**6. Conclusions**

Clinically and pathologically, atherosclerosis is an important disease in a worldwide aging society. It has been shown that innate immune factors and adaptive immune factors are associated with the atherosclerotic process since inflammatory mechanisms are identified as major causes in patients. A number of studies have identified several potential targets for therapy. Unfortunately, however, inflammation is an independent risk factor for atherosclerosis progression in humans. Researchers have tried to evaluate the mechanism of immunerelated therapies in atherosclerotic cardiovascular disease. Along with inflammation-related mechanisms, autophagy in atherosclerosis is also responsible for the foam cell formation and insoluble oxLDL uptake and clearance in human atherosclerotic lesions. Autophagic macrophages produce pro-inflammatory cytokines such as TNF-beta and interleukin-6, and these cytokines are not immunologically silenced during the autophagic process. Lipid droplets are spilled from lipid-overloaded macrophages in the plaques. Based on previous research, future studies are focusing on therapeutic advantages of autophagic microphages in unstable atherosclerotic plaques.

Despite efforts to develop strong therapeutic targets, it is not feasible to establish respective contributors to degeneration and vascular disease onset and progression in each patient. Today, in our aging society, dementia has becoming an important issue in the public heath, economics, and social aspects, and also in political fields. With careful converging and treating on vascular risk factors containing atherosclerosis, it would get available therapeutic strategies for prognosis and diagnosis in patients with progressive dementia.
