Abstract
While oxidative stress is implicated in aging, the impact of oxidative stress on aging in the peripheral nervous system is not well understood. To determine a potential mechanism for age-related deficits in the peripheral nervous system, we examined both functional and morphological changes and utilized microarray technology to compare normal aging in wild-type mice to effects in copper/zinc superoxide dismutase-deficient (Sod1−/−) mice, a mouse model of increased oxidative stress. Sod1−/− mice exhibit a peripheral neuropathy phenotype with normal sensory nerve function and deficits in motor nerve function. Our data indicate that a decrease in the synthesis of cholesterol, which is vital to myelin formation, correlates with the structural deficits in axons, myelin, and the cell body of motor neurons in the Sod1+/+ mice at 30 months and the Sod1−/− mice at 20 months compared with mice at 2 months. Collectively, we have demonstrated that the functional and morphological changes within the peripheral nervous system in our model of increased oxidative stress are manifested earlier and resemble the deficits observed during normal aging.
Highlights
Neuromuscular system function declines with age and manifests as dramatic decreases in muscle strength and size, often referred to as sarcopenia [1]
Increasing oxidative stress is implicated in normal aging, sarcopenia, and decreased neuromuscular function
Building on our previous observation that denervation of the muscle resulted in the loss of muscle fibers and muscle atrophy [10,12], in the current study we compared normal age-related deficits in the peripheral nervous system superimposed on those observed in an established model of increased systemic oxidative stress, the Sod12/2 mouse
Summary
Neuromuscular system function declines with age and manifests as dramatic decreases in muscle strength and size, often referred to as sarcopenia [1]. Age-related changes in the central nervous system are well documented and include neuronal loss, demyelination, and deficits in cognitive function; little has been reported concerning age-related changes in the peripheral nervous system beyond a decline in nerve conduction velocities (NCVs) [3]. Oxidative stress is the result of an imbalance between pro-oxidants and antioxidants [5]. To date, both invertebrate and vertebrate models have been generated in which one or more antioxidants are either ablated or overexpressed; the role of oxidative stress in aging vertebrates, including rat, mouse, and human, remains unclear, likely due to the complexity of the aging process [7]
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