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
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
The amyloid beta protein and the amyloid beta-protein precursor (APP) are major constituents of senile plaques and cerebrovascular deposits in 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
The modified questionnaire and interview instruments capture a range of impairment in DS adults, including subthreshold symptomatology, and the instruments provide complementary information relevant to the ascertainment of dementia in DS. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Caspase cleaved amyloid precursor protein (APPcc) and SET are increased and mislocalized in the neuronal cytoplasm in Alzheimer Disease (AD) brains. 1 key finding →
Evidence: low
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Unlike other research, in this study higher body mass index was also found to increase the chance of prodromal dementia and dementia. 4 key findings →
Participants: 66 Evidence: low
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As people with Down syndrome (DS) age, they are at greater risk for Alzheimer disease (AD) than the general population. 3 key findings →
Participants: 231 Evidence: low
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Down syndrome (DS), caused by trisomy 21, is the most prevalent genetic condition associated with accelerated aging and near-universal development of early-onset Alzheimer's disease (AD). 1 key finding →
Evidence: low
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BackgroundIndividuals with Down syndrome (DS) generally show neuropathological features of Alzheimer disease (AD). 1 key finding →
Participants: 120 Evidence: low
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Specific health plans for DS and conducting clinical and translational research on the challenges of aging, including AD, are necessary and feasible. 1 key finding →
Participants: 114 Evidence: moderate
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Down syndrome (DS), caused by trisomy 21, is the most prevalent genetic condition associated with accelerated aging and near-universal development of early-onset Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an urgent need for objective markers of Alzheimer’s disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression and assess response to disease-modifying therapies. 4 key findings →
Participants: 80 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A variety of clinically-defined predementia syndromes, with differing diagnostic criteria and nomenclature, have been proposed to describe nondisabling symptomatic cognitive deficits arising in elderly persons. 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is a clinical condition with a high risk of progression to dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To assess the contribution of hyperammonemia and inflammation to induction of mild cognitive impairment (or MHE). 2 key findings →
Evidence: low
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Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls. 4 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →