2025 American Academy of Neurology Abstract Website

Objective:

This study was conducted on whether changes in the activity of autophagy/mitophagy are induced in sarcopenia including muscle disease. In addition, we observed how changes in muscle cell-specific autophagy/mitophagy are involved in increased muscle inflammation.

Background:

A decrease in GSTO1 activity has been observed in various degenerative cerebral diseases and muscle diseases.

Design/Methods:

A. Fly Stocks

B. Western blot analysis

C. Immunohistochemistry

D. In vivo ubiquitination assay

E Locomotive Activity

Results:

1. Decreased mRNA and protein amount of GSTO1 gene in patients with muscle disease.

2. Protein amount of GstO2 in muscle tissue significantly decreases as aging progresses.
In fruit flies, it is suggested that the function of GstO2 may be important in the process of muscle cell damage due to aging.

3. We build a GSTO1/GstO2 RNAi fruit fly model that can specifically control expression in muscle tissue.

4. The results of GSTO1 reduction in various muscle diseases and GstO2 expression in aging fruit fly muscles indicate that GSTO1/GstO2 may play an important role in the stability and survival of muscle cells.

5. The reduction/inactivation of GSTO1/GstO2 in muscle cells in the development of muscle disease including sarcopenia due to aging is important for mitophage control.

6. GstO2 Restored Defective Locomotive Activity in Motor Neuron-Specific hTDP-43-Induced Flies.

Conclusions:

The GSTO1/GstO2 gene maintains mitochondrial function by controlling autophagy/mitophagy in muscle cells, and through anti-inflammatory action in muscle, it is important for the survival and stability of muscle cells during the aging process, and is involved in the development of sarcopenia.