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down
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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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.
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Cross-sectional and longitudinal analyses were used to compare age-related changes in adaptive functioning in institutionalized adults with and without Down syndrome.
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Neuropeptide Y (NPY)-containing neurons are depleted in the cortices of individuals with Alzheimer disease (AD), yet spared in the striatum of patients with Huntington chorea.
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S100 beta is a calcium-binding protein that is expressed at high levels in brain primarily by astrocytes.
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Down syndrome (DS) is a major cause of mental retardation and congenital heart disease.
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Evolutionary aspects of menopause are considered from several perspectives.
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Two groups of subjects, 14 young (ages 20 to 31 years) and 14 adults (ages 32 to 54 years), both groups with Down Syndrome, were examined on a matching and naming olfactory task.
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Correlational analysis of cerebral metabolic (rCMRglc) data obtained with positron emission tomography (PET) assesses group differences and has demonstrated reduced frontal-parietal rCMRglc interdependencies in Alzheimer's disease (AD).
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Neuropsychologic tests were performed in subjects with Down syndrome in order to assess the effect of a 90-day treatment with L-acetyl-carnitine (LAC).
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It has been reported that the Down syndrome occurs more often than expected among relatives of individuals with Alzheimer disease.
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A major component of amyloid deposits found in Alzheimer disease and Down syndrome is the beta/A4 peptide, which is derived from the Alzheimer amyloid protein precursor (APP).
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Platelets are the main source of 5-hydroxytryptamine (5-HT) and amyloid precursor protein (APP) found in plasma.
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Frequencies of chromatid aberrations in response to G2-phase x-irradiation were compared in PHA-stimulated blood lymphocytes from healthy control subjects, Down syndrome (DS) patients, and Alzheimer disease (AD) patients.
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IgG subclasses were measured in sera from 33 persons with Down syndrome (DS) (mean age 55 +/- 7 years) and 33 age- and sex-matched control individuals using a mouse monoclonal antibody based sandwich enzyme linked immunosorbent assay.
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38/100
Down syndrome remains one of the most common causes of mental retardation.
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The association cortex of Down's syndrome (DS) predictably and prematurely undergoes neurofibrillary degeneration of Alzheimer type.
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We previously observed low level mosaicism (2-4% normal cells) in phytohemagglutinin-stimulated peripheral blood lymphocytes (PBL) in 29% of a small group of elderly persons with Down syndrome (DS).
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Human carbonyl reductase (CBR) belongs to a group of NADPH-dependent enzymes called aldo-keto reductases.
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Recent reports suggest that cultivated nonneuronal cells from individuals with Alzheimer disease (AD) and other specific hereditary neurodegenerative disorders show hypersensitivity to DNA-damaging agents such as x-rays and radiomimetic chemicals.
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Mice trisomic for Chromosome (Chr) 16 have been used extensively as an animal model for human Down Syndrome (Trisomy 21).
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It has been suggested that this increment, by accelerating hydrogen peroxide formation, might promote oxidative damage within DS cells and might be involved in the various neurobiological abnormalities found in DS such as premature aging and Alzheimer-type neurological lesions.
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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.
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To determine whether neurodegeneration in Alzheimer disease brain is associated with degradation of structural cell membrane molecules, we measured tissue levels of the major membrane phospholipids and their metabolites in three cortical areas from postmortem brains of Alzheimer disease patients and matched controls.
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Down syndrome (DS) is a major cause of congenital heart and gut disease and mental retardation.
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Vulnerability of specific brain regions and neuronal populations is a characteristic feature of Alzheimer disease and Down syndrome.
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The brains of individuals with Down's syndrome in their 40's and 50's begin to develop changes that are otherwise seen only in patients with Alzheimer disease.
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Age-related declines in language and other neuropsychological variables were examined in 60 adults with Down syndrome.
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The amyloid precursor protein (APP) is thought to be processed aberrantly to yield the major constituent of the amyloid plaques observed in the brains of patients with Alzheimer disease and Down syndrome.
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It was suggested that increased Cu-Zn superoxide dismutase (SOD-1) might be involved in the various biological abnormalities found in Down's syndrome (DS) such as premature aging and Alzheimer-type neurological lesions.
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A German family with 21 members affected by Alzheimer disease (AD) was studied clinically and genetically.
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In Alzheimer's disease, in Down syndrome and in normal aging, scattered deposits of amyloid fibril precursors occur in both cerebral cortex and subcortical grey structures.
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Cognitive profiles of performances were obtained from a selected group of adult Down syndrome (DS) subjects (n = 20; mean age: 34.5 years; s.d.: 7.7) by means of an ad hoc neuropsychological battery.
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Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology.
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Individuals with Down syndrome develop neuropathologic and in some cases clinical evidence of Alzheimer disease after age 40.
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Serum tests of thyroid function were compared in Down syndrome (DS) patients with and without manifestations of Alzheimer disease (AD).
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Paired helical filaments (PHF), which constitute neurofibrillary tangles (NFT) and neuritic plaque (NP) neurites, serve as a useful marker for Alzheimer disease (AD).
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The activities of red blood cell enzymes that scavenge the superoxide radical and hydrogen peroxide were measured in severely to profoundly retarded adult Down syndrome (DS) patients with and without manifestations of Alzheimer disease (AD), and control individuals matched for sex, age, and time of blood sampling.
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The plasma distribution of gallium (as an analogue of aluminium) was investigated in patients with Alzheimer disease, Down syndrome, or stroke dementia, in subjects on haemodialysis for chronic renal failure, and in healthy controls.
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A blind study was set up to examine the in vitro growth characteristics of skin fibroblasts from 2 individuals with and 9 at risk for familial Alzheimer disease, 4 individuals with sporadic Alzheimer disease, 18 with Down syndrome as well as 5 younger and 6 older controls.
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Regional CMRglc (rCMRglc) values were measured with [18F]2-fluoro-2-deoxy-D-glucose (18FDG) and positron emission tomography (PET), using a Scanditronix PC-1024-7B scanner, in 14 healthy, noninstitutionalized subjects with trisomy 21 (Down syndrome; DS) (mean age 30.0 years, range 25-38 years) and in 13 sex-matched, healthy volunteers (mean age 29.5 years, range 22-38 years).
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In a prospective longitudinal study with death as the end point in 17 middle-aged patients with Down's syndrome, dementia was clinically diagnosed in 15 patients, by means of careful observations in daily circumstances.
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In past decades, most individuals with Down syndrome were usually not afforded adequate medical care.
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Immunohistochemical staining with polyclonal antibodies to synthetic amyloid (residues 1-28 of A4) was performed on normal and Down syndrome brains from fetuses to adults.
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Patients with Down syndrome (DS) over 40 years of age, prematurely and consistently develop neurofibrillary tangles (NFT), intracytoplasmic inclusions of highly insoluble straight or paired helical 12-16 nm filaments, and senile plaques (SP) composed of abnormal neurites surrounding a core of beta amyloid.
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Numerous intraneuronal neurofibrillary tangles and senile (neuritic) plaques are the two characteristic lesions in Alzheimer disease (AD) and adult Down syndrome (DS).
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Review of the clinical cytogenetic literature provides compelling evidence for a specific relationship between imbalance of particular chromosomes or chromosomal regions and the appearance of defined patterns of phenotypic abnormalities.
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Chromosome 21-specific yeast artificial chromosomes (YACs) have been constructed by a method that performs all steps in agarose, allowing size selection by pulsed-field gel electrophoresis and the use of nanogram to microgram quantities of DNA.
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48/100
Interleukin 1, an immune response-generated cytokine that stimulates astrocyte proliferation and reactivity (astrogliosis), was present in up to 30 times as many glial cells in tissue sections of brain from patients with Down syndrome and Alzheimer disease compared with age-matched control subjects.
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We have evaluated serum alpha 1-antichymotrypsin content in dementia of the Alzheimer type (DAT).
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Studies of Alzheimer amyloid protein precursor mRNA expression in the human brain have provided compelling evidence for a neural origin of beta amyloid.
From across this tag
9 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 9. The same 9 appear here every time.
- Fecal corticosterone levels in RCAN1 mutant mice
- The effects of mosaicism on biological and clinical markers of Alzheimer's disease in adults with Down syndrome
- Neurodegenerative disorders associated with diabetes mellitus
- Increased amyloid beta protein levels in children and adolescents with Down syndrome
- Clinical and biomarker changes of Alzheimer's disease in adults with Down syndrome: a cross-sectional study
- Balance and Gait: Associations With Cognitive Impairment and Dementia in Individuals With Down Syndrome
- Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration
- Mapping of the gene encoding the beta-amyloid precursor protein and its relationship to the Down syndrome region of chromosome 21
- Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome