Inflammaging-associated mitochondrial degeneration occurs in hypoglossal motor neurons prior to tongue muscle.

Matthew J Fogarty, Debanjali Dasgupta, Trace A Christensen, Genesis A Hernandez-Vizcarrondo, Sanjana Mahadev Bhat, Kathryn D Rooker, Gary C Sieck

Department of Physiology and Biomedical Engineering, Mayo Clinic, 200 1st St SW, Rochester, MN, 55905, USA. [email protected]. · pubmed

Paper

Abstract

Mitochondrial degeneration and dysfunctions are increasingly linked with neurodegenerative diseases, with the greatest risk factor being increased age. Mitochondrial dysfunction is also implicated in sarcopenia, the age-associated weakness and atrophy of striated muscle. Untangling the pathophysiological effects of age-related mitochondrial degeneration and dysfunction is of huge interest in gerontology. In elderly humans and Fischer 344 (F344) rats, motor neuron (MN) death and denervation effects are becoming increasingly implicated in sarcopenia. We have previously demonstrated that MN loss and muscle weakness are prevalent in respiratory MNs and muscles; however, the chronology and mechanism of MN death and muscle weakness are relatively unexplored. We evaluated inflammaging (inflammatory cytokine release via ELISA), the endoplasmic reticulum (ER) stress response (via western blotting), mitochondrial degeneration (via serial block-face scanning electron microscopy), mitochondrial function (via SDH

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Research summary

The paper claims that mitochondrial degeneration in hypoglossal motor neurons occurs before muscle degeneration in the context of aging. This research is relevant as it explores the underlying mechanisms of mitochondrial dysfunction and neurodegeneration associated with aging, which are critical for understanding and potentially addressing the root causes of age-related diseases.

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