Therapeutic Actions of the Thiazolidinediones in Alzheimer’s Disease

Figure 1

Targets of thiazolidinediones drugs in Alzheimer’s disease. The TZDs can bind to PPARγ receptors and other pathways that regulate energy metabolism, in cellular and animal models of AD. In cognition and behavioral test, these drugs increase the memory performance of the animals and also decrease the Aβ deposits accelerating the amyloid plaque clearance. At more cellular levels, TZDs promote the neuronal survival, differentiation, and synaptic plasticity and also increase the phagocytosis and reduce neuroinflammation both in astrocytes and in microglia. In the mitochondria, TZDs induce biogenesis and enhance the mitochondrial function observed by a rise in the respiratory complex activities and reduction of the oxidative stress. Finally, TZDs are capable of reducing tau phosphorylation through the inhibition of different kinases activities and the later formation of the neurofibrillary tangles presented in AD.