The Molecular Biology of Down Syndrome: Journal of Neural Transmission. Supplementa, cartea 57
Editat de G. Lubecen Limba Engleză Paperback – 2 dec 1999
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Specificații
ISBN-13: 9783211833773
ISBN-10: 3211833773
Pagini: 380
Ilustrații: X, 366 p.
Dimensiuni: 210 x 280 x 20 mm
Greutate: 1 kg
Ediția:Softcover reprint of the original 1st ed. 1999
Editura: SPRINGER VIENNA
Colecția Springer
Seria Journal of Neural Transmission. Supplementa
Locul publicării:Vienna, Austria
ISBN-10: 3211833773
Pagini: 380
Ilustrații: X, 366 p.
Dimensiuni: 210 x 280 x 20 mm
Greutate: 1 kg
Ediția:Softcover reprint of the original 1st ed. 1999
Editura: SPRINGER VIENNA
Colecția Springer
Seria Journal of Neural Transmission. Supplementa
Locul publicării:Vienna, Austria
Public țintă
ResearchCuprins
Molecular abnormalities of the brain in Down Syndrome: relevance to Alzheimer’s neurodegeneration.- Reduced aldehyde dehydrogenase levels in the brain of patients with Down Syndrome.- The Down Syndrome critical region.- Neuropathology.- c-fos expression in brains of patients with Down Syndrome.- Neuronal cell death in Down’s syndrome.- Altered Gene expression in fetal Down Syndrome brain as revealed by the Gene huntinG technique of subtractive hybridization.- Gene expression in fetal Down Syndrome brain as revealed by subtractive hybridization.- Molecular misreadinG of Genes in Down syndrome as a model for the Alzheimer type of neurodegeneration.- Expression of the dihydropyrimidinase related protein 2 (DRP-2) in Down Syndrome and Alzheimer’s disease brain is downregulated at the mRNA and dysregulated at the protein level.- Gene expression relevant to Down Syndrome: problems and approaches.- Isolation and analysis of chromosome 21 Genes potentially involved in Down Syndrome.- Differential display reveals deteriorated mRNA levels of NADH3 (complex I) in cerebellum of patients with Down Syndrome.- Serotonin (5-HT) in brains of adult patients with Down Syndrome.- Mechanisms of neuronal death in Down’s syndrome.- Impaired brain Glucose metabolism in patients with Down Syndrome.- Oxidative stress and neural dysfunction in Down Syndrome.- Expression of the transcription factor ETS2 in brain of patients with Down Syndrome — evidence against the overexpression-Gene dosage hypothesis.- Neuronal apoptosis inhibitory protein (NAIP)-like immunoreactivity in brains of adult patients with Down Syndrome.- The “Gene dosage effect” hypothesis versus the “amplified developmental instability” hypothesis in Down Syndrome.- Downregulation of the transcription factorscleraxis in brain of patients with Down Syndrome.- Heat-shock protein 70 levels in brain of patients with Down Syndrome and Alzheimer’s disease.- Increased levels of 14-3-3 Gamma and epsilon proteins in brain of patients with Alzheimer’s disease and Down Syndrome.- Application of Alu-splice PCR on chromosome 21: DSCR1 and Intersectin.- Overexpression of DNAse I in brain of patients with Down Syndrome.