Duchenne muscular dystrophy (DMD) is a neuromuscular disorder caused by dystrophin loss—notably within muscles and CNS neurons. DMD presents as cognitive weakness, progressive skeletal and cardiac muscle degeneration until pre-mature death from cardiac or respiratory failure. Innovative therapies improved life expectancy, but this is accompanied by increased late-onset heart failure and emergent cognitive degeneration. Thus, there is an increasing need to both better understand and track disease pathophysiology in the dystrophic heart and brain prior to onset of severe degenerative symptoms. Chronic inflammation is strongly associated with skeletal and cardiac muscle degeneration, however chronic neuroinflammation’s role is largely unknown in DMD despite being prevalent in other neurodegenerative diseases. Considering the well-known consequences of unchecked chronic inflammation, inflammation’s contribution towards multi-organ degeneration must be explored. Thus, this study explored inflammatory marker translocator protein positron emission tomography (TSPO-PET) to evaluate immune cell infiltration within the hearts and brains of DMD murine models. Four DMD and six healthy mice underwent whole-body PET imaging using the TSPO radiotracer [18F]FEPPA. Confirmatory TSPO-immunofluorescence staining of cardiac and neural tissues were also conducted. Our results indicated that DMD mice showed significant elevations in heart and brain [18F]FEPPA activity, which correlated with increased ex-vivo fluorescence intensity. In summary, this study suggests cardiac and neuroinflammation presence in DMD and highlights TSPO-PET’s utility as a tool for in-vivo assessment of inflammation in several organs simultaneously within DMD
