This represents the largest U.S.-based, multi-site, biomarker initiative of AD in DS. 1 key finding →
Design: longitudinal study Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This represents the largest U.S.-based, multi-site, biomarker initiative of AD in DS. 1 key finding →
Design: longitudinal study Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome over age 40 years are at risk for developing dementia of the Alzheimer type and have evidence for chronic oxidative stress. 4 key findings →
Participants: 53 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Virtually all adults with Down syndrome (DS) show the neuropathological changes of Alzheimer disease (AD) by the age of 40 years. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Improvements in medical interventions for people with Down's syndrome have led to a substantial increase in their longevity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These findings suggest significant binding of lecanemab to cerebral amyloid angiopathy in DS. 5 key findings →
Participants: 15 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) with age. 2 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
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
There is evidence to suggest that certain shared features exist in the pathogenesis of vascular disease and Alzheimer disease (AD) in the general population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Aged individuals with Down syndrome (DS) develop senile plaques and neurofibrillary tangles consistent with Alzheimer disease (AD). 1 key finding →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Beta-amyloid (Aβ) deposition in brain accumulates as a function of age in people with Down syndrome (DS) with subsequent development into Alzheimer disease neuropathology, typically by 40 years of age. 3 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Acetylcholinesterase inhibitors may be helpful in reversing the symptoms of dementia during early and middle stages of cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Adults with Down syndrome (DS) develop Alzheimer disease (AD) pathology progressively with age but clinical signs of dementia are delayed by at least 10 years after the first signs of disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Adults with Down syndrome (DS) develop Alzheimer's disease (AD) neuropathology by 40 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrovascular pathology is a significant mediator in Alzheimer's disease (AD) in the general population. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This is one of the first formal studies to evaluate research attitudes among relatives of individuals with DS and shows the feasibility of using this approach to answer important questions that will guide trialists developing treatments for AD in DS. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A subset of aged individuals with Down syndrome (DS) exhibits the clinical features of Alzheimer's disease (AD) but our ability to detect dementia in this population is hampered by developmental differences as well as the sensitivity of existing test tools. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) provides a model for studying important aspects of Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Individuals with Down syndrome (DS) have high levels of oxidative stress throughout the lifespan. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
This chapter reviews the neurological phenotype of Down syndrome (DS) in early development, childhood, and aging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is characterized by increased mortality rates, both during early and later stages of life, and age-specific mortality risk remains higher in adults with DS compared with the overall population of people with mental retardation and with typically developing populations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence is implicating mitochondrial dysfunction as a central factor in the etiology of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous research has revealed similarities in the neuropathology, clinical presentation, and risk factors between persons with Alzheimer disease from the general population (GP-AD) and those with Down syndrome (DS-AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
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.
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.
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 →