ArticleThe Kaohsiung journal of medical sciences2025
Association Between Angiotensin-Converting Enzyme (ACE) Gene Insertion/Deletion (I/D) Polymorphism Genotypes With Brain Volume and Hypertension in Alzheimer's Disease-A Retrospective Study.
Article in The Kaohsiung journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Association Between Angiotensin-Converting Enzyme (ACE) Gene Insertion/Deletion (I/D) Polymorphism Genotypes With Brain Volume and Hypertension in Alzheimer's Disease-A Retrospective Study.The Kaohsiung journal of medical sciences · 2025Article
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4 authors.
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Abstract
This study investigates the role of the ACE I/D polymorphism in Alzheimer's disease (AD) patients, particularly in relation to hypertension and its influence on brain volume. Seventy-seven AD patients, diagnosed based on Aging and Alzheimer's Association criteria, were enrolled from the Kaohsiung Municipal Ta-Tung Hospital Dementia Cohort. ACE I/D genotypes were identified through polymerase chain reaction, and various factors such as age, sex, education, brain volume, and neuropsychological test scores were analyzed. The results indicated that ACE genotypes, presence of apolipoprotein epsilon 4 (APOEε4), and brain volume did not significantly differ between patients with and without hypertension. While age and sex were associated with gray matter volume, cerebrospinal fluid volume correlated with age, sex, and hypertension. Total cranial volume was linked to sex, and the cerebrospinal fluid-to-total intracranial volume ratio was influenced by sex and education. Overall, ACE I/D genotypes and APOEε4 did not have a significant impact on brain volume in AD patients, regardless of hypertension status. Instead, brain atrophy was associated with sex, age, education, and hypertension. These findings suggest that although ACE may not significantly influence brain volume in AD patients, further large-scale studies are needed to clarify its role in AD pathogenesis.
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