Intima thickening and constrictive geometric remodeling of the artery wall are primary changes associated with the decreased lumen. Expansive remodeling of the wall tends to preserve the lumen in the face of increased lesion burden. Therefore, the thicker intima-media and lower wall stress in diabetics may partly explain the protective effect of diabetes against AbMole Povidone iodine aneurysm development. Hypertension is considered a risk for aneurysmal rupture. Previous studies have found that hypertension is more common in the diabetic population than in the general nondiabetic population, and hypertension and/or insulindependent diabetes mellitus significantly increases cerebral IA formation. In the current study, we investigated the effects of T1DM alone on the regulation of IA formation. The effects of diabetes in combination with hypertension on the IA formation and progression warrants further investigation. In addition, tPA thrombolysis could induce rupture of 
cerebral aneurysms and also increase IA formation. While tPA treatment of ischemic stroke in T1DM stroke rats significantly increases brain hemorrhage formation, whether the brain hemorrhage formation induced by tPA treatment is related with IA formation in T1DM animals, requires further investigation. AGEs accumulate in the vessel wall and are implicated in both the microvascular and macrovascular complications of diabetes. The expression of the AGE receptor RAGE is upregulated in endothelial cells, smooth muscle cells, and mononuclear phagocytes in diabetic vasculature, and such upregulation is linked to the inflammatory response, and it accelerates the development of atherosclerosis in patients with diabetes. It has been generally accepted that the occurrence of aneurysm is related to the presence of severe atherosclerosis in the circulation. Increased RAGE expression was detected in aneurysm formation in animal models and in human patients. RAGE affects the aneurysmal formation via nuclear factor kappa-light-chainenhancer of activated B cells pathway to activate MMP9 expression. In addition, TLR4 initiates inflammation in diabetics and plays an important role in arteriosclerosis by inducing inflammation responses. TLR4 expression is apparently upregulated in the endothelial cell layer and adventitia of aneurysm walls, and increases MMP9 expression in macrophages, which promote aneurysmal formation. MMP9 degrades especially type IV collagen, the main constituent of the basement membrane, and contributes to development of vascular lesions. MMP9 is also involved in abdominal aortic aneurysm formation. Inhibition of MMP9 therapy results in attenuation of aneurysm formation by suppression of inflammation of the aortic wall. We found that diabetes significantly resulted in increased expression of RAGE, TLR4 and MMP9 in damaged arteries which also correlated with intracranial formation of aneurysms.