Impaired hypoxic tolerance and altered protein binding of NADH in presymptomatic APP23 transgenic mice

It is being discussed whether impairment of energy metabolism is a final common pathway of neurodegeneration or initiates the neurodegenerative cascade. The goal was to investigate hypoxic tolerance and oxidative energy metabolism in 4-month-old, presymptomatic B6-Tg(ThylAPP)23Sdz (APP23) mice, a tr...

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Veröffentlicht in:	Neuroscience 2002-01, Vol.114 (2), p.285-289
Hauptverfasser:	Büchner, M, Huber, R, Sturchler-Pierrat, C, Staufenbiel, M, Riepe, M.W
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - genetics Alzheimer Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - metabolism Animals Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Energy Metabolism - genetics Female Hippocampus - metabolism Hippocampus - physiopathology hypoxia Hypoxia, Brain - genetics Hypoxia, Brain - metabolism Hypoxia, Brain - physiopathology Ischemic Preconditioning Male Medical sciences Mice Mice, Transgenic NAD - antagonists & inhibitors NAD - metabolism NADH Neurology Neurons - metabolism Nitro Compounds preconditioning Propionates - pharmacology Protein Binding - genetics Recovery of Function - genetics spectrum Spectrum Analysis
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Zusammenfassung:	It is being discussed whether impairment of energy metabolism is a final common pathway of neurodegeneration or initiates the neurodegenerative cascade. The goal was to investigate hypoxic tolerance and oxidative energy metabolism in 4-month-old, presymptomatic B6-Tg(ThylAPP)23Sdz (APP23) mice, a transgenic mouse model of Alzheimer’s disease. Posthypoxic recovery of the population spike amplitude in hippocampal region CA1 upon stimulation of Schaffer collaterals in region CA3 (15 min hypoxia, 45 min recovery) was 43±46% (mean±S.D.) vs. 19±35% ( P
ISSN:	0306-4522 1873-7544
DOI:	10.1016/S0306-4522(02)00280-4