A new study from the University of California, Riverside, reveals that mitochondrial impairment plays a critical role in the progressive brain damage observed in multiple sclerosis (MS). Published in the Proceedings of the National Academy of Sciences, the research highlights how energy deficits in neurons contribute to motor impairments and cerebellar degeneration in MS patients.
MS, a chronic inflammatory disease affecting more than 2.3 million people worldwide, often damages the cerebellum, a brain region essential for movement and balance. The study found that inflammation and demyelination disrupt mitochondrial function in Purkinje cells, specialized neurons crucial for coordination. This energy deficiency leads to cell death and worsening motor symptoms, such as tremors and ataxia.
Using post-mortem brain tissue from MS patients and a mouse model of the disease, researchers observed a significant loss of the mitochondrial protein Cytochrome C Oxidase Subunit IV (COXIV) in Purkinje cells. “Mitochondrial dysfunction appears early in the disease, accelerating neurodegeneration,” explained lead author Dr. Seema Tiwari-Woodruff.
The findings suggest that therapies targeting mitochondrial health could slow or prevent neurological decline in MS. Future research will explore whether other brain cells, such as oligodendrocytes and astrocytes, are similarly affected.
“Protecting mitochondrial function may offer new ways to preserve mobility and improve quality of life for MS patients,” said Tiwari-Woodruff. The team emphasizes the importance of continued funding for scientific research to advance such discoveries.
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