Diego Mastroeni1, Omar M Khdour2, Elaine Delvaux3, Jennifer Nolz3, Gary Olsen4, Nicole Berchtold5, Carl Cotman5, Sidney M Hecht2, Paul D Coleman6. 1. ASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA; Banner Sun Health Research Institute, Sun City, AZ, USA. Electronic address: diego.mastroeni@asu.edu. 2. Biodesign Institute, and Department of Chemistry and Biochemistry, Arizona State University, Tempe, AZ, USA. 3. ASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA. 4. Banner Sun Health Research Institute, Sun City, AZ, USA. 5. Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, USA. 6. ASU-Banner Neurodegenerative Disease Research Center, Biodesign Institute and School of Life Sciences, Arizona State University, Tempe, AZ, USA; Banner Sun Health Research Institute, Sun City, AZ, USA.
Abstract
INTRODUCTION: We have comprehensively described the expression profiles of mitochondrial DNA and nuclear DNA genes that encode subunits of the respiratory oxidative phosphorylation (OXPHOS) complexes (I-V) in the hippocampus from young controls, age matched, mild cognitively impaired (MCI), and Alzheimer's disease (AD) subjects. METHODS: Hippocampal tissues from 44 non-AD controls (NC), 10 amnestic MCI, and 18 AD cases were analyzed on Affymetrix Hg-U133 plus 2.0 arrays. RESULTS: The microarray data revealed significant down regulation in OXPHOS genes in AD, particularly those encoded in the nucleus. In contrast, there was up regulation of the same gene(s) in MCI subjects compared to AD and ND cases. No significant differences were observed in mtDNA genes identified in the array between AD, ND, and MCI subjects except one mt-ND6. DISCUSSION: Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. Published by Elsevier Inc.
INTRODUCTION: We have comprehensively described the expression profiles of mitochondrial DNA and nuclear DNA genes that encode subunits of the respiratory oxidative phosphorylation (OXPHOS) complexes (I-V) in the hippocampus from young controls, age matched, mild cognitively impaired (MCI), andAlzheimer's disease (AD) subjects. METHODS: Hippocampal tissues from 44 non-AD controls (NC), 10 amnestic MCI, and 18 ADcases were analyzed on Affymetrix Hg-U133 plus 2.0 arrays. RESULTS: The microarray data revealed significant down regulation in OXPHOS genes in AD, particularly those encoded in the nucleus. In contrast, there was up regulation of the same gene(s) in MCI subjects compared to ADandNDcases. No significant differences were observed in mtDNA genes identified in the array between AD, ND, and MCI subjects except one mt-ND6. DISCUSSION: Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. Published by Elsevier Inc.
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