ted receptors (PPARs) are ligand-directed transcription factors pertaining for the class of nuclear hormone receptors (NHR), and are implicated in the modulation of mitochondrial operation, inflammation, wound healing, redox equilibrium, and metabolism of blood sugar and lipids. Several PPAR agonists have been recognized to safeguard nerve cells from oxidative destruction, inflammation, and programmed cell death in PD and other neurodegenerative ailments. On top of that, different investigations recommend that common administration of PPAR-activating non-steroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, indomethacin), and leukotriene receptor antagonists (montelukast) were connected to the de-escalated evolution of neurodegenerative ailments. The present review elucidates the emerging evidence enlightening the neuroprotective outcomes of PPAR agonists in in vivo and in vitro models experiencing PD. Existing articles up to the present have been procured via PubMed, MEDLINE, etc., using particular keywords and phrases spotlighted within this overview. Additionally, the authors aim to provide insight into the neuroprotective actions of PPAR agonists by outlining the pharmacological mechanism. As a conclusion, PPAR agonists exhibit neuroprotection by means of modulating the expression of a group of genes implicated in cellular survival pathways, and could possibly be a propitious target inside the therapy of incapacitating neurodegenerative diseases like PD. Keyword phrases: neurodegenerative illnesses; peroxisome proliferator-activated receptors; oxidative pressure; mitochondrial dysfunction; Parkinson’s disease; neuroprotectionCopyright: 2021 by the authors. Licensee MDPI, Basel, Switzerland. This short article is definitely an open access article distributed beneath the terms and circumstances in the Creative Commons Attribution (CC BY) license ( creativecommons.org/licenses/by/ 4.0/).Int. J. Mol. Sci. 2021, 22, 10161. doi.org/10.3390/ijmsmdpi/journal/ijmsInt. J. Mol. Sci. 2021, 22,2 of1. Introduction Parkinson’s disease (PD) is a common, intricate, progressive, multifaceted, and debilitating neurodegenerative illness, which is portrayed by the forfeiture of dopamine (DA) creating nerve cells in the substantia nigra pars compacta (SN-PC). Furthermore, a pathogenic feature of PD will be the accumulation of protein named -synuclein in Lewy bodies (LBs) and Lewy neurites pinpointed inside the nerve cells [1]. Tremor, bradykinesia, rigor, and postural abnormalities emerge as an integral manifestation related with PD [2]. In these below the age of 40, PD is MMP Storage & Stability exceedingly rare, but it impacts almost 1 of individuals more than 605 years of age and presents a comparative larger danger of creating PD in individuals beyond 85 years of age worldwide [3]. The incidence of PD differs amongst genders, with ladies exhibiting lesser vulnerability to establishing PD than men, because of the neuroprotective outcomes rendered by estrogen in the case of ladies [4]. Although the exact etiology of PD is unclear, a variety of genetic and environmental aspects are PARP3 Purity & Documentation believed to play a pivotal function in the progression on the illness [5]. Despite the fact that the vital pathways involved inside the commencement and progression of PD are still unknown, enhanced oxidative stress, ubiquitin-proteasome system (UPS) dysfunction, autophagy-lysosome method dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction are presumed to become actively engaged inside the pathogenesis of PD [5]. Existing pharmacotherapy can only furnish symptomatic relief, and no treat