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Neurodegeneration and Countermeasures to Slow Down Its Onset

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

Deadline for manuscript submissions: 10 June 2024 | Viewed by 1620

Special Issue Editors


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Guest Editor
Department of Systems Medicine, “Tor Vergata” University of Rome, 00133 Rome, Italy
Interests: neurophysiology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Systems Medicine, “Tor Vergata” University of Rome, 00133 Rome, Italy
Interests: neuromuscular conditioning
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Systems Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
Interests: exercise; aging; whole body vibration; musculoskeletal diseases; osteoporosis; sarcopenia; neurodegeneration; quality of life; microgravity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the last century, the quality of life has improved considerably and with it the possibility of leading a longer and more comfortable life. Unfortunately, longer life expectancy has a “dark side”: an aging population. Indeed, the average age of the world’s population is increasing, which inevitably leads to the prevalence of numerous age-dependent pathological conditions. One of the main problems afflicting the elderly population is cognitive decline, which markedly affects psycho-physical well-being, predisposing affected individuals to isolation and rapidly worsening health conditions. Unfortunately, the molecular mechanisms responsible for this cognitive impairment have not yet been fully elucidated, making it difficult to develop countermeasures to both prevent and/or delay its onset and counter its progression. Adopting a healthy lifestyle from a young age, based on constant exercise and a healthy diet, maybe the most powerful weapon in our possession. Indeed, regular exercise can promote the production of numerous neurotrophic factors that protect against neurodegeneration. Similarly, a diet based on regular consumption of omega-3 fatty acids, antioxidants, and polyphenols improves cognitive performance and reduces the onset of neurodegenerative diseases. Nevertheless, an in-depth study of these strategies is needed to optimize their potential, as well as to explore further avenues that could promote cognitive well-being. Therefore, this special issue aims to bring together the latest evidence on the molecular processes leading to neurodegeneration and potential countermeasures to counter its adverse course.

Prof. Dr. Giovanna D'Arcangelo
Prof. Dr. Giuseppe Annino
Dr. Ida Cariati
Guest Editors

Manuscript Submission Information

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Keywords

  • neurodegeneration
  • cognitive decline
  • aging
  • countermeasures
  • physical exercise
  • nutrition
  • prevention

Published Papers (1 paper)

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Research

21 pages, 4094 KiB  
Article
Aerobic Exercise Facilitates the Nuclear Translocation of SREBP2 by Activating AKT/SEC24D to Contribute Cholesterol Homeostasis for Improving Cognition in APP/PS1 Mice
by Zelin Hu, Yangqi Yuan, Zhen Tong, Meiqing Liao, Shunling Yuan, Weijia Wu, Yingzhe Tang, Yirong Wang, Changfa Tang and Wenfeng Liu
Int. J. Mol. Sci. 2023, 24(16), 12847; https://doi.org/10.3390/ijms241612847 - 16 Aug 2023
Cited by 1 | Viewed by 1291
Abstract
Impaired cholesterol synthesizing ability is considered a risk factor for the development of Alzheimer’s disease (AD), as evidenced by reduced levels of key proteases in the brain that mediate cholesterol synthesis; however, cholesterol deposition has been found in neurons in tangles in the [...] Read more.
Impaired cholesterol synthesizing ability is considered a risk factor for the development of Alzheimer’s disease (AD), as evidenced by reduced levels of key proteases in the brain that mediate cholesterol synthesis; however, cholesterol deposition has been found in neurons in tangles in the brains of AD patients. Although it has been shown that statins, which inhibit cholesterol synthesis, reduce the incidence of AD, this seems paradoxical for AD patients whose cholesterol synthesizing capacity is already impaired. In this study, we aimed to investigate the effects of aerobic exercise on cholesterol metabolism in the brains of APP/PS1 mice and to reveal the mechanisms by which aerobic exercise improves cognitive function in APP/PS1 mice. Our study demonstrates that the reduction of SEC24D protein, a component of coat protein complex II (COPII), is a key factor in the reduction of cholesterol synthesis in the brain of APP/PS1 mice. 12 weeks of aerobic exercise was able to promote the recovery of SEC24D protein levels in the brain through activation of protein kinase B (AKT), which in turn promoted the expression of mem-brane-bound sterol regulatory element-binding protein 2 (SREBP2) nuclear translocation and the expression of key proteases mediating cholesterol synthesis. Simultaneous aerobic exercise restored cholesterol transport capacity in the brain of APP/PS1 mice with the ability to efflux excess cholesterol from neurons and reduced neuronal lipid rafts, thereby reducing cleavage of the APP amyloid pathway. Our study emphasizes the potential of restoring intracerebral cholesterol homeostasis as a therapeutic strategy to alleviate cognitive impairment in AD patients. Full article
(This article belongs to the Special Issue Neurodegeneration and Countermeasures to Slow Down Its Onset)
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