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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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An extra copy of the amyloid precursor protein gene (APP) is present in Down syndrome (DS) and APP duplication (APPdup), increasing the risk of Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA).
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Individuals with Down syndrome (DS) are at high risk for Alzheimer's disease (AD), yet accessible tools for routine clinical screening of AD in individuals with DS remain limited.
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This first evaluation of 18 F-MK6240 in DS demonstrates its suitability as a sensitive biomarker for Alzheimer's disease tau pathology.
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Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability.
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Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability.
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42/100
Recent Findings Recent observational data in adults with Down syndrome indicate that obstructive sleep apnoea is associated with adverse cardiometabolic, mortality and Alzheimer disease outcomes.
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47/100
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer’s disease.
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67/100
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer's disease.
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Alzheimer’s disease (AD) pathology including amyloid beta (Aβ) plaques and tau tangles accumulate with age in Down Syndrome (DS).
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47/100
There is a need for early, objective markers of Alzheimer's disease (AD)-related synapse dysfunction in adults with Down syndrome (DS).
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In DS, longitudinal characterization of all previously identified proteins revealed distinct trajectories over time and an association of baseline levels with future cognitive decline.
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Epilepsy was associated with higher subsequent recording of dementia and mortality over 2 years.
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Individuals with Down syndrome (DS) display developmental delay, intellectual disability, premature brain ageing, and an increased risk of Alzheimer-like neurodegeneration.
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Frailty in DS is associated with both ID severity and acquired cognitive decline.
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Down syndrome (DS), caused by trisomy of chromosome 21, is characterized by early-onset oxidative stress, impaired neuronal development, and an increased risk of Alzheimer's disease (AD)-like neuropathology.
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How do clinicians distinguish early-stage dementia from the expected cognitive variability seen in ageing adults with Down syndrome?
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Dementia in individuals with Down syndrome (DS) is the leading cause of early-onset cognitive decline occurring before the age of 50.
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The majority of the participants met criteria for obesity.
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials.
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Of 115 participants (mean age 40.0 ± 9.2 years; 43.5% female), higher interdaily stability was associated with higher DSMSE scores B = 20.6 (95% CI 5.0-36.2).
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Our study is the first one showing that dietary supplements improve cognition and sleep in a mouse model of DS.
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These findings suggest that circadian rhythm disruption as measured via 24-hour RAR is associated with plasma and imaging biomarkers of AD in DS.
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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).
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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).
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Down syndrome (DS), caused by trisomy 21, is the most frequent genetic cause of intellectual disability worldwide.
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48/100
Individuals with Down syndrome (DS) have an increased risk of developing Alzheimer disease (AD), with nearly all individuals exhibiting AD neuropathology, including amyloid beta (Aβ) plaques and neurofibrillary tangles (NFT), by age 40 years.
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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).
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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.
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Down syndrome is one of the most common chromosomal abnormalities in humans in which an extra copy of chromosome 21 is present.
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42/100
Down syndrome is the most common viable autosomal trisomy, resulting from an extra copy of chromosome 21, and is the leading genetic cause of intellectual disability.
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Presence of CHD may influence AD progression in DS.
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46/100
This cross-sectional study examines data for participants in the Alzheimer Biomarker Consortium–Down Syndrome study to gauge the concordance of clinical and biological Alzheimer disease staging.
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Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration.
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Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS).
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Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability.
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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.
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In partial correlations adjusted for age, there was a significant positive association between the cardiovascular composite (r = .156, p = .016) and resistance score; higher cardiovascular composite was associated with greater than expected Aβ for age.
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During alteplase administration, the patient experienced clinical deterioration.
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Amyloid pathology in aDS individuals is linked to frontal‐predominant atrophy without clear hypometabolism.
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Iron was 2-fold higher in DSAD. Iron storage proteins and lipid peroxidation were increased in prefrontal cortex, but not in the cerebellum.
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PSMD was more strongly associated with age in DS (rho=0.56; p <0.001) than in HC (rho=0.38, p <0.001; Figure 1A), with regression lines starting to diverge at age 42.
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In DS, PSMD changed approximately 10‐15 years before the onset of AD symptoms and linearly increased with AD clinical stages, AD pathology, and SVD metrics.
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= 49.17) had a higher incidence of psychotic disorder (p = .028) compared to non-progressors and progressors.
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There was a significant interaction between OSA and diagnosis for within- and between-DMN FC (p-values<0.05).
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We observed higher within‐ and between‐DMN FC in the CS‐OSA compared to the CI‐OSA group; however, this difference was not observed between the CS‐nonOSA and CI‐nonOSA groups.
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MOLDI-MS identified eighty-five proteins represented by multiple tryptic peptides, twenty-five of which showed significant differences between DS and controls, confirmed by WB and ELISA analysis.
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We found that a higher baseline sum of stress events was associated with greater risk of conversion from baseline stable cognition to mild cognitive impairment (MCI) or dementia at follow up, even when controlling for age, sex, premorbid level of intellectual disability, site, clinical latency between assessments, and the presence of anxiety or depression (odds ratio = 1.53, p = 0.021).
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Participant and visit numbers varied by measure, with 455 participants evaluated over 1178 data points.
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Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology.
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Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology.
From across this tag
7 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 7. The same 7 appear here every time.
- Global differential expression of genes located in the Down Syndrome Critical Region in normal human brain
- Use of a Screening Tool for Dementia in a Down Syndrome Specialty Clinic
- Shaping down syndrome brain cognitive and molecular changes due to aging using adult animals from the Ts66Yah murine model
- Emerging roles for intersectin (ITSN) in regulating signaling and disease pathways
- A stereological study of the mediodorsal thalamic nucleus in Down syndrome
- Transcriptome and metabolome analysis of crGART, a novel cell model of de novo purine synthesis deficiency: Alterations in CD36 expression and activity
- New Horizons: Gonadotropin-Releasing Hormone and Cognition