Abstract: The increasing incidence of Alzheimer’s disease (AD) in the aging population, indicates the critical need for the development of novel targeted molecular therapies for ameliorating AD pathology. Moreover, clinical and pre-clinical evidence demonstrates that peroxisomal proliferator activating receptors (PPAR) agonists regulate energy and lipid homeostasis in models of diabetes, as well as improve spatial memory in animal models of AD (Khan et al., 2019). Mechanistically, PPARs are nuclear transcription factors that form heterodimeric complexes with retinoid X receptors. PPARs are key mediators responsible for the activation of genes involved in cell metabolism, differentiation, and development. More specifically they regulate the transcription of genes associated with energy homeostasis e.g., glucose metabolism, lipid transport, insulin sensitivity, mitochondrial biogenesis, and thermogenesis. They exists in three highly conserved isoforms, gamma (γ), delta (δ/β), and alpha (α). These highly conserved isoforms are well known for their clinical importance for example; PPARα agonists include the fibrates class of drugs (hypercholesterolemia) and PPARα consist of the thiazolidinedione class of drugs for type 2 diabetes (Zhang et al., 2020). Considering these findings, extensive investigation on PPAR agonists, showed reduced levels of amyloid plaques and tau hyperphosphorylation i.e., pathological hallmarks of AD via exhibiting anti-inflammatory properties, regulating ATP metabolism by reducing oxidative stress in mitochondria and improving symptoms associated with behavioral deficits and cognitive decline (Zhen et al., 2023).