Molecular Mechanisms Involved in Pathogenesis of Parkinson's Disease

Abstract

Listen

Translate article

A variety of age-related disorders can include Parkinson's disease, which is regarded as by a gradual but irreversible decline in brain function. It is primarily linked to many biochemical pathways that underlie the deterioration of dopaminergic neurons substantia nigra pars compacta (SNpc) in the brain. These chemical processes that underlie neuronal loss remain mysterious. The Parkinson's disease treatments now on the market are not always helpful or suitable for all Parkinson's sufferers. These treatments simply address the symptoms; they neither slow the progression of the disease nor replace the destroyed dopaminergic neurons. We would like to provide an extensive summary of the different molecular mechanisms involved in Parkinson’s disease such as oxidative stress, protein aggregation, mitochondrial dysfunction, ferroptosis, and gut dysbiosis that lead to the deterioration of dopaminergic neurons. The intricate interactions between these molecular pathways further complicate the pathogenesis of Parkinson's disease (PD) and pose considerable obstacles for therapeutic development. Furthermore, the pathophysiology of Parkinson's disease has been observed in relation to several neurotransmitters, including but not limited to dopamine, acetylcholine, serotonin, glutamate, and gamma amino butyric acid. This review spur research into a wide range of ligands that may improve treatment outcomes and/or lessen adverse effects in Parkinson's disease.