in Alzheimer disease and Down syndrome patients. 4 key findings →

Evidence: low

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

Alzheimer degeneration in Down syndrome. Electrophysiologic alterations and histopathologic findings

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Archives of neurology 1975-09-01

Progressive electroencephalographic disorganization and decreased voltage amplitude in the late components of the averaged visual evoked potentials were recorded in the last two years of life of a patient with Down disease and Alzheimer degeneration. 3 key findings →

Evidence: low

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

Hypothesis: Alzheimer's disease is a phylogenetic disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Medical hypotheses 1989-07-01

It is hypothesized that Alzheimer's disease is a human phylogenetic disease which has a common multifactorial pathogenesis in sporadic and familial cases and in Down syndrome, related to a genomic character function G(x). 1 key finding →

Evidence: low

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

Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Current Alzheimer research 2016-01-01

Down syndrome (DS) is the most common non-lethal genetic condition that affects approximately 1 in 700 births in the United States of America. 1 key finding →

Evidence: low

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

Expression of APP in brains of transgenic mice containing the entire human APP gene

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Biochemical and biophysical research communications 1993-12-01

A major component of amyloid deposits found in Alzheimer disease and Down syndrome is the beta/A4 peptide, which is derived from the Alzheimer amyloid protein precursor (APP). 3 key findings →

Evidence: low

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

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

The amyloid percursor protein of Alzheimer disease is expressed as a 130 kDa polypeptide in various cultured cell types

✓ Peer-reviewed alzhub usefulness score 37 out of 100. FEBS letters 1988-12-01

The vascular and parenchymal amyloid deposits in Alzheimer disease (AD), normal aging and Down syndrome are mainly composed of a 4 kDa polypeptide (A4), which derives from a larger precursor protein (APP). 2 key findings →

Evidence: low

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

Brain t-complex polypeptide 1 (TCP- 1) related to its natural substrate beta1 tubulin is decreased in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Life sciences 2001-06-01

The t-complex polypeptide 1 is a selective molecular chaperone in tubulin biogenesis, by that nascent tubulin subunits are bound to t-complex polypeptide 1 and released in assembly competent forms. 2 key findings →

Evidence: low

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

Modulation of blood-brain barrier permeability

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of drug targeting 1996-01-01

Genetic and other defects leading to brain changes in Down syndrome, Alzheimer disease, amyotrophic lateral sclerosis, Huntington disease, Gaucher disease, hypertension and other disorders are rapidly being identified. 3 key findings →

Evidence: low

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

Genome-wide expression analysis of cultured trophoblast with trisomy 21 karyotype

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Human reproduction (Oxford, England) 2007-07-17

Our results demonstrate that gene expression in trisomy 21 affected placentas significantly differs from that of chromosomally normal placentas, and this difference is only partially explained by over-expression of genes from chromosome 21. 5 key findings →

Evidence: low

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

LIM homeobox 8 (Lhx8) is a key regulator of the cholinergic neuronal function via a tropomyosin receptor kinase A (TrkA)-mediated positive feedback loop

✓ Peer-reviewed alzhub usefulness score 37 out of 100. The Journal of biological chemistry 2013-11-21

Basal forebrain cholinergic neurons play an important role in cognitive functions such as learning and memory, and they are affected in several neurodegenerative diseases, including Alzheimer disease and Down syndrome. 1 key finding →

Evidence: low

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

Expression of human Cu-Zn superoxide dismutase gene in transgenic mice: model for gene dosage effect in Down syndrome

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Free radical research communications 1991-01-01

It was suggested that increased Cu-Zn superoxide dismutase (SOD-1) might be involved in the various biological abnormalities found in Down's syndrome (DS) such as premature aging and Alzheimer-type neurological lesions. 2 key findings →

Evidence: low

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

The 129 codon polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neurology 2003-06-01

Recently, a frequent prion protein gene (PRNP) polymorphism consisting of a methionine (M) for valine (V) substitution at codon 129 has been associated with cognitive impairment in elderly individuals. 4 key findings →

Evidence: low

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

Proteomic signatures and aberrations of mouse embryonic stem cells containing a single human chromosome 21 in neuronal differentiation: an in vitro model of Down syndrome

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Neuroscience 2004-01-01

Neurodegeneration in fetal development of Down syndrome (DS) patients is proposed to result in apparent neuropathological abnormalities and to contribute to the phenotypic characteristics of mental retardation and premature development of Alzheimer disease. 1 key finding →

Evidence: low

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

Age, adaptive behavior, and Alzheimer disease in Down syndrome: cross-sectional and longitudinal analyses

✓ Peer-reviewed alzhub usefulness score 37 out of 100. American journal of mental retardation : AJMR 1994-09-01

Cross-sectional and longitudinal analyses were used to compare age-related changes in adaptive functioning in institutionalized adults with and without Down syndrome. 2 key findings →

Design: cross-sectional Evidence: moderate

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

Transcriptome and metabolome analysis of crGART, a novel cell model of de novo purine synthesis deficiency: Alterations in CD36 expression and activity

✓ Peer-reviewed alzhub usefulness score 37 out of 100. PloS one 2021-07-20

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. 3 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. 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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