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The Molecular Mechanism of Dementia and Age-Related Comorbidity
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The Molecular Mechanism of Dementia and Age-Related Comorbidity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 8441

Special Issue Editor

Prof. Dr. Shin Murakami

E-Mail Website
Guest Editor
Department of Basic Sciences, College of Osteopathic Medicine, Touro University California, Vallejo, CA, USA
Interests: aging; stress resistance; age-related memory impairment (AMI); dementia in basic and medical sciences
Special Issues, Collections and Topics in MDPI journals

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

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

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Published Papers (1 paper)

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Review

10 pages, 893 KiB  
Review
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://doi.org/10.3390/ijms222413178 - 7 Dec 2021
Cited by 30 | Viewed by 7860
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 [...] Read more.
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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