BackgroundLifetime incidence of Alzheimer's disease (AD) in Down syndrome (DS) exceeds 90%. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
BackgroundLifetime incidence of Alzheimer's disease (AD) in Down syndrome (DS) exceeds 90%. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with DS may have unique neuro- and cardio- protective factors that deserve future investigation. 4 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with DS are often supported by family caregiver(s), who face challenges including lack of awareness of the increased risk of developing AD, difficulty in obtaining a timely diagnosis, limited resources for psychosocial support, and lack of access to clinical trials. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To study the use of a dementia screening tool in our clinic cohort of adults with Down syndrome. 1 key finding →
Participants: 14 Evidence: moderate
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The objective of this study was to use high-resolution MRI techniques to determine whether children with Down syndrome exhibit decreases in hippocampal and amygdala volumes similar to those demonstrated in recent studies of adults with this condition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ts65Dn mouse displays a partial triplication of chromosome 16 and is adopted as a model for Down syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology. 3 key findings →
Evidence: low
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Down syndrome (DS) provides a model for studying important aspects of Alzheimer disease (AD). 2 key findings →
Evidence: low
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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
The presence of abundant intraneuronal amyloid in the form of neurofibrillary tangles (NFT) in the brains of Guamanian parkinsonism-dementia patients and the absence of extraneuronal amyloid in the form of vascular amyloid deposits or senile plaques permit the purification of NFT without contamination with extraneuronal amyloid. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is the most common chromosomal abnormality associated with early mental retardation and neurological abnormalities followed by precocious age dependent Alzheimer-type neurode generation later in life. 1 key finding →
Evidence: low
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The Alzheimer amyloid protein precursor (APP) has previously been localized to human chromosome 21q11.2-q21. 1 key finding →
Evidence: low
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Clinical trials with drugs aimed at treatment of Alzheimer disease to decelerate cognitive decline and translated mimetically to demented and young nondemented Down syndrome patients have been unable to demonstrate improvements in cognitive performance and functioning. 1 key finding →
Evidence: low
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In Alzheimer's disease, in Down syndrome and in normal aging, scattered deposits of amyloid fibril precursors occur in both cerebral cortex and subcortical grey structures. 1 key finding →
Evidence: low
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Intersectins (ITSNs) represent a family of multi-domain adaptor proteins that regulate endocytosis and cell signaling. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frameshift (+1) proteins such as APP(+1) and UBB(+1) accumulate in sporadic cases of Alzheimer disease (AD) and in older subjects with Down syndrome (DS). 3 key findings →
Evidence: low
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In general, there was only a moderate alteration of gene expression in ADAM10 overexpressing mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Oxidative stress is known to play a relevant role in Down syndrome (DS) and its effects are documented from embryonic life. 3 key findings →
Evidence: low
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The amyloid precursor protein (APP) is thought to be processed aberrantly to yield the major constituent of the amyloid plaques observed in the brains of patients with Alzheimer disease and Down syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
During a study of the familial aggregation of Down syndrome (DS) and Alzheimer disease (AD), we observed an increase in mosaicism for disomy 21 in older individuals with DS. 3 key findings →
Participants: 15 Evidence: low
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A 53-year-old Japanese woman with a point mutation in mitochondrial DNA (tRNALeu(UUR), nt3243) consistent with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and Alzheimer-type brain pathology is reported. 1 key finding →
Evidence: low
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Down syndrome (DS) is one of the most common causes of intellectual disability, owing to trisomy of all or part of chromosome 21. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study examines cortical organoids generated from a panel of isogenic trisomic and disomic iPSC lines (subclones) as a model of early fetal brain development in Down syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Collagenous Alzheimer amyloid plaque component (CLAC) is a unique non-Abeta amyloid component of senile plaques (SP) derived from a transmembrane collagen termed CLAC-precursor. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These data point to significant reductions in KLC1 in AD and AD-DS. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 527 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.
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 →