Down syndrome (DS) subjects develop Alzheimer disease (AD) histopathology before they develop dementia. 2 key findings →
Evidence: low
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Down syndrome (DS) subjects develop Alzheimer disease (AD) histopathology before they develop dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Thirty-four unique-sequence microclones were isolated from a previously described microdissection library of human chromosome 21 and were regionally mapped using a cell hybrid mapping panel which consists of six cell hybrids and divides chromosome 21 into eight regions. 3 key findings →
Evidence: low
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However, bed rest results in many alterations which are disadavantageous. 2 key findings →
Evidence: low
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Recent data have allowed speculating that amyloid Aβ induces apoptosis via opening type-1 VDAC in cell membranes of hypo-metabolic neurons, a process most likely running over life time--as leaves fall from trees in the tropics--and ending in Alzheimer's disease whenever critical brain regions are affected. 5 key findings →
Evidence: low
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Tau-like protein levels from 40 Down syndrome (DS) persons (31-70 years old), 40 non-DS age-matched normal controls, 18 non-DS mentally retarded (MR) persons (26-91 years old), 25 probable Alzheimer disease (AD) patients (55-99 years old) and 24 non-demented elderly controls (54-79 years old) were measured using a sandwich enzyme linked immunosorbent assay. 1 key finding →
Evidence: low
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Despite frequent neuropathological findings, the prevalence of dementia in people with Down syndrome is thought to be no higher than in the general population. 5 key findings →
Evidence: low
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Patients with Down syndrome (human trisomy 21) develop neuropathological and cholinergic functional defects characteristic of Alzheimer's disease, which has been attributed to the location of the Alzheimer beta-amyloid precursor protein on chromosome 21. 4 key findings →
Evidence: low
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Through deinstitutionalization, more adults with mental retardation are living in the community under the care of family physicians. 3 key findings →
Design: case report Evidence: low
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In humans, GART [phosphoribosylglycinamide formyltransferase (EC 2.1.2.2) / phosphoribosylglycinamide synthetase (EC 6.3.4.13) / phosphoribosylaminoimidazole synthetase (EC 6.3.3.1)] is a trifunctional protein which catalyzes the second, third, and fifth reactions of the ten step de novo purine synthesis (DNPS) pathway. 4 key findings →
Evidence: low
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Down syndrome, as a phenotypic result of trisomy 21, is a complex condition with a set of over 30 phenotypic features, which manifest themselves with varying frequencies among affected individuals. 3 key findings →
Evidence: low
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Down syndrome (DS) brains, from 19 gestational weeks to 50 years of age were studied by immunohistochemical methods with a polyclonal antibody against synthetic peptide comprising part of the Kunitz-type protease inhibitor (KPI) domain of Alzheimer disease amyloid precursor protein (APP), residues 301 to 323 of APP 770. 1 key finding →
Evidence: low
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A fifteen-year follow up of the linguistic and cognitive profile of a woman, named Françoise, with standard trisomy 21. 1 key finding →
Evidence: low
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Impaired glucose metabolism in adult Down Syndrome (DS) has been well-documented in vivo and information on the underlying biochemical defect i.e. aberrant glucose handling enzymes is already available. 2 key findings →
Evidence: low
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There are few published data available about simultaneous bilateral hip fractures. 1 key finding →
Evidence: low
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Alzheimer’s disease is the most common type of dementia, characterized by a progressive decline in cognitive function, particularly memory and impacting daily life. 5 key findings →
Evidence: low
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No entanto, os resultados dos estudos clínicos apresentam divergências entre si, além de limitações metodológicas, pequeno tamanho amostral e variabilidade na definição dos desfechos. 5 key findings →
Evidence: low
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Using anti-SP28 (a polyclonal antibody to a 28 residue synthetic peptide homologous to the NH2-terminal region of Alzheimer amyloid beta-protein) to investigate the cerebral cortex of 8 Alzheimer and 6 Down patients and 13 nondemented individuals, we found that, besides senile plaques and congophilic vessels, extracellular deposits unrelated to degenerating neurites, tangle-bearing neurons or congophilic vessels were labelled. 1 key finding →
Evidence: low
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The present study investigated the frequency and distribution of TUNEL-positive neurons in brains of dementia with Lewy bodies (DLB) in comparison with those in brains of Alzheimer's disease (AD), Down syndrome (DS) and non-demented elderly persons. 2 key findings →
Evidence: low
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This study sought to test the hypothesis that adults with Down Syndrome may age faster than the general population by comparing the rate of increase in their mortality with age with that of the general population by the method originally described by Gompertz. 1 key finding →
Evidence: low
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Some individuals with Down syndrome develop an Alzheimer-type dementia in the third and fourth decades of life. 2 key findings →
Participants: 21 Evidence: low
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Cytonectin is a novel 35,000 molecular weight protein that displays remarkable ion-independent adherence properties. 1 key finding →
Evidence: low
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Para psychotic troubles in Mentally Handicapped Persons (particularly in Down syndrome)-Clinical examples of M.H.P. which had no trouble until their 25-40 (years) except their intellectual defect and then, slide in psychiatric or para psychiatric behaviour. 5 key findings →
Evidence: low
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(1) GARS-AIRS-GART is an important candidate gene in studies of Down syndrome (DS)-related Alzheimer's disease (AD), due to its chromosomal localization (21q22.1) in the Down syndrome critical region, involvement in de novo purine biosynthesis, and over-expression in DS brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It has been reported that the Down syndrome occurs more often than expected among relatives of individuals with Alzheimer disease. 3 key findings →
Evidence: low
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In recent years, it has been possible for patients with Down syndrome to live longer with advanced medical treatment and social support. 5 key findings →
Evidence: low
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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 →