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534 studies tagged down, dated 1975-09-01 to 2026-10-30. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Differential endothelial cell remodeling in Down syndrome and APP duplication drives distinct blood brain barrier dysfunction 2026-10-30
- Memory and Plasma pTau217 Refine Prognosis in Down Syndrome 2026-10-02
- Tau extent is associated with lower cognition in Down syndrome-related Alzheimer's disease 2026-10-01
Studies
534 studies carry this tag.
Date range
1975 to 2026
Top journals
- Proceedings of the National Academy of Sciences of the United States of America 21
- Alzheimer s & Dementia 20
- Alzheimer's & dementia : the journal of the Alzheimer's Association 15
- Neurology 14
- Neuroscience letters 14
239 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Senile myoclonic epilepsy of Genton is a newer epileptic syndrome of the older patients with Down syndrome associated with an Alzheimer-type dementia.
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The mechanisms by which trisomy 21 leads to the characteristic Down syndrome (DS) phenotype are unclear.
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Most individuals with Down syndrome show early onset of Alzheimer disease (AD), resulting from the extra copy of chromosome 21.
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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.
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This study highlights the similarities in the clinical presentation of dementia among the general population and people with DS with a particular emphasis on the earlier appearance of symptoms associated with the frontal lobe dysfunction among adults with DS.
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The number of people over the age of 60 years with lifelong developmental delays is predicted to double by 2030.
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Our results demonstrate that gene expression in trisomy 21 affected placentas significantly differs from that of chromosomally normal placentas, and this difference is only partially explained by over-expression of genes from chromosome 21.
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Elevations in plasma Abeta(42) peptide levels are associated with earlier onset of AD and increased risk of death.
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Down syndrome (DS), or trisomy 21, is the most common identifiable genetic cause of mental retardation.
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Down syndrome, or trisomy 21, is the most common chromosomal abnormality associated with intellectual impairment.
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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.
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The over expression of APP gene in DS leads to increases in plasma Abeta40 and Abeta42 levels before plaque formation in DS brain.
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This review discusses the laboratory and clinical research supporting the rationale for the efficacy of donepezil (Aricept USA) in enhancing cognition in autism, Alzheimer disease, Down syndrome, traumatic brain injury, Attention Deficit Hyperactivity Disorder (ADHD), and schizophrenia.
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Down syndrome (DS) provides a model for studying important aspects of Alzheimer disease (AD).
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We scanned throughout chromosome 21 to assess genetic associations with late-onset Alzheimer disease (AD) using 374 Japanese patients and 375 population-based controls, because trisomy 21 is known to be associated with early deposition of beta-amyloid (Abeta) in the brain.
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Myoclonic epilepsy is being increasingly recognized as a late-onset complication in middle-aged or elderly patients with Down syndrome, in association with cognitive decline.
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36/100
Our findings suggest that, with respect to this putative marker of central cholinergic activity, dementia in aging DS shares pathophysiological similarities to AD in the general population.
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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.
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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.
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Since previous investigations reported improvements in cognition of patients with dementia after acetyl-L-carnitine therapy and since there is an increased risk for persons with Down syndrome to develop Alzheimer disease, this study was designed to investigate the effect of acetyl-L-carnitine administration on neurological, intellectual, and social functions in adults with Down syndrome.
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Neuronal oxidative stress occurs early in the progression of Alzheimer disease (AD), significantly before the development of the pathologic hallmarks, neurofibrillary tangles, and senile plaques.
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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).
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Researchers since the 1990s have predominantly focused on the amyloid hypothesis and the formation of amyloid fibrils as the culprit behind AD when we began working on soluble Abeta (sAbeta).
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Adults with DS have a significantly increased brain concentration of myo-inositol, and this is associated with reduced cognitive ability.
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DYRK1A, dual-specificity tyrosine-regulated kinase 1A, maps to human chromosome 21 within the Down syndrome (DS) critical region.
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Down syndrome (DS) patients suffer from mental retardation, but also display enhanced beta-APP production and develop cortical amyloid plaques at an early age.
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Familial Danish dementia is an early onset autosomal dominant neurodegenerative disorder linked to a genetic defect in the BRI2 gene and clinically characterized by dementia and ataxia.
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Beta-secretase (BACE1) is the rate-limiting protease for the generation of the amyloid beta-peptide (Abeta) in Alzheimer disease.
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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).
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There is evidence to suggest that certain shared features exist in the pathogenesis of vascular disease and Alzheimer disease (AD) in the general population.
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Individuals with Down syndrome (DS) are at a high risk for developing Alzheimer disease (AD) after the age 40; however, low levels of intellectual functioning, coupled with impaired language ability, confound the detection of AD.
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Alzheimer disease (AD) and Down syndrome (DS) brains contain deposits of amyloid-beta peptide that are located extracellularly in the neuropil and in blood vessels walls.
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The present findings demonstrate several fundamental parallels between lens and neuron vesicle trafficking cell biology and development, and suggest that more extensive AbetaPP related vesicle trafficking disease mechanisms may be shared by lens and brain.
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An important aspect of brain cholinesterase function is related to enzymatic differences.
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31/100
Mutations in the human prion protein gene (PRNP) are responsible for hereditary diseases called transmissible spongiform encephalopathies (TSE) and a polymorphic site at codon 129 determines sensitivity to infectious forms of these maladies.
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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.
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40/100
In fetuses with Down syndrome, neurons fail to show normal dendritic development, yielding a "tree in winter" appearance.
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More than 20 syndromes among the significant and increasing number of degenerative diseases of neuronal tissues are known to be associated with diabetes mellitus, increased insulin resistance and obesity, disturbed insulin sensitivity, and excessive or impaired insulin secretion.
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An important lesion in Alzheimer's disease (AD) patient brains is the neurofibrillary tangle (NFT).
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APP is an important locus predicting the age at onset of dementia in people with Down syndrome.
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It has been clearly established that there is an increased incidence of early onset dementia of the Alzheimer type (DAT) in people who have Down syndrome.
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41/100
Our data supported the presumption of increased oxidative stress in DS.
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Neurodegeneration in fetal development of Down syndrome (DS) patients is proposed to result in apparent neuropathological abnormalities and to contribute to the phenotypic characteristics of mental retardation and premature development of Alzheimer disease.
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Aged individuals with Down syndrome (DS) develop senile plaques and neurofibrillary tangles consistent with Alzheimer disease (AD).
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In persons with Down syndrome, soluble Abeta peptides, which result from the processing of the amyloid precursor protein, appear in the brain decades before the extracellular deposition of neuritic plaques.
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Dementia of the Alzheimer type (DAT) is common in older persons with Down syndrome (DS).
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Recently, a frequent prion protein gene (PRNP) polymorphism consisting of a methionine (M) for valine (V) substitution at codon 129 has been associated with cognitive impairment in elderly individuals.
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Plasma amyloid beta protein 1-40 (Abeta40) and Abeta42 levels were quantitated from 28 young Down syndrome (DS) (20-40 years old), 28 age-matched controls, 32 old DS (41-65 years old) and 32 age-matched controls in a sandwich enzyme-linked immunosorbent assay.
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36/100
We immunohistochemically studied the expression of beta-amyloid precursor protein (APP), Abeta40, Abeta42, and Abeta43 in the frontal lobes of 20 Down syndrome (DS) patients and 13 controls.
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Individuals with DS have a substantially increased risk of mortality due to specific causes and may have an elevated risk of other incident cancers in addition to leukemia.
From across this tag
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.
- Motion perception deficit in Down Syndrome
- The joint association of obesity and physical activity on cognitive function in Down syndrome
- Life-long overexpression of S100beta in Down's syndrome: implications for Alzheimer pathogenesis
- Poor Sleep as a Precursor to Cognitive Decline in Down Syndrome : A Hypothesis
- Alzheimer Abeta peptide induces chromosome mis-segregation and aneuploidy, including trisomy 21: requirement for tau and APP
- A pilot study of the reliability and validity of the Caregiver Activity Survey - Intellectual Disability (CAS-ID)
- Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons: Converging Insights From Alternative Hypotheses
- The evolution of ovarian oocyte decline with aging and possible relationships to Down syndrome and Alzheimer disease
- Change in plasma Aß peptides and onset of dementia in adults with Down syndrome
- Presenilin 1 and alpha-1-antichymotrypsin polymorphisms in Down syndrome: no effect on the presence of dementia