Objective: Angiotensin-converting enzyme(ACE) insertion/deletion(I/D) polymorphisms are considered biomarkers of late-onset Alzheimer's disease(AD). However, the results of studies of these polymorphisms have been...Objective: Angiotensin-converting enzyme(ACE) insertion/deletion(I/D) polymorphisms are considered biomarkers of late-onset Alzheimer's disease(AD). However, the results of studies of these polymorphisms have been inconsistent. The ACE protein directly degrades beta-amyloid and thereby slows the progression of AD and its onset. However, it also activates the renin–angiotensin–aldosterone system, which can contribute to hypertension and/or cardiovascular events that increase the risk for developing AD. Methods: In this study, we examined the bidirectional association of the ACE gene and AD in patients with AD with and without hypertension. Results: Patients who were clinically diagnosed with AD(n = 983) underwent ACE I/D genotyping. The distribution of the ACE I/D genotypes(P = 0.355 for I/I vs. D/D; P = 0.888 for I/D vs. D/D) and I alleles(P = 0.895) did not significantly differ between hypertensive patients with AD and patients with AD without hypertension. Conclusions: In contrast to traditional theories, the results of this study suggested that the contribution of the ACE gene to the development of AD was not associated with hypertension and similar cardiovascular effects.展开更多
基金Supported by the Kaohsiung Medical University Hospital 2T05
文摘Objective: Angiotensin-converting enzyme(ACE) insertion/deletion(I/D) polymorphisms are considered biomarkers of late-onset Alzheimer's disease(AD). However, the results of studies of these polymorphisms have been inconsistent. The ACE protein directly degrades beta-amyloid and thereby slows the progression of AD and its onset. However, it also activates the renin–angiotensin–aldosterone system, which can contribute to hypertension and/or cardiovascular events that increase the risk for developing AD. Methods: In this study, we examined the bidirectional association of the ACE gene and AD in patients with AD with and without hypertension. Results: Patients who were clinically diagnosed with AD(n = 983) underwent ACE I/D genotyping. The distribution of the ACE I/D genotypes(P = 0.355 for I/I vs. D/D; P = 0.888 for I/D vs. D/D) and I alleles(P = 0.895) did not significantly differ between hypertensive patients with AD and patients with AD without hypertension. Conclusions: In contrast to traditional theories, the results of this study suggested that the contribution of the ACE gene to the development of AD was not associated with hypertension and similar cardiovascular effects.
