Another characteristic feature of PD is the accumulation of abnormal protein aggregates known as Lewy bodies within neurons. Lewy bodies primarily consist of misfolded αsynuclein protein and are found in various brain regions, including the substantia nigra and other structures involved in motor and cognitive function. The presence of Lewy bodies is thought to contribute to neuronal dysfunction and degeneration, although the exact role they play in the pathogenesis of PD is still under investigation. Chronic inflammation and oxidative stress are also believed to play significant roles in the progression of Parkinson's disease. Inflammatory processes in the brain, mediated by activated microglia and astrocytes, can lead to neuronal damage and contribute to the degenerative cascade. Oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) and antioxidant defenses, can damage cellular components and exacerbate neuronal dysfunction and death. Dysfunction of mitochondria, the cellular organelles responsible for energy production, has been implicated in the pathophysiology of PD. Mitochondrial impairment can lead to energy deficits, increased oxidative stress, and activation of cell death pathways, contributing to neuronal degeneration. Mutations in genes associated with mitochondrial function, such as PINK1 and Parkin, have been linked to familial forms of Parkinson's disease.