Cerebral palsy (CP) is the most common cause of childhood-onset physical disability. It results from injury to the developing brain and is characterized by motor impairments, muscle weakness, and fatigue.

CP is commonly associated with marked deficits in muscle mass and function, and many individuals experience early declines in physical performance and functional ability as they age. These features resemble changes observed in age-related muscle loss, that is, sarcopenia, raising the possibility of shared underlying mechanisms.

This paper hypothesizes that skeletal muscles of individuals with CP undergo accelerated aging, driven by cellular and molecular pathways similar to those implicated in sarcopenia. To support this hypothesis, we highlight emerging evidence of phenotypic overlap between CP and aging muscle, including neuromuscular changes, impaired satellite cell function, altered niche components, chronic inflammation, and metabolic deficits such as reduced capillarization and mitochondrial dysfunction.

To test this hypothesis, we propose cross-sectional and longitudinal studies targeting both baseline aging markers and the rate of aging-related changes. These studies should focus on established hallmarks of aging, such as mitochondrial dysfunction, DNA methylation, and markers of cellular senescence.

If confirmed, this hypothesis could reshape our understanding of muscle pathology in CP. It may also open up the possibility of repurposing therapeutic strategies demonstrated to be effective in geriatric care for children and young adults with CP.