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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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Thyroid hormone abnormalities are strongly associated with Down Syndrome (DS) with elevated thyroid stimulating hormone (TSH) levels as the most consistent finding.
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There is convincing epidemiological and in vitro evidence of chronic oxidative stress in individuals with Down syndrome (DS).
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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.
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40/100
To gain insights into the different forms of modified amyloid beta peptides (A beta) in the Alzheimer disease (AD) and Down syndrome (DS) brain, we used two-site ELISAs with antibodies specific for isomerized (i.e. A beta with L-isoaspartate at positions 1 and 7) and pyroglutamate-modified (i.e. A beta beginning with pyroglutamate at position 3) forms of A beta to quantitate the levels of these different A beta peptides in formic acid extracts of AD and DS frontal cortex.
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36/100
The presenilin-1 (PS1) gene mutation (Pro117Leu), recently identified in a Polish family is characterized by the earliest reported onset (from 24-31 years) of Alzheimer disease (AD) and a very short duration of disease (4-6 years).
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Ts65Dn mouse displays a partial triplication of chromosome 16 and is adopted as a model for Down syndrome (DS).
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46/100
Chronic overexpression of the neurite growth-promoting factor S100beta has been implicated in the pathogenesis of neuritic plaques in Alzheimer's disease.
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However, bed rest results in many alterations which are disadavantageous.
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An increased risk of Alzheimer disease (AD) has been reported in young mothers of Down syndrome (DS) probands.
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40/100
Circulating glucose concentrations regulate many brain functions, including learning and memory.
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Previous research has hypothesized an association between Alzheimer's disease and the amyloid precursor protein (APP) gene found on chromosome 21.
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The Rivermead Behavioural Memory Test for Children (RBMT-C) was used to assess a population-based sample of 74 people with Down syndrome (DS) aged 30 years and over (range 30-65 years) living in the Cambridge health district.
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Tau protein promotes microtubule assembly.
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Trisomy 21 (Down syndrome) is associated with a high incidence of Alzheimer disease and with deficits in cholinergic function in humans.
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In Down syndrome (DS), oxidative DNA-damage may play a role in the pathogenesis of characteristic mental retardation and precocious dementia of Alzheimer type.
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Some individuals with Down syndrome develop an Alzheimer-type dementia in the third and fourth decades of life.
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Growth inhibitory factor, a new metallothioneinlike protein, was investigated at postmortem examination in the brains of 18 patients with Down syndrome ranging in age from 18 weeks gestation to 50 years of age and in 20 age-matched normal controls by developmental immunohistochemistry.
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Patients with Alzheimer disease (AD) show visual impairments in color discrimination (blue hues), stereoacuity, and contrast sensitivity.
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Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome.
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Monoclonal antibodies (mAbs) D3G6 and C8A5, specific for amino acid residues 160-168 of S182 protein, immunolabeled neurons, ependymal and choroid plexus cells, and myocytes in brain sections from normal subjects and people with Alzheimer disease or Down syndrome and in rats and mice.
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31/100
Down syndrome, trisomy of chromosome 21, is well investigated because it is a genetic disease with characteristic mental retardation and precocious dementia of Alzheimer type.
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In order to study whether Alzheimer-like neuropathological changes involve the central histaminergic system we measured the concentration of histamine, its precursor histidine as well as the activity of histidine decarboxylase (HDC) and histamine-N-methyl-transferase (HMT) in frontal cortex of aging Down syndrome (DS) patients, Alzheimer patients and control individuals.
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38/100
Neuritic pathology is a major neuroanatomical correlate of dementia in Alzheimer disease (AD).
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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.
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Institutionalized patients with Down syndrome (n = 307) were monitored for 5 to 10 years prospectively to determine prevalence of Alzheimer-type dementia.
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Magnetic resonance imaging is potentially a valuable tool in the diagnosis of Alzheimer disease in adults with Down syndrome, particularly in individuals for whom standard intellectual assessments are not possible.
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A consistent alteration in platelet APP isoforms has been found in Alzheimer disease and Down syndrome.
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40/100
To identify changes in brain functions associated with the development of dementia, brain metabolism and cognition were assessed repeatedly in 12 adults with Down syndrome (DS) using positron emission tomography and neuropsychological tests.
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49/100
To study the pathogenesis of central nervous system abnormalities in Down syndrome (DS), we have analyzed a new genetic model of DS, the partial trisomy 16 (Ts65Dn) mouse.
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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.
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In order to study whether phosphokinases might be involved in the neuropathology of Down Syndrome (DS) and Alzheimer disease (AD), cyclin dependent kinase (CDK) activity and protein, phosphokinase C (PKC) and phosphokinase A (PKA) activities have been determined in frontal lobes of DS, AD and control brains.
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32/100
On the basis of what is known about the neural circuitry essential or normally involved in eyeblink classical conditioning (EBCC), the pattern of neurodegeneration in Huntington's disease (HD) would not appear to interfere with this type of learning.
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29/100
Through deinstitutionalization, more adults with mental retardation are living in the community under the care of family physicians.
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Individual differences in the development of neurofibrillary changes were examined in eight cortical regions in the brains of 43 subjects with Down syndrome (DS; age range, 15-69 years) using sections stained with monoclonal antibodies (mAb) tau-1 and 3-39.
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The neurodegeneration and amyloid deposition of sporadic Alzheimer disease (AD) also occur in familial AD and in all trisomy-21 Down syndrome (DS) patients, suggesting a common pathogenetic mechanism.
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Down syndrome (DS) subjects develop Alzheimer disease (AD) histopathology before they develop dementia.
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Polyamines may play an important role in brain development, mature brain function and also in neurodegenerative conditions.
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Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein.
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We report on the clinical and cytogenetic assessment of five cases of Down syndrome phenotype with either a partial duplication of chromosome 21 or a normal karyotype, and we quote a case of del (21q) syndrome.
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The main purpose of this study was to investigate differences regarding endogenous opioids in post-mortem frontal cortex of adult patients with Down syndrome (DS), patients with Alzheimer disease (AD) and neurologically healthy persons, respectively, using specific radioimmunoassays.
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Declines in adaptive behavior were examined in a study of dementia in adults with Down syndrome and other forms of mental retardation.
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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.
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In addition to clinical and neuropathological similarities between Alzheimer's disease and Down syndrome there are genetic and biochemical data which suggest common disease mechanism.
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Trisomy 21 or Down syndrome (DS) is the most frequent genetic cause of mental retardation, affecting one in 800 live born human beings.
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38/100
The survival of cultured mouse hippocampal neurons was found to be greatly enhanced by micromolar concentrations of the excitatory neurotransmitter glutamate.
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The purpose of this study was to determine cerebral myo-inositol (mI) in adults with Down syndrome (DS), and to trace the chronobiology of DS to Alzheimer disease (AD).
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A comprehensive baseline of emotional functioning was established for adults with Down syndrome.
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The discovery that the epsilon 4 allele of the apolipoprotein E (apoE) gene is a putative risk factor for Alzheimer disease (AD) in the general population has highlighted the role of genetic influences in this extremely common and disabling illness.
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Dementia is seen earlier and more often in patients with Down syndrome (DS) than in the general population.
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Cognitive processes and their decline with aging were studied in individuals with Down Syndrome (DS) and individuals of comparable mental handicap without Down Syndrome (NonDS).
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.
- The evolution of ovarian oocyte decline with aging and possible relationships to Down syndrome and Alzheimer disease
- Impact of Triplicated DYRK1A on Neurogenesis and Intellectual Disability in Down Syndrome and Therapeutic Potential
- Chr21 protein-protein interactions: enrichment in products involved in intellectual disabilities, autism and Late Onset Alzheimer Disease
- Paving the Way for Therapy: The Second International Conference of the Trisomy 21 Research Society
- APOE genotype and gender effects on Alzheimer disease in 100 adults with Down syndrome
- Segmental trisomy as a mouse model for Down syndrome
- Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome
- The effect of acetyl-L-carnitine administration on persons with Down syndrome
- Oxidative stress and mitochondrial dysfunction in Down syndrome
- Down syndrome fibroblast model of Alzheimer-related endosome pathology: accelerated endocytosis promotes late endocytic defects