Etiopathogenetic factors and neurobiological links between traumatic brain injury and Parkinson’s Disease: The Case of Muhammad Ali

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Parkinson’s Disease (PD) is a neurological disorder characterized by the loss of dopaminergic neurons of the substantia nigra pars compacta (SNc). Several predisposing and pathogenic factors have been implicated in PD, all of which lead to the activation of the intracellular machinery of programmed cell death, eventually killing the dopaminergic neurons. These etiopathogenetic factors include oxidative stress associated with mitochondrial dysfunction, proteolytic stress associated with ubiquitin-proteasome system dysfunction, local inflammation, environmental factors such as pesticides, and genetic mutations. Moreover, there has been a strong molecular association between the pathogenesis of traumatic brain injury (TBI) and the development of Parkinson’s Disease. In particular, TBI affects the molecular mechanisms that are fundamental to the formation of pathological proteins, such as amyloid-β plaques, tau proteins, and Lewy Bodies which are implicated in dementia and PD. An icon in the boxing industry who was diagnosed with Parkinson’s Disease was Muhammad Ali. The clinical and neuropathological reasons that led to Muhammad Ali’s diagnosis of the disease remain controversial. In this work, we conduct a detailed review of the literature and examine pieces of evidence of the roles of the various etiopathogenetic factors in the neuronal loss that lead to Parkinson’s, and then illustrate synopses from Muhammad Ali’s personal life that are medically relevant to his PD case which might explain his diagnosis with the disease. The review is aimed to highlight from a neuroscience lens the dynamic interactions between the environmental, genetic, and inflammatory factors that the boxer had been exposed to during his personal and career lives, which might have been involved in the progression of his neurodegenerative disease.

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