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Biomolecules
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Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies...
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Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies 2.0

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 December 2023) | Viewed by 3907

Special Issue Editor

Prof. Dr. Undurti N. Das

E-Mail Website
Guest Editor
1. UND Life Sciences, 2221 NW 5th St, Battle Ground, WA 98604, USA
2. Department of Medicine, Omega Hospitals, Gachibowli, Hyderabad-500032, India
3. Department of Biotechnology, Indian Institute of Technology, Sangareddy 502284, India
Interests: bioactive lipids; essential fatty acids; polyunsaturated fatty acids; prostaglandins; lipoxins; resolvins; protectins and maresins; reactive oxygen species; lipid peroxidation; cancer; rheumatology; inflammation; immune response; immune checkpoint inhibitors; lupus; radiation induced injury; diabetes mellitus; insulin resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

With the increasing age of the population throughout the world, aging-associated diseases are becoming common. Some of these diseases/disorders include obesity, insulin resistance, type 2 diabetes mellitus, hypertension, metabolic syndrome, coronary heart disease, chronic obstructive lung disease (COPD), gastrointestinal disorders such as lack of appetite, inflammatory bowel disease, and constipation, hepatic disorders (due to alcoholism and previous viral diseases such as HBV and HCV), Alzheimer’s disease, depression, dementia, sarcopenia, osteoporosis, immunodeficiency, autoimmune disorders, and cancer. It is known that some of these diseases do occur in the young, but when they occur in the elderly, they are more difficult to manage due to other associated health issues, such as diabetes mellitus, obesity, osteoporosis, and immunodeficiency. Aging is also associated with reduced wound healing, atherosclerosis, peripheral vascular disease, and decreased ability to fight infections. As the population is aging and with many elderly people actively working, it is essential that the elderly remain healthy, active, and contribute to the economy. In view of this, understanding the pathobiology of aging-associated diseases/disorders is important for the development of newer therapeutic interventions.

In this Special Issue devoted to age-related diseases, we are expecting contributions from scientists, physicians, and others on all aspects of aging. We are particularly interested in receiving manuscripts that describe the molecular events that occur in various age-related diseases/disorders and their potential therapeutic applications. Thus, we wish to bridge the gap between the lab and the clinic and, at the same time, understand the molecular events in various diseases that may also have relevance when those diseases occur in the younger population.

Prof. Dr. Undurti N. Das
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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • aging inflammation
  • cytokines resolution
  • homeostasis
  • diabetes mellitus
  • hypertension diseases disorders

Published Papers (2 papers)

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Research

14 pages, 2345 KiB  
Article
Alzheimer’s Amyloid-β Accelerates Cell Senescence and Suppresses SIRT1 in Human Neural Stem Cells
by Rongyao Li, Yi Li, Haowei Zuo, Gang Pei, Shichao Huang and Yujun Hou
Biomolecules 2024, 14(2), 189; https://doi.org/10.3390/biom14020189 - 04 Feb 2024
Viewed by 1185
Abstract
As a lifelong source of neurons, neural stem cells (NSCs) serve multiple crucial functions in the brain. The senescence of NSCs may be associated with the onset and progression of Alzheimer’s disease (AD). Our study reveals a noteworthy finding, indicating that the AD-associated [...] Read more.
As a lifelong source of neurons, neural stem cells (NSCs) serve multiple crucial functions in the brain. The senescence of NSCs may be associated with the onset and progression of Alzheimer’s disease (AD). Our study reveals a noteworthy finding, indicating that the AD-associated pathogenic protein amyloid-β (Aβ) substantially enhances senescence-related characteristics of human NSCs. These characteristics encompass the enhanced expression of p16 and p21, the upregulation of genes associated with the senescence-associated secretory phenotype (SASP), increased SA-β-gal activity, and the activation of the DNA damage response. Further studies revealed that Aβ treatment significantly downregulates the SIRT1 protein which plays a crucial role in regulating the aging process and decreases downstream PGC-1α and FOXO3. Subsequently, we found that SIRT1 overexpression significantly alleviates a range of Aβ-induced senescent markers in human NSCs. Taken together, our results uncover that Aβ accelerates cellular senescence in human NSCs, making SIRT1 a highly promising therapeutic target for senescent NSCs which may contribute to age-related neurodegenerative diseases, including AD. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies 2.0)
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20 pages, 2927 KiB  
Article
3α,7-Dihydroxy-14(13→12)abeo-5β,12α(H),13β(H)-cholan-24-oic Acids Display Neuroprotective Properties in Common Forms of Parkinson’s Disease
by Andreas Luxenburger, Hannah Clemmens, Christopher Hastings, Lawrence D. Harris, Elizabeth M. Ure, Scott A. Cameron, Jan Aasly, Oliver Bandmann, Alex Weymouth-Wilson, Richard H. Furneaux and Heather Mortiboys
Biomolecules 2023, 13(1), 76; https://doi.org/10.3390/biom13010076 - 30 Dec 2022
Cited by 2 | Viewed by 2264
Abstract
Parkinson’s Disease is the most common neurodegenerative movement disorder globally, with prevalence increasing. There is an urgent need for new therapeutics which are disease-modifying rather than symptomatic. Mitochondrial dysfunction is a well-documented mechanism in both sporadic and familial Parkinson’s Disease. Furthermore, ursodeoxycholic acid [...] Read more.
Parkinson’s Disease is the most common neurodegenerative movement disorder globally, with prevalence increasing. There is an urgent need for new therapeutics which are disease-modifying rather than symptomatic. Mitochondrial dysfunction is a well-documented mechanism in both sporadic and familial Parkinson’s Disease. Furthermore, ursodeoxycholic acid (UDCA) has been identified as a bile acid which leads to increased mitochondrial function in multiple in vitro and in vivo models of Parkinson’s Disease. Here, we describe the synthesis of novel C-nor-D-homo bile acid derivatives and the 12-hydroxy-methylated derivative of lagocholic acid (7) and their biological evaluation in fibroblasts from patients with either sporadic or LRRK2 mutant Parkinson’s Disease. These compounds boost mitochondrial function to a similar level or above that of UDCA in many assays; notable, however, is their ability to boost mitochondrial function to a higher level and at lower concentrations than UDCA specifically in the fibroblasts from LRRK2 patients. Our study indicates that novel bile acid chemistry could lead to the development of more efficacious bile acids which increase mitochondrial function and ultimately cellular health at lower concentrations proving attractive potential novel therapeutics for Parkinson’s Disease. Full article
(This article belongs to the Special Issue Aging and Aging-Associated Diseases: From Molecular Mechanisms to Therapies Strategies 2.0)
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