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Special Issue Information

Dear Colleagues,

This Special Issue aims to develop our understanding of the transition of middle-life processes from normal aging to disease. Recent studies on the human genome, including on genome-wide association studies (GWAS), have identified the metabolism and diabetes genes that are risk indicators of dementia. These represent the comorbidities of multiple diseases that are associated with dementia. A goal of those studies is to apply to direct-to-consumer (DTC) genomics in which we could predict the risk of each disease by looking at the genetic data. However, how the genes mediate the transition of middle-life to late-life problems such as dementia has yet to be adequately explored. This Special Issue emphasizes but is not limited to the involvement or association of metabolism and diabetes with dementia, including neurodegenerative diseases such as Alzheimer’s disease. Particularly, model systems will be useful to understand the mechanisms in humans. We would like to invite a collection of heritable knowledge toward the middle-life crisis theory of aging, which explains the transition from young to old.

Prof. Shin Murakami
Guest Editor

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Keywords

meta-analysis
genome-wide association studies (GWAS)
genetics
dyslipidemia
hypertension
molecular mechanisms
model systems

Published Papers (1 paper)

Review

10 pages, 893 KiB

Open AccessReview

Two Opposing Functions of Angiotensin-Converting Enzyme (ACE) That Links Hypertension, Dementia, and Aging

by Duc Le, Lindsay Brown, Kundan Malik and Shin Murakami

Int. J. Mol. Sci. 2021, 22(24), 13178; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413178 - 07 Dec 2021

Cited by 19 | Viewed by 5591

Abstract

A 2018 report from the American Heart Association shows that over 103 million American adults have hypertension. The angiotensin-converting enzyme (ACE) (EC 3.4.15.1) is a dipeptidyl carboxylase that, when inhibited, can reduce blood pressure through the renin–angiotensin system. ACE inhibitors are used as a first-line medication to be prescribed to treat hypertension, chronic kidney disease, and heart failure, among others. It has been suggested that ACE inhibitors can alleviate the symptoms in mouse models. Despite the benefits of ACE inhibitors, previous studies also have suggested that genetic variants of the ACE gene are risk factors for Alzheimer’s disease (AD) and other neurological diseases, while other variants are associated with reduced risk of AD. In mice, ACE overexpression in the brain reduces symptoms of the AD model systems. Thus, we find two opposing effects of ACE on health. To clarify the effects, we dissect the functions of ACE as follows: (1) angiotensin-converting enzyme that hydrolyzes angiotensin I to make angiotensin II in the renin–angiotensin system; (2) amyloid-degrading enzyme that hydrolyzes beta-amyloid, reducing amyloid toxicity. The efficacy of the ACE inhibitors is well established in humans, while the knowledge specific to AD remains to be open for further research. We provide an overview of ACE and inhibitors that link a wide variety of age-related comorbidities from hypertension to AD to aging. ACE also serves as an example of the middle-life crisis theory that assumes deleterious events during midlife, leading to age-related later events. Full article

(This article belongs to the Special Issue The Molecular Mechanism of Dementia and Age-Related Comorbidity)

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