Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder,
characterized by the deposition of amyloid-β within the brain parenchyma resulting in a significant
decline in cognitive functions. The pathophysiological conditions of the disease are recognized by
the perturbation of synaptic function, energy and lipid metabolism. In Addition deposition of amyloid
plaques also triggers inflammation upon the induction of microglia. Peroxisome proliferatoractivated
receptors (PPARs) are ligand-activated transcription factors known to play important role
in the regulation of glucose absorption, homeostasis of lipid metabolism and are further known to
involved in repressing the expression of genes related to inflammation. Therefore, agonists of this
receptor represent an attractive therapeutic target for AD. Recently, both clinical and preclinical
studies showed that use of Peroxisome proliferator-activated receptor gamma (PPARγ) agonist
improves both learning and memory along with other AD related pathology. Thus, PPARγ signifies
a significant new therapeutic target in treating AD. In this review, we have shed some light on the
recent progress of how, PPARγ agonist selectively modulated different cellular targets in AD and
its amazing potential in the treatment of AD.
Keywords: Alzheimer's disease, Peroxisome proliferator-activated receptors, Transactivation, β-amyloid, Thiazolidinedione,
Insulin sensitivity, Rosiglitazone, Blood-brain-barrier.
Toledo EM, Inestrosa NC. 2010.
Fehm HL, Kern W, Peters A. The selfish brain: competition for energy resources. 2006.
Tong M, Dominguez C, Didsbury J, de la Monte SM. Targeting alzheimer’s disease Neuro-Metabolic Dysfunction with a small molecule nuclear receptor agonist (T3D-959) reverses disease pathologies. J Alzheimers Dis Parkinsonism 2016; 6(3): 238.
Rights & PermissionsPrintExport