Association between genetic polymorphism of angiotensin-converting enzyme gene and Parkinson's disease

The insertion/deletion polymorphism in the angiotensin-converting enzyme and susceptibility to schizophrenia or Parkinson’s disease: A meta-analysis

“…[11][12][13][14][15][16][17][18][19][20][21][22][23][31][32][33] Three studies were excluded because they contained no data. [31][32][33] Thus, a total of 13 studies met our inclusion criteria: [11][12][13][14][15][16][17][18][19][20][21][22][23] eight schizophrenia studies and five PD studies ( Figure 1). With regard to ethnicity, three European, four Asian, and three Turkish studies, as well as one Jewish, one Australian, and one Latin American study, were analyzed.…”

The angiotensin-converting enzyme (ACE) I/D polymorphism in Parkinson’s disease

“…Most studies indicated a nonsignificant association in Caucasians or Latin Americans, 4,[6][7][8] while one study suggested significant association in a Chinese population. 5 Thus, the aim of the present study using meta-analysis was to clarify the relationship between ACE I/D polymorphism and PD across different ethnic populations.…”

The role of the central renin-angiotensin system in Parkinson’s disease

“…Substance P can also be hydrolysed by ACE, 22 and this feature might be important since a primary loss of substance P has been linked with the pathogenesis of several neurological diseases including Parkinson's disease. 29,30 Fourthly, an association between genetic polymorphism of the ACE gene and Parkinson's disease has been described in Taiwan. 29 However, in the Australian and Italian population, no correlation between genetic polymorphism of the ACE gene and Parkinson's disease could be detected.…”

“…29,30 Fourthly, an association between genetic polymorphism of the ACE gene and Parkinson's disease has been described in Taiwan. 29 However, in the Australian and Italian population, no correlation between genetic polymorphism of the ACE gene and Parkinson's disease could be detected. 31,32 Finally, stimulation of AT 1 receptors by angiotensin II has been shown to activate NADPH-dependent oxidases which are a major source of reactive oxygen species (ROS).…”