Neuroprotection by Drugs, Nutraceuticals and Physical Activity

Dear Colleagues,

Acute and chronic neurodegenerative diseases, such as stroke, brain trauma, amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, and Alzheimer's disease are associated with high morbidity and mortality rates. A characteristic of these neurodegenerative diseases is selective neuronal dysfunction and death. The symptoms and the exacerbations of these diseases are, however, very different according to their specific pathways of neuronal impairment. Several mechanisms can lead to neuronal dysfunction and death, including calcium overload, excitatory amino acid release, oxidative stress, inflammation and microglial activation, protein misfolding, proteostasis and mitochondrial disfunction. The clinical management of these diseases is currently very critical as therapeutic strategies are often limited to relieving symptoms rather than treating the disease. Hence, the development of neuroprotective strategies to prevent or delay the neuronal impairment is at the epicenter of the current 21st-century research agenda in biomedicine. The scientific community, in addition to focusing on the development of effective new neuroprotective drugs, is also exploring non-pharmacological approaches by food components, such as nutraceuticals, and physical activity. In this regard, several studies show that nutraceuticals and physical activity have similar or complementary neuroprotection mechanisms, suggesting new integrated approaches with the pharmacological interventions to enhance neuroprotective effects. We invite you to submit your research findings to this Special Issue, which has the aim to present the updated state-of-the-art research on the potential mechanisms of neuroprotection at pre-clinical and clinical level mediated by drugs, nutraceuticals and physical activity. Original research articles, review articles, clinical trials, and meta-analyses are welcome.

Dr. Cristina Angeloni
Dr. Andrea Tarozzi
Topic Editors

Deadline for abstract submissions: 30 July 2022.
Deadline for manuscript submissions: 30 September 2022.

Topic Board

Keywords

  • old and new drugs
  • food supplements, nutraceuticals, and functional foods
  • physical activity and exercise
  • integrated neuroprotective interventions
  • neuroprotective mechanisms
  • neuroprotective strategies
  • new targets for neuroprotection
  • prevention of eurodegeneration
  • neurodegenerative diseases

Relevant Journals List

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Biomedicines
biomedicines
6.081 3.6 2013 16.34 Days 2000 CHF Submit
Current Issues in Molecular Biology
cimb
2.081 4.3 1999 16.15 Days 1600 CHF Submit
International Journal of Molecular Sciences
ijms
5.923 6.0 2000 14.32 Days 2000 CHF Submit
Neurology International
neurolint
- 1.7 2009 22.29 Days 1000 CHF Submit
Pharmaceuticals
pharmaceuticals
5.863 4.6 2004 13.7 Days 1800 CHF Submit

Published Papers (1 paper)

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Article
Farnesol Ameliorates Demyelinating Phenotype in a Cellular and Animal Model of Charcot-Marie-Tooth Disease Type 1A
Curr. Issues Mol. Biol. 2021, 43(3), 2011-2021; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb43030138 (registering DOI) - 13 Nov 2021
Abstract
Charcot-Marie-Tooth disease (CMT) is a genetically heterogeneous disease affecting the peripheral nervous system that is caused by either the demyelination of Schwann cells or degeneration of the peripheral axon. Currently, there are no treatment options to improve the degeneration of peripheral nerves in [...] Read more.
Charcot-Marie-Tooth disease (CMT) is a genetically heterogeneous disease affecting the peripheral nervous system that is caused by either the demyelination of Schwann cells or degeneration of the peripheral axon. Currently, there are no treatment options to improve the degeneration of peripheral nerves in CMT patients. In this research, we assessed the potency of farnesol for improving the demyelinating phenotype using an animal model of CMT type 1A. In vitro treatment with farnesol facilitated myelin gene expression and ameliorated the myelination defect caused by PMP22 overexpression, the major causative gene in CMT. In vivo administration of farnesol enhanced the peripheral neuropathic phenotype, as shown by rotarod performance in a mouse model of CMT1A. Electrophysiologically, farnesol-administered CMT1A mice exhibited increased motor nerve conduction velocity and compound muscle action potential compared with control mice. The number and diameter of myelinated axons were also increased by farnesol treatment. The expression level of myelin protein zero (MPZ) was increased, while that of the demyelination marker, neural cell adhesion molecule (NCAM), was reduced by farnesol administration. These data imply that farnesol is efficacious in ameliorating the demyelinating phenotype of CMT, and further elucidation of the underlying mechanisms of farnesol’s effect on myelination might provide a potent therapeutic strategy for the demyelinating type of CMT. Full article
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