Antioxidant Capability and Physical Exercise in Neurobiology: A Focus in Neurodegeneration II

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (20 April 2023) | Viewed by 2100

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Guest Editor
Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy
Interests: oxidative stress; brain function; neurodegeneration; antioxidant capability; physical exercise
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Special Issue Information

Dear Colleagues,

Neurodegenerative processes have been linked not only to genetic factors, but also to environmental ones. Among these, a pivotal role has been largely attributed to oxidative stress, which arises from an imbalance between an excessive generation of reactive oxygen species (ROS) and the biological system’s capability to eliminate the reactive intermediates. Oxidative stress leads to a progressive decline in cell physiology by damaging cellular macromolecular components such as DNA, lipids, and proteins.

Several studies have demonstrated that regular exercise is an important preventive and therapeutic tool in neurodegeneration and cerebrovascular diseases. The adaptive response to regular exercise involves the upregulation of the enzymatic antioxidant system and modulation of oxidative damage, which culminate in a recovered redox state of brain cells. In addition to a reduction in oxidative damage, the effects of exercise seem to be quite intricate, including an increase in neurogenesis and capillarization and an enhanced proteolytic degradation of toxic oligomers that characterize aging and neurodegenerative processes. All together, these data highlight the link between neurodegeneration, oxidative stress, and physical exercise.

This Special Issue aims to provide an overview of the current knowledge on the physiological, metabolic, and epigenetic modifications in response to physical activity and its final effects on brain functionality, both in physiological and in pathological conditions.

Potential topics include, but are not limited to, the following:

  • Studies of the cellular and molecular mechanisms associated with oxidative stress in neurodegenerative diseases;
  • Clinical or preclinical studies showing physical exercise properties in brain functionality.

Dr. Ferdinando Franzoni
Guest Editor

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Keywords

  • physical exercise
  • oxidative stress
  • brain function
  • neurodegeneration
  • antioxidant capability

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Published Papers (1 paper)

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Research

17 pages, 12441 KiB  
Article
JAC4 Alleviates Rotenone-Induced Parkinson’s Disease through the Inactivation of the NLRP3 Signal Pathway
by Lu Zou, Zhen Che, Kun Ding, Chao Zhang, Xia Liu, Luman Wang, Aiping Li and Jianwei Zhou
Antioxidants 2023, 12(5), 1134; https://doi.org/10.3390/antiox12051134 - 20 May 2023
Cited by 2 | Viewed by 1794
Abstract
Parkinson’s disease (PD) is the fastest-growing neurodegeneration disease, characterized typically by a progressive loss of dopaminergic neurons in the substantia nigra, and there are no effective therapeutic agents to cure PD. Rotenone (Rot) is a common and widely used pesticide which can directly [...] Read more.
Parkinson’s disease (PD) is the fastest-growing neurodegeneration disease, characterized typically by a progressive loss of dopaminergic neurons in the substantia nigra, and there are no effective therapeutic agents to cure PD. Rotenone (Rot) is a common and widely used pesticide which can directly inhibit mitochondrial complex I, leading to a loss of dopaminergic neurons. Our previous studies proved that the JWA gene (arl6ip5) may play a prominent role in resisting aging, oxidative stress and inflammation, and JWA knockout in astrocytes increases the susceptibility of mice to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. JWA-activating compound 4 (JAC4) is a small-molecule activator of the JWA gene, but its role in and mechanism against PD have not yet been clarified. In the present study, we showed that the JWA expression level is strongly related to tyrosine hydroxylase (TH) in different growth periods of mice. Additionally, we constructed models with Rot in vivo and in vitro to observe the neuroprotective effects of JAC4. Our results demonstrated that JAC4 prophylactic intervention improved motor dysfunction and dopaminergic neuron loss in mice. Mechanistically, JAC4 reduced oxidative stress damage by reversing mitochondrial complex I damage, reducing nuclear factor kappa-B (NF-κB) translocation and repressing nucleotide-binding domain, leucine-rich-containing family and pyrin domain-containing-3 (NLRP3) inflammasome activation. Overall, our results provide proof that JAC4 could serve as a novel effective agent for PD prevention. Full article
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