From mitochondrial dysfunction to neuroinflammation in Parkinson’s disease: Pathogenesis and mitochondrial therapeutic approaches

Parkinson's disease (PD) is a prevalent and intricate neurological condition resulting from a combination of several factors, such as genetics, environment, and the natural process of aging. Degeneration of neurons in the substantia nigra pars compacta (SN) can cause motor and non-motor impairments in patients with PD. In PD's etiology, inflammation and mitochondrial dysfunction play significant roles in the disease's development. Studies of individuals with PD have revealed increased inflammation in various brain areas. Furthermore, mitochondrial dysfunction is an essential part of PD pathophysiology. Defects in the components of the mitochondrial nucleus, its membrane or internal signaling pathways, mitochondrial homeostasis, and morphological alterations in peripheral cells have been extensively documented in PD patients. According to these studies, neuroinflammation and mitochondrial dysfunction are closely connected as pathogenic conditions in neurodegenerative diseases like PD. Given the mitochondria's role in cellular homeostasis maintenance in response to membrane structural flaws or mutations in mitochondrial DNA, their dynamic nature may present therapeutic prospects in this area. Recent research investigates mitochondrial transplantation as a potential treatment for Parkinson's disease in damaged neurons. This review delves into the impact of inflammation and mitochondrial dysfunction on PD occurrence, treatment approaches, and the latest developments in mitochondrial transplantation, highlighting the potential consequences of these discoveries.