In addition, it was found that overexpression of a-synuclein in a transgenic mice model WY 14643 caused inclusion body formation in hippocampal neurons, suggesting that high expression of a-synuclein is important for the intracellular accumulation and formation of LBs. Recently, accumulation of a-synuclein was observed at the presynaptic terminals expressing vGluT-1in SNARE protein mutant mice. These reports seem to be consistent with our present results. Intracellular aggregate formation composed of a-synuclein might be related to the endogenous expression level of a-synuclein, which is cell-type specific. In conclusion, we have demonstrated differential expression patterns of a-synuclein between excitatory and inhibitory neurons in vitro. Further studies will elucidate how a-synuclein works differently in the synaptic machinery of excitatory and inhibitory neurons, including in the regulation of the membrane recycling pool. Further analysis of the regulation of intracellular expression of a-synuclein will provide new insights for understanding the pathological conditions of neurodegenerative disorders including PD and DLB. Atherosclerosis is a chronic inflammatory disease in blood vessels that is related to the renin-angiotensin system. Through the angiotensin II type 1 receptor, angiotensin II promotes endothelial dysfunction, induces inflammation, and stimulates the oxidation of plasma lipoproteins in atherosclerotic plaques. Since the endothelial dysfunction denotes the initiation of atherosclerosis, enhanced inflammation promotes the development of vulnerable plaques, and reactive oxygen species exert harmful effects such as the induction of the apoptosis of macrophage and smooth muscle cells, the blockade of the AT1 receptor may suppress atherosclerosis progression and stabilize vulnerable plaques. In agreement with this concern, several experimental studies and clinical trials demonstrated that treatment with angiotensin II AT1 receptor blockers can attenuate atherosclerotic plaque formation, reduce cytokine expression and inflammation levels, and suppress oxidative stress in the vessel wall. Irbesartan, one of the most widely used ARBs, has been suggested as a peroxisome proliferator-activated receptor gamma ligand in addition to its role in the blockade of the AT1 receptor. Since PPARc activation also exerts anti-inflammatory effects and reduces the ROS production, irbesartan may further reduce inflammatory chemokine expression level and suppress apoptotic cell death in atherosclerotic plaque. The antiatherogenic effects of irbesartan, however, have not been fully investigated, and the mechanisms underlying the therapeutic effects remain unclear. Although the beneficial effects of irbesartan can be confirmed by the pathological examination of samples collected after surgery or by the indirect assessment of patient outcomes in clinical settings.