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Protective mechanism against age-associated changes in the peripheral nerves
Kenji Goto1, Kiyohito Naito1, Shinji Nakamura2
1Department of Orthopaedics, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Life Sciences
|May 7, 2020
Summary
Aging preserves peripheral nerve function through increased REST/NRSF expression, not oxidative stress. This study investigated age-related changes in mouse sciatic nerves and protective mechanisms against aging.
Area of Science:
- Neuroscience
- Aging Research
- Cell Biology
Background:
- Senescence, a normal decline in physiological functions with aging, leads to cell dysfunction.
- Age-associated changes in peripheral nerves remain largely unelucidated.
- Understanding these changes is crucial for addressing age-related neurological decline.
Purpose of the Study:
- To investigate histological changes in sciatic nerves of young and aged mice.
- To evaluate the protective mechanisms of peripheral nerves against aging.
- To elucidate age-related alterations in peripheral nerve structure and function.
Main Methods:
- Sciatic nerves from young (8-week-old) and aged (78-week-old) female C57BL/6 mice were examined histologically.
- Axon number and density were assessed using hematoxylin and eosin staining.
- Immunofluorescence staining evaluated nerve-specific proteins, oxidative stress markers, and the neuronal aging marker REST/NRSF, with fluorescence intensity quantified.
Main Results:
- Axon number and density were lower in aged mice, though not statistically significant.
- Expression of most markers did not differ significantly between age groups.
- Significantly higher expression of REST/NRSF was observed in aged mice compared to young mice (p < 0.05).
Conclusions:
- Peripheral nerve function appears preserved in aging mice due to increased REST/NRSF expression.
- The protective effects of REST/NRSF are suggested to be independent of oxidative stress levels.
- This highlights a potential intrinsic mechanism protecting peripheral nerves during senescence.
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