ABSTRACTPD (PD) is a debilitating progressive age-related neurodegenerative disorder that negatively impacts bodily movement. It is the second most common type of neurodegenerative disease after Alzheimer's disease. Although the etiology and pathogenesis of PD remain unknown, a vast body of evidence indicates that oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, and proteasomal dysfunction all play a role in the disease's pathogenesis. Because of the multifactorial nature of the disease, current drug treatment can only offer symptomatic relief and cannot stop or delay the disease progression. The Peroxisome proliferator-activated receptors (PPARs) are the member of the receptor’s superfamily called, nuclear receptors, regulates the growth, differentiation of the tissues, inflammation, mitochondrial function, wound healing, lipid metabolism, and glucose metabolism. Several PPAR agonists have recently been shown to protect neurons from oxidative damage, inflammation, and apoptosis in Alzheimer's disease, PD, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. We review the research on the neuroprotective effects of PPAR agonists in in-vitro and in-vivo models of PD in this paper. Similarly, the pharmacological mechanism of PPAR agonists' neuroprotective effects is examined. Finally, PPAR agonists exert neuroprotective effects by controlling the expression of a set of genes involved in cell survival processes, suggesting that they may be a potential therapeutic target in crippling neurodegenerative diseases like PD.Keywords: Parkinson’s disease, neuroprotective, neuro inflammatory, oxidative stress, PPAR agonist