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
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Presence of CHD may influence AD progression in DS. 1 key finding →
Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
48/100
Individuals with Down syndrome (DS) have an increased risk of developing Alzheimer disease (AD), with nearly all individuals exhibiting AD neuropathology, including amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT), by age 40 years. 5 key findings →
Design: cross-sectional Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
48/100
This study provided a preliminary examination of indices of obstructive sleep apnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology. 3 key findings →
Design: longitudinal study Participants: 22 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Prior authorization criteria for Federal Drug Administration (FDA) approved immunotherapeutics, among the class of anti-amyloid monoclonal antibodies (mAbs), established by state drug formulary committees, are tailored for adults with late-onset Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down syndrome (DS) are more likely to experience earlier onset of multiple facets of physiological aging. 3 key findings →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
While post mortem studies have identified the major cell types and functional systems affected in Alzheimer's disease (AD) the initial sites and molecular characteristics of pathology are still unclear. 1 key finding →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Epidemiological and experimental studies suggest that a disease-aggravating neuroinflammatory process is present at preclinical stages of Alzheimer's disease. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
This study was designed to provide information on the prevalence and nature of psychiatric disorders in 497 individuals with Down syndrome. 1 key finding →
Participants: 497 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), trisomy of human chromosome 21 (HSA21), is characterized by lifelong cognitive impairments and the development of the neuropathological hallmarks of Alzheimer's disease (AD). 4 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Trisomy 21 (T21) gives rise to Down syndrome (DS), the most commonly occurring chromosomal abnormality in humans. 2 key findings →
Participants: 400 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is the result of triplication of chromosome 21 (trisomy 21) and is the prevailing cause of mental retardation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is convincing epidemiological and in vitro evidence of chronic oxidative stress in individuals with Down syndrome (DS). 5 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Down syndrome (DS) is the most common genetic cause of intellectual disability in children, and the number of adults with DS reaching old age is increasing. 4 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
These findings demonstrate that chronic InRapa administration is able to exert a neuroprotective effect on Ts65Dn hippocampus by reducing AD pathological hallmarks and by restoring protein homeostasis, thus ultimately resulting in improved cognition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
Transactive response DNA-binding protein 43 pathology occurs in FAD and DS, similar to that observed in sporadic Alzheimer disease. 2 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
On November 8-9, 2007, a meeting entitled "Setting a Public Health Research Agenda for Down Syndrome" was held to review current knowledge, identify gaps, and develop priorities for future public health research related to Down syndrome. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
People with Down syndrome (DS) are at high risk for developing Alzheimer disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
47/100
Adults with Down syndrome (DS) have an exceptionally high prevalence of Alzheimer disease (AD), with an earlier age of onset compared with the neurotypical population. 4 key findings →
Participants: 339 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The prevalence of MetS was low in adults with DS. 5 key findings →
Participants: 389 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
47/100
This study provided a preliminary examination of indices of obstructive sleep apsnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology. 3 key findings →
Design: longitudinal study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
47/100
There is a need for early, objective markers of Alzheimer's disease (AD)-related synapse dysfunction in adults with Down syndrome (DS). 1 key finding →
Design: cross-sectional Participants: 131 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Demonstrated utility of the mCRT warrants further investigation into comparisons between the A and B versions, free versus cued recall and changes in performance over time to better understand sensitivity for tracking memory decline over time based on age and AD clinical status. 5 key findings →
Design: longitudinal study Participants: 272 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Chromosome 21, triplicated in Down Syndrome, contains several genes that are thought to play a critical role in the development of AD neuropathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 534 studies in this tag, 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.
- Gene expression profiling in the adult Down syndrome brain
- Cognitive deficits and associated neurological complications in individuals with Down's syndrome
- Alzheimer dementia in Down's syndrome: the relevance of cognitive ability
- Cardiovascular Risk Composite and Time of Amyloid Accumulation and Cognitive Decline in Down Syndrome Alzheimer's Disease
- Down syndrome: age-dependence of PiB binding in postmortem frontal cortex across the lifespan
- Telemedicine, dementia and Down syndrome: implications for Alzheimer disease
- Constitutive Dyrk1A is abnormally expressed in Alzheimer disease, Down syndrome, Pick disease, and related transgenic models
- Down syndrome
- Absence of familial association between dementia of Alzheimer type and Down syndrome
- Lysosomal Dysfunction in Down Syndrome Is APP-Dependent and Mediated by APP-βCTF (C99)
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 →