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syndrome
534 studies tagged syndrome, 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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The DABNI cohort included 1,135 participants with a mean age of 42.82 years (SD = 11.56), 46.3% of whom are female.
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Down syndrome (DS) stands out as the most prevalent genetic contributor to intellectual disability, marked by the presence of an extra copy of chromosome 21 (HSA21).
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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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BackgroundMost adults with Down syndrome will develop Alzheimer's disease (AD) due to the triplication of the amyloid precursor protein in the 21 st chromosome.
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40/100
BackgroundLifetime incidence of Alzheimer's disease (AD) in Down syndrome (DS) exceeds 90%.
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The prevalence of MetS was low in adults with DS.
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The patterns of FDG decline are distinct in these 2 genetically determined forms of AD.
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A bidirectional relationship has been identified between dementia and epilepsy.
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To study the use of a dementia screening tool in our clinic cohort of adults with Down syndrome.
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Gene dysregulation in trisomy 21 can cause disorders of genes that are members of the heat-shock proteins (HSPs) family and contribute to the early onset of Alzheimer's disease (AD) in Down syndrome (DS).
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Down syndrome is a condition caused by trisomy of chromosome 21 and is the most common genetic cause of intellectual disability.
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48/100
This study provided a preliminary examination of indices of obstructive sleep apnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology.
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47/100
This study provided a preliminary examination of indices of obstructive sleep apsnea (OSA) and sleep disruptions in adults with Down syndrome (DS), and their associations with Alzheimer's disease (AD) pathology and symptomatology.
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Disturbances of the single sugar modification of proteins, O-GlcNAc, have been identified as a potential connection between disrupted brain metabolism and intellectual decay.
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Fourteen individuals with DS and five age-matched euploid controls were studied, with all DS cases showing HFOs.
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Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life.
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Down syndrome (DS), caused by trisomy of chromosome 21, exhibits significant phenotypic variability, including intellectual disability, early-onset Alzheimer disease (AD), congenital heart defects (CHDs), haematological malignancies, and immune dysregulation.
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These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition.
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Individuals with Down syndrome (DS) have a genetically determined form of Alzheimer's disease (AD) due to the amyloid precursor protein (APP) gene dose effect.
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Inter-rater agreement for ID level classification was 95% within sites but 60% between sites.
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Adults with DS may have unique neuro- and cardio- protective factors that deserve future investigation.
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Down syndrome (DS) is a genetic form of Alzheimer's disease (AD) that offers crucial insights into AD pathogenesis.
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Demonstrated utility of the mCRT warrants further investigation into comparisons between the A and B versions, free versus cued recall and changes in performance over time to better understand sensitivity for tracking memory decline over time based on age and AD clinical status.
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Down syndrome (DS), caused by trisomy of chromosome 21 (HSA21), is a complex condition associated with neurodevelopmental impairments and accelerated brain aging, often culminating in early-onset Alzheimer's disease (AD).
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BackgroundIndividuals with Down syndrome (DS) generally show neuropathological features of Alzheimer disease (AD).
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Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB.
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16/100
Adults with Down syndrome carry high risk of developing Alzheimer’s disease and efforts to include this population in clinical trials remain limited.
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The brain metabolic decline in DS with age reflects Alzheimer's pathological processes and involves temporoparietal regions in a similar pattern to that found in other forms of AD.
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Virtually all people with Down syndrome will develop Alzheimer disease pathology during their lifetime.
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35/100
This chapter discusses the dependency of basal forebrain cholinergic neurons (BFCNs) on endogenous nerve growth factor (NGF) for the structural and physiologic maintenance of the neuronal cell somata, axonal projections, and terminal synapses.
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45/100
This well-characterized case of PCA syndrome due to AD in a very young patient with DS demonstrates the occurrence of atypical presentations in DS that might be overshadowed by the baseline intellectual disability associated with DS.
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Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [ 11 C]PiB PET imaging, which has not been replicated with [ 18 F]florbetapir (FBP).
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Down syndrome (DS), characterised by compromised brain development and intellectual challenges, often manifests Alzheimer's disease (AD) -like symptoms.
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The amyloid cascade hypothesis as the etiological underpinning of Alzheimer disease (AD) is supported by a large body of literature, the most influential of which are genetic studies of the 1980s and 1990s. Other evidence includes the neuropathology of Down syndrome, apparent toxicity of oligomeric amyloid-β (Aβ), interactions with apolipoprotein E, and the analogy of cardiac amyloidosis.
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For both cohorts, the prevalence of mosaicism was 40 and Aβ 42 concentrations.
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The identified deficits in the medical care of the target population and the approaches to solving them will be incorporated into the development of health policy recommendations in order to optimize the care situation of those affected in the long term.
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Early increases in plasma NfL may reflect early white matter microstructural changes prior to dementia in DS.
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These findings suggest significant binding of lecanemab to cerebral amyloid angiopathy in DS.
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Down syndrome (DS) is the most common genetic cause of intellectual impairment, characterised by an extra copy of chromosome 21.
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There were 132 720 unique adults with Down syndrome from 2011 to 2019: 79 578 (53.2%) were male, 17 090 (11.7%) were non-Hispanic Black, 20 777 (15.7%) were Hispanic, 101 120 (68.8%) were non-Hispanic White, and 47 692 (23.3%) had ever had an Alzheimer dementia diagnosis.
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Adults with Down syndrome (DS) are at risk for Alzheimer’s disease (AD).
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The anterior thalamic nuclei are important for cognition, and memory in particular.
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Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05).
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Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes.
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These findings emphasize the necessity of tailoring mAb trials for DS, considering age-related AD characteristics.
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Currently available literature shows limited information on aging in RGNDs, with relatively many reports of young-onset dementia.
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Down syndrome (DS) is the most common condition with intellectual disability and is caused by trisomy of Homo sapiens chromosome 21 (HSA21).
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Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease.
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Since its first description in 1906 by Dr. Alois Alzheimer, Alzheimer’s disease (AD) has been the most common type of dementia.
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Adult individuals with Down syndrome (DS) develop Alzheimer disease (AD).
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.
- Tubulin immunopositive structures resembling intracellular neurofibrillary tangles
- Relevance of donepezil in enhancing learning and memory in special populations: a review of the literature
- X-ray-induced chromatid damage in cells from Down syndrome and Alzheimer disease patients in relation to DNA repair and cancer proneness
- The natural history of dementia in Down's syndrome
- Carbohydrate handling enzymes in fetal Down syndrome brain
- Down syndrome and Alzheimer disease: response to donepezil
- Oligodendrocyte Enriched Brain Organoids Reveal Impaired Oligodendroglial Maturation and Altered Neural Network Activity in Down Syndrome
- Alzheimer-type neuropathology and clinical symptoms of dementia in mentally retarded people without Down syndrome
- Parallel compensatory and pathological events associated with tau pathology in middle aged individuals with Down syndrome
- Differences between GABA levels in Alzheimer's disease and Down syndrome with Alzheimer-like neuropathology