alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

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

Find studies

Showing 1–25 of 25 studies in Down syndrome and Alzheimer's · tagged Digital Tools · 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.

Allelic variability in D21S11, but not in APP or APOE, is associated with cognitive decline in Down syndrome

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neuroreport 1997-05-01

Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome. 3 key findings →

Design: longitudinal study Evidence: moderate

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

Novel predictors of Alzheimer's disease in Down syndrome identified using machine learning

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of Alzheimer's disease : JAD 2025-10-17

BackgroundMost adults with Down syndrome will develop Alzheimer's disease (AD) due to the triplication of the amyloid precursor protein in the 21 st chromosome. 1 key finding →

Design: case-control study Evidence: moderate

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

The Impact of APP on Alzheimer-like Pathogenesis and Gene Expression in Down Syndrome iPSC-Derived Neurons

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Stem cell reports 2018-05-31

Early-onset Alzheimer disease (AD)-like pathology in Down syndrome is commonly attributed to an increased dosage of the amyloid precursor protein (APP) gene. 5 key findings →

Evidence: low

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

Partial BACE1 reduction in a Down syndrome mouse model blocks Alzheimer-related endosomal anomalies and cholinergic neurodegeneration: role of APP-CTF

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of aging 2015-12-02

β-amyloid precursor protein (APP) and amyloid beta peptide (Aβ) are strongly implicated in Alzheimer's disease (AD) pathogenesis, although recent evidence has linked APP-βCTF generated by BACE1 (β-APP cleaving enzyme 1) to the development of endocytic abnormalities and cholinergic neurodegeneration in early AD. 1 key finding →

Evidence: low

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

APP mutations in the Aβ coding region are associated with abundant cerebral deposition of Aβ38

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica 2012-11-13

Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →

Evidence: low

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

Down Syndrome, Partial Trisomy 21, and Absence of Alzheimer's Disease: The Role of APP

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of Alzheimer's disease : JAD 2017-01-01

Overexpression of the amyloid precursor protein (APP) gene on chromosome 21 in Down syndrome (DS) has been linked to increased brain amyloid levels and early-onset Alzheimer's disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Sleep Health in Adults with Intellectual Disability: Recent Advances and Persistent Evidence Gaps

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Current Treatment Options in Neurology 2026-09-25

Recent Findings Recent observational data in adults with Down syndrome indicate that obstructive sleep apnoea is associated with adverse cardiometabolic, mortality and Alzheimer disease outcomes. 2 key findings →

Design: cohort study Evidence: moderate

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

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

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

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

Telemedicine, dementia and Down syndrome: implications for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2006-07-01

This study supports the need for formal reliability and validity studies of TM preparatory to the consideration of this modality for use in clinical trials for AD. 1 key finding →

Participants: 90 Evidence: low

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

Alzheimer's-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-12-28

An additional copy of the beta-amyloid precursor protein (APP) gene causes early-onset Alzheimer's disease (AD) in trisomy 21 (DS). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

BACE2, as a novel APP theta-secretase, is not responsible for the pathogenesis of Alzheimer's disease in Down syndrome

✓ Peer-reviewed alzhub usefulness score 36 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2006-07-01

Amyloid beta protein (Abeta), the major component of neuritic plaques in Alzheimer's disease (AD), is derived from APP by sequential cleavages of beta- and gamma-secretases. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Activation of the Notch pathway in Down syndrome: cross-talk of Notch and APP

✓ Peer-reviewed alzhub usefulness score 34 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2005-09-01

Down syndrome (DS) patients suffer from mental retardation, but also display enhanced beta-APP production and develop cortical amyloid plaques at an early age. 3 key findings →

Evidence: low

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

Characterization of a mouse model overexpressing beta-site APP-cleaving enzyme 2 reveals a new role for BACE2

✓ Peer-reviewed alzhub usefulness score 34 out of 100. Genes, brain, and behavior 2009-09-22

BACE2 is homologous to BACE1, a beta-secretase that is involved in the amyloidogenic pathway of amyloid precursor protein (APP), and maps to the Down syndrome critical region of chromosome 21. 1 key finding →

Evidence: low

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

Chronic elevation of S100 beta protein does not alter APP mRNA expression or promote beta-amyloid deposition in the brains of aging transgenic mice

✓ Peer-reviewed alzhub usefulness score 33 out of 100. Brain research 1995-12-01

S100 beta protein, a member of a Ca(2+)-binding protein family present primarily in the nervous system, affects the survival and differentiation of both neurons and glia cells. 2 key findings →

Evidence: low

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

Digital and palmar dermatoglyphics in dementia of the Alzheimer type

✓ Peer-reviewed alzhub usefulness score 32 out of 100. American journal of medical genetics 1988-07-01

Digital and palmar dermatoglyphics were examined in 29 men and 27 women with dementia of the Alzheimer type (DAT) and 112 age-, sex-, and racial group-matched controls. 1 key finding →

Evidence: low

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

Differential endothelial cell remodeling in Down syndrome and APP duplication drives distinct blood brain barrier dysfunction

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30

An extra copy of the amyloid precursor protein gene (APP) is present in Down syndrome (DS) and APP duplication (APPdup), increasing the risk of Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

APP Dosage and Extracellular Domain Variants Drive Distinct Defects in Neurogenesis modeled in Down Syndrome iPS cells

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-06

The amyloid precursor protein (APP) is heavily studied as the source of amyloid beta in Alzheimer’s disease (AD), however, the complex functions of APP remain poorly understood, as does the impact of APP dosage on neurodevelopment. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

↑ 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 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