Analysis Tools
mortality/aging
| N |
• mice exhibit normal aging and life span
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cellular
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• deletions in mitochondrial DNA accumulate unlike in wild-type mice
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• at 18 months, mice exhibit COX-SDH+, markers of decreased respiratory function and increased proliferation, muscles and brain cells unlike wild-type mice
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• deletions in mitochondrial DNA accumulate unlike in wild-type mice
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• at 18 months, mice exhibit COX-SDH+, markers of decreased respiratory function and increased proliferation, muscles and brain cells unlike wild-type mice
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muscle
| N |
• despite mitochondrial defects, mice exhibit normal muscle strength and performance
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• at 18 months, muscle fibers exhibit an increase in the number and size of mitochondria compared to in wild-type mice
• severely affected muscle fibers exhibit large mitochondria with concentric cristae and electron-dense inclusions unlike in wild-type mice
• however, total respiration capacity of the muscle is normal
• at 18 months, mice exhibit COX-SDH+, markers of decreased respiratory function and increased proliferation, muscles cells unlike wild-type mice
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nervous system
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• at 18 months, 1% of Purkinje cells in the cerebellum and a few neurons in the olfactory bulbs, substantia nigra, and hypothalamus are COX-SDH+ unlike in wild-type mice that have no COX-SDH+ brain cells
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homeostasis/metabolism
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• deletions in mitochondrial DNA accumulate unlike in wild-type mice
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behavior/neurological
| N |
• despite mitochondrial defects, mice exhibit normal muscle strength and performance
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