ors. The PKD1 Storage & Stability molecular mechanisms, encompassing oxidative anxiety, UPS dysfunction, autophagy-lysosome program dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction are actively engaged within the pathogenesis of PD. On account of the single target regulation offered by current pharmacotherapy, this makes the abolition of disease progression all but impossible. Hence, neuronal protection could be correctly achieved using the help of such pharmacological substances that hold the prospective to regulate a number of molecular and pathogenic mechanisms in the exact same time. New expanding corroborations have revealed that PPAR agonists have the prospective to alter and regulate multiple molecular mechanisms at the transcriptional level by means of prompting gene expression. Many PPAR agonists/substances, as an illustration, pioglitazone, rosiglitazone, GW-501516, L-165041, GW0742, fenofibrate, benzafibrate, and MHY908 have been reported to act in the transcriptional level and thereby emerge as neoteric and propitious targets inside the therapy of neurodegenerative illnesses. Additional experimental studies are necessary to achieve an in-depth understanding of PPARs, their agonists, their neuroprotective outcomes, and their benefits and shortcomings so that you can overcome neuronal degeneration. Eventually, a comprehensive knowledge in the molecular pathways by means of which PPARs render neuronal protection would help in the development of a potentially efficient remedy into clinical practice for the therapy of PD.Author Contributions: Conceptualization, T.B. and P.M.; methodology, T.B. and S.G.B.; investigation, T.B. and P.M..; resources, T.B.; information curation, S.S., N.S. and S.B.; writing–original draft preparation, T.B., P.M. and S.G.B.; writing–review and editing, T.B., A.A.-H. and S.G.B.; visualization, A.S., S.C. and I.A.; supervision, T.B. and S.G.B. All authors have read and agreed for the published version of the manuscript. Funding: This study received no external funding. University of Oradea, Oradea, Romania, Internal plan. Institutional Evaluation Board Statement: Not applicable. Informed Consent Statement: Not applicable. Acknowledgments: The authors are thankful to Chitkara College of Pharmacy, Chitkara University, Punjab, India for giving the many sources for completion with the short article and to University of Oradea, Oradea, Romania for supporting its publication. Conflicts of Interest: The authors declare no conflict of interest.AbbreviationsPD, Parkinson’s illness; DA, dopamine; SN-PC, substantia nigra pars compacta; UPS, ubiquitinproteasome program; PPARs, Peroxisome proliferator-activated receptors; NHR, nuclear hormone receptors; NSAIDs, non-steroidal anti-inflammatory drugs; LBs, lewy S1PR4 Source bodies; RXR, retinoid X receptors; PPREs, peroxisome proliferator response components; FA, fatty acids; H2 O2 , hydrogen peroxide; N, amino; DNA, deoxyribonucleic acid; C, carboxy; L-165041, [4-[3-(4-Acetyl-3-hydroxy-2propylphenoxy)propoxy]phenoxy]acetic acid; GW-501516, 2-[2-methyl-4-[[4-methyl-2-[4-(trifluorom ethyl)phenyl]-1,3-thiazol-5-yl]methylsulfonyl]phenoxy]acetic acid; TZDs, thiazolidinediones; NFB, nuclear factor kappa B; ATF-1, activating transcription factor-1; ATF-4, activating transcription factor-4; STAT, signal transducer and activator of transcription; COX-2, cyclooxygenase-2; NO, nitric oxide; CREB, cyclic AMP-response element binding protein; RELA, REL-associated protein; IB, IkappaB alpha; AP-1, activator protein-1; O2 , oxygen; mtDNA,
