| Literature DB >> 29031832 |
Kirsten Thomsen1, Takashi Yokota2, Md Mahdi Hasan-Olive3, Niloofar Sherazi4, Nima Borhan Fakouri5, Claus Desler6, Christine Elisabeth Regnell7, Steen Larsen8, Lene Juel Rasmussen6, Flemming Dela8, Linda Hildegard Bergersen9, Martin Lauritzen10.
Abstract
Brain aging is accompanied by declining mitochondrial respiration. We hypothesized that mitochondrial morphology and dynamics would reflect this decline. Using hippocampus and frontal cortex of a segmental progeroid mouse model lacking Cockayne syndrome protein B (CSBm/m) and C57Bl/6 (WT) controls and comparing young (2-5 months) to middle-aged mice (13-14 months), we found that complex I-linked state 3 respiration (CI) was reduced at middle age in CSBm/m hippocampus, but not in CSBm/m cortex or WT brain. In hippocampus of both genotypes, mitochondrial size heterogeneity increased with age. Notably, an inverse correlation between heterogeneity and CI was found in both genotypes, indicating that heterogeneity reflects mitochondrial dysfunction. The ratio between fission and fusion gene expression reflected age-related alterations in mitochondrial morphology but not heterogeneity. Mitochondrial DNA content was lower, and hypoxia-induced factor 1α mRNA was greater at both ages in CSBm/m compared to WT brain. Our findings show that decreased CI and increased mitochondrial size heterogeneity are highly associated and point to declining mitochondrial quality control as an initial event in brain aging.Entities:
Keywords: Brain aging; Cockayne syndrome B; Complex I-linked respiration; Mitochondrial dynamics; Mitochondrial morphology; mtDNA copy numbers
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Year: 2017 PMID: 29031832 DOI: 10.1016/j.neurobiolaging.2017.08.004
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673