This review article explores the significant link between mitochondrial dysfunction and Parkinson's disease (PD). PD is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Mitochondrial dysfunction, particularly the inhibition of the electron transport chain, is a key factor in this process. This dysfunction leads to the generation of reactive oxygen species (ROS) and depletion of cellular energy, causing oxidative stress and excitotoxicity, which ultimately result in neuronal damage and death. The article highlights several genetic links between mitochondrial proteins and PD, including mutations in genes encoding proteins involved in mitochondrial function. Environmental toxins, such as MPTP, rotenone, paraquat, diquat, and TaClo, have also been shown to cause PD-like symptoms by inhibiting the electron transport chain and leading to mitochondrial dysfunction. The review discusses the mechanisms by which mitochondrial dysfunction contributes to PD, including the generation of ROS, calcium overload, and the involvement of proteins like α-synuclein, Parkin, PINK1, and DJ-1. It also examines the role of iron and calcium in exacerbating mitochondrial dysfunction and excitotoxicity. Additionally, the article explores the relationship between mitochondrial dysfunction and Lewy body formation, suggesting that mitochondria may play a direct role in the early stages of Lewy body development. The review concludes by emphasizing the need for further research to understand the exact mechanisms of mitochondrial dysfunction in PD and to explore potential therapeutic targets.This review article explores the significant link between mitochondrial dysfunction and Parkinson's disease (PD). PD is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Mitochondrial dysfunction, particularly the inhibition of the electron transport chain, is a key factor in this process. This dysfunction leads to the generation of reactive oxygen species (ROS) and depletion of cellular energy, causing oxidative stress and excitotoxicity, which ultimately result in neuronal damage and death. The article highlights several genetic links between mitochondrial proteins and PD, including mutations in genes encoding proteins involved in mitochondrial function. Environmental toxins, such as MPTP, rotenone, paraquat, diquat, and TaClo, have also been shown to cause PD-like symptoms by inhibiting the electron transport chain and leading to mitochondrial dysfunction. The review discusses the mechanisms by which mitochondrial dysfunction contributes to PD, including the generation of ROS, calcium overload, and the involvement of proteins like α-synuclein, Parkin, PINK1, and DJ-1. It also examines the role of iron and calcium in exacerbating mitochondrial dysfunction and excitotoxicity. Additionally, the article explores the relationship between mitochondrial dysfunction and Lewy body formation, suggesting that mitochondria may play a direct role in the early stages of Lewy body development. The review concludes by emphasizing the need for further research to understand the exact mechanisms of mitochondrial dysfunction in PD and to explore potential therapeutic targets.