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Research

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

Find studies

Showing 326–350 of 544 studies (page 14 of 22) · 30,580 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)

Showing 544 studies tagged syndrome — clear

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.

Synaptic actin stabilization protein loss in Down syndrome and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Brain pathology (Zurich, Switzerland) 2019-09-08

Reduced spine densities and age-dependent accumulation of amyloid β and tau pathology are shared features of Down syndrome (DS) and Alzheimer's disease (AD). 3 key findings →

Evidence: low

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

Cerebral amyloidosis, amyloid angiopathy, and their relationship to stroke and dementia

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Alzheimer's disease : JAD 2001-02-01

Cerebral amyloid angiopathy (CAA) is the common term used to define the deposition of amyloid in the walls of medium- and small-size leptomeningeal and cortical arteries, arterioles and, less frequently, capillaries and veins. 1 key finding →

Evidence: low

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

Elevated expression of beta-site amyloid precursor protein cleaving enzyme 2 in brains of patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neuroscience letters 2002-06-01

The gene encoding the beta-site amyloid precursor protein cleaving enzyme 2 (BACE2) has been determined to be located on the long arm of chromosome 21 at 21q22.3. 5 key findings →

Evidence: low

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

Mouse model of neurodegeneration: atrophy of basal forebrain cholinergic neurons in trisomy 16 transplants

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1992-02-01

Vulnerability of specific brain regions and neuronal populations is a characteristic feature of Alzheimer disease and Down syndrome. 3 key findings →

Evidence: low

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

Signalling Pathways Implicated in Alzheimer's Disease Neurodegeneration in Individuals with and without Down Syndrome

✓ Peer-reviewed alzhub usefulness score 38 out of 100. International journal of molecular sciences 2020-09-20

Down syndrome (DS), the most common cause of intellectual disability of genetic origin, is characterized by alterations in central nervous system morphology and function that appear from early prenatal stages. 1 key finding →

Evidence: low

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

Serotonin (5-HT) in brains of adult patients with Down syndrome

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of neural transmission. Supplementum 1999-01-01

Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration. 5 key findings →

Evidence: low

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

GATA1-mediated transcriptional regulation of the γ-secretase activating protein increases Aβ formation in Down syndrome

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Annals of neurology 2015-10-29

Because of an extra copy of the Aβ precursor protein gene on chromosome 21, Down syndrome (DS) individuals develop high levels of Aβ peptides and Alzheimer disease-like brain amyloidosis early in life. 3 key findings →

Evidence: low

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

Cerebral cortical astroglia from the trisomy 16 mouse, a model for down syndrome, produce neuronal cholinergic deficits in cell culture

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-11-01

Trisomy 21 (Down syndrome) is associated with a high incidence of Alzheimer disease and with deficits in cholinergic function in humans. 3 key findings →

Evidence: low

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

Quantitative proteomics characterization of a mouse embryonic stem cell model of Down syndrome

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Molecular & cellular proteomics : MCP 2008-11-10

Down syndrome, caused by the trisomy of chromosome 21, is a complex condition characterized by a number of phenotypic features, including reduced neuron number and synaptic plasticity, early Alzheimer disease-like neurodegeneration, craniofacial dysmorphia, heart development defects, increased incidence of childhood leukemia, and powerful suppression of the incidence of most solid tumors. 3 key findings →

Participants: 1,661 Evidence: low

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

Senile myoclonic epilepsy of Genton: two cases in Down syndrome with dementia and late onset epilepsy

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Epilepsy research 2007-10-24

Senile myoclonic epilepsy of Genton is a newer epileptic syndrome of the older patients with Down syndrome associated with an Alzheimer-type dementia. 1 key finding →

Evidence: low

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

Down syndrome with partial duplication and del (21) syndrome: study protocol and call for collaboration. Study I: Clinical assessment

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Clinical genetics 1996-01-01

We report on the clinical and cytogenetic assessment of five cases of Down syndrome phenotype with either a partial duplication of chromosome 21 or a normal karyotype, and we quote a case of del (21q) syndrome. 5 key findings →

Evidence: moderate

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

A combination of long- and short-read genomics reveals frequent p-arm breakpoints within chromosome 21 complex genomic rearrangements

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Genetics in medicine open 2024-06-28

Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes. 3 key findings →

Evidence: low

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

Early Detection of White Matter Integrity Changes in Down Syndrome: The Promise of PSMD as a Sensitive Biomarker

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s & Dementia 2025-12-01

In DS, PSMD changed approximately 10‐15 years before the onset of AD symptoms and linearly increased with AD clinical stages, AD pathology, and SVD metrics. 4 key findings →

Participants: 70 Evidence: low

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

Neuronal and glial gene expression in neocortex of Down's syndrome and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Journal of neuropathology and experimental neurology 1993-05-01

The association cortex of Down's syndrome (DS) predictably and prematurely undergoes neurofibrillary degeneration of Alzheimer type. 3 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

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

From across this tag

10 of the 537 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ Change the filters

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 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