**6. Concluding remarks**

In conclusion, this chapter has provided a broad overview of the role of oxidative stress, ROS, and lipoprotein oxidation in the pathophysiology of disease states such as atherosclerosis, Alzheimer's disease and diabetes. While Ox-LDL and inflammation seem to be bona fide factors in the development of atherosclerosis, the role of dysfunctional HDL in these disease states is not known at this point. There are several points of uncertainty regarding the *in vivo* source of ROS and oxidative stress, the physiological behavior of oxidized lipoproteins, particularly in Alzheimer's disease and diabetes, and the line-up of antioxidants and autoantibodies in response to the oxidized factors. It is anticipated that the next decade will provide more insights into the molecular and mechanistic basis of the effect of oxidative damage on lipoprotein in disease states. This would pave the way for new therapeutic options for preventing and treating these diseases.
