Our data did not show a significant difference in Hcy and CRP between the PD and VP groups. This result demonstrates that the inflammatory mediators Hcy and CRP might contribute equally to the progression of these two diseases. Interestingly, when we separated the subjects into two groups according to age, we noticed that the CRP levels in PD subjects above 60 years old were much higher than those patients under 60, whereas the Hcy levels in VP subjects above GSK864 were less than those under 60. Two reasons probably led to the discrepancy in the CRP and Hcy levels in patients with PD. First, as a neurodegenerative disease, PD exacerbates with age, and the inflammatory process aggravates the progression in PD patients above 60 when compared to patients under 60. This exacerbated inflammatory response in PD patients above 60 can be reflected in the obviously elevated levels of CRP,GSK864 a biomarker of systemic inflammation. Second, Hcy, though recognized as an indicator of neurotoxic mediator, is profoundly affected by several factors, such as some B-vitamin deficiencies, genetic polymorphisms of MTHFR and CßS, and L-dopa intake. These influences may have lead to the unchanged level of Hcy between PD patients above and under 60 in this study. We did not observe a significantly changed level of CRP, but we did observe a significant upregulation of Hcy in VP patients above CD1530 when compared with those under 67. The precise reasons remain unclear, but it may reflect a different pathogenesis for PD and VP, the latter of which mainly results from subcortical vascular causes; additionally, Hcy is obviously increased in cerebral-vascular diseases. Our findings suggest that the chronic inflammatory response may be worse in older PD patients and that an anti-inflammatory strategy would be useful in the management of PD. The prevalence of obesity, type 2 diabetes mellitus and risk factors associated with the metabolic syndrome has increased dramatically over the past 30 years. Insulin resistance is associated with obesity and is the main indicator of early stages of type 2 diabetes. Intracellular lipid accumulation in non-adipose tissue, such as liver and skeletal muscle, is one of the most likely causes of dysfunction of these tissues with regards to insulin resistance.