Journal
CURRENT NEUROPHARMACOLOGY
Volume 17, Issue 3, Pages 232-246Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570159X16666180828100002
Keywords
Alzheimer's disease; Peroxisome proliferator-activated receptors; Transactivation; beta-amyloid; Thiazolidinedione; Insulin sensitivity; Rosiglitazone; Blood-brain-barrier
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Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder, characterized by the deposition of amyloid-beta 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 proliferator-activated 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 (PPAR gamma) agonist improves both learning and memory along with other AD related pathology. Thus, PPAR gamma signifies a significant new therapeutic target in treating AD. In this review, we have shed some light on the recent progress of how, PPAR gamma agonist selectively modulated different cellular targets in AD and its amazing potential in the treatment of AD.
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