30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Several lines of evidence suggest a shared genetic susceptibility to Down syndrome (DS) and Alzheimer disease (AD). 2 key findings →
Participants: 168 Evidence: low
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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 aim of this study was to test whether there is an excess of dementia of Alzheimer type (DAT) cases in Down syndrome (DS) relatives. 1 key finding →
Design: case-control study Evidence: moderate
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For these neurodegenerative dementias, we observed that the chronological age did not align with their biological age, which was determined based on hippocampal transcript levels (i.e., transcriptional age). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) has been proposed by George Martin as a segmental progeroid syndrome since 1978. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Circulating glucose concentrations regulate many brain functions, including learning and memory. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuropathologically, Alzheimer-type abnormalities are demonstrated in patients with Down syndrome (DS), both demented and nondemented and more than a half of patients with DS above 50 years develop Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Down syndrome (DS) is a major cause of congenital heart and gut disease and mental retardation. 2 key findings →
Evidence: low
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The dendritic atrophy seen in childhood continued into adulthood, with a marked decrease in dendritic branching, dendritic length, and spine frequency in elderly adults with the Down syndrome. 1 key finding →
Evidence: low
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Down syndrome (DS) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age-dependent Alzheimer-type neurodegeneration. 4 key findings →
Evidence: low
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In fetuses with Down syndrome, neurons fail to show normal dendritic development, yielding a "tree in winter" appearance. 1 key finding →
Evidence: low
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Down syndrome (DS) is the leading cause of genetically-defined intellectual disability and congenital birth defects. 1 key finding →
Evidence: low
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Institutionalized patients with Down syndrome (n = 307) were monitored for 5 to 10 years prospectively to determine prevalence of Alzheimer-type dementia. 5 key findings →
Participants: 307 Evidence: low
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Increased SOD-1 levels in patients with DS may reflect the overexpression by the trisomic state, as a response to the oxidative stress, as has been proposed in DS by several authors. 1 key finding →
Evidence: low
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To gain insights into the different forms of modified amyloid beta peptides (A beta) in the Alzheimer disease (AD) and Down syndrome (DS) brain, we used two-site ELISAs with antibodies specific for isomerized (i.e. A beta with L-isoaspartate at positions 1 and 7) and pyroglutamate-modified (i.e. A beta beginning with pyroglutamate at position 3) forms of A beta to quantitate the levels of these different A beta peptides in formic acid extracts of AD and DS frontal cortex. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The purpose of this study was to determine cerebral myo-inositol (mI) in adults with Down syndrome (DS), and to trace the chronobiology of DS to Alzheimer disease (AD). 5 key findings →
Evidence: low
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Chromosome 21-specific yeast artificial chromosomes (YACs) have been constructed by a method that performs all steps in agarose, allowing size selection by pulsed-field gel electrophoresis and the use of nanogram to microgram quantities of DNA. 1 key finding →
Evidence: low
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In Down syndrome (DS), enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic mental retardation and precocious dementia of Alzheimer-type. 4 key findings →
Evidence: low
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Florbetapir PET can be used to detect increased cerebral-to-cerebellar fibrillar Aβ burden in a Down syndrome patient with Alzheimer disease, even in the presence of frequent amyloid angiopathy and diffuse plaques in the cerebellum. 3 key findings →
Evidence: low
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Down syndrome (DS) is a common genetic condition caused by the presence of three copies of chromosome 21 (trisomy 21). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Down syndrome (DS), oxidative DNA-damage may play a role in the pathogenesis of characteristic mental retardation and precocious dementia of Alzheimer type. 3 key findings →
Evidence: low
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The human amyloid beta protein is the major constituent of the brain amyloid plaques found in Alzheimer disease. 4 key findings →
Evidence: low
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In adults with DS, early amyloid-β accumulation in the striatum is divergent from sporadic AD; however, despite the early striatal amyloid-β, glucose hypometabolism was confined to the typical AD-associated regions, which occurs similarly in autosomal dominant AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
People with Down syndrome (DS) have increased risk of Alzheimer disease (AD), presumably conferred through genetic predispositions arising from trisomy 21. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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