PD (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
A Review on Chemistry of Anti-malarials
