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Research Advances in Neurodegeneration and Neuropathy
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Research Advances in Neurodegeneration and Neuropathy

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: closed (20 January 2025) | Viewed by 4190

Special Issue Editor

Dr. Yi-Hung Chen

E-Mail Website
Guest Editor
Chinese Medicine Research Center, China Medical University, Taichung 40402, Taiwan
Interests: neuropharmacology; stem cell; neurodegeneration; itching; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over the past few years, some medications have been shown to have the effect of neuroprotection on neurodegenerative diseases through the regulation of synaptic plasticity, mitochondria functions, orexin systems, autophagocytosis, neuroinflammation, intestinal microbiota, etc. Furthermore, the application of the human gene project, the development of artificial intelligence, and new automatic behavior monitors rapidly expanded the vision of clinical and basic molecular research of neurodegenerative diseases and neuropathy.

For an upcoming Issue in the International Journal of Molecular Sciences, we encourage researchers to submit original research articles on neurobiology, as well as review articles.

Topics for this Special Issue include, but are not limited to:

  • Molecular mechanisms on neuroprotection such as: synaptic proteins, DNA repair, apoptosis, autophagy, mitochondria, gene expression, signaling pathway, neuroinflammation, neuron regeneration, vascular remodeling, and Tau protein
  • Mechanisms of neurohormonal, neurotransmitter, and neuropeptides 
  • High-throughput technologies: genomics, epigenomics, proteomics, metabolomics, microarray, next-generation sequencing, and other omics technologies
  • Genomic and proteomic databases and applications
  • Automatic behavior monitors in the neurodegenerative or neuropathy animal model study

Dr. Yi-Hung Chen
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.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • mechanism
  • neurodegenerative disease
  • neuropathy

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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19 pages, 2929 KiB  
Article
TRPM8′s Role in the Shift Between Opioid and Cannabinoid Pathways in Electroacupuncture for Inflammatory Pain in Mice
by Dinh-Trong Pham, Rae-Mann Hsu, Mao-Feng Sun, Chien-Chen Huang, Yi-Hung Chen and Jaung-Geng Lin
Int. J. Mol. Sci. 2024, 25(23), 13000; https://doi.org/10.3390/ijms252313000 - 3 Dec 2024
Viewed by 1355
Abstract
The TRPM8 channel, a temperature-sensitive ion channel, plays a crucial role in various physiological processes, particularly in the modulation of inflammation and nociception. Although electroacupuncture (EA) is a recognized analgesic treatment for pain conditions, its interaction with TRPM8 remains underexplored. This study aims [...] Read more.
The TRPM8 channel, a temperature-sensitive ion channel, plays a crucial role in various physiological processes, particularly in the modulation of inflammation and nociception. Although electroacupuncture (EA) is a recognized analgesic treatment for pain conditions, its interaction with TRPM8 remains underexplored. This study aims to determine TRPM8′s role in EA-induced analgesia using a murine model of inflammatory pain. Mechanical allodynia, evidenced by a reduced paw withdrawal threshold (PWT), was induced in both wild-type and Trpm8−/− mice through CFA injection. EA applied at the GB34 and LR3 acupoints significantly alleviated mechanical allodynia in both groups. In wild-type mice, the analgesic effects of EA were partially reversed by naloxone (an opioid receptor antagonist) or AM251 (a CB1 receptor antagonist) and fully reversed by their combination. In contrast, only AM251 reversed EA-induced analgesia in Trpm8−/− or TRPM8-inhibited wild-type mice (via AMTB treatment, a TRPM8 antagonist), indicating no involvement of the opioid pathway. Additionally, the combination of menthol, a partial TRPM8 agonist, and EA enhanced analgesia in wild-type mice. In Trpm8−/− or AMTB-pretreated mice, the CB1 receptor agonist WIN 55,212-2 (WIN) exhibited stronger analgesic effects compared to wild-type controls. These findings suggest that EA at LR3 and GB34 mediates analgesia through both opioid and endocannabinoid pathways. TRPM8 is critical for EA to activate the opioid pathway, while its inhibition or deletion shifts the analgesic mechanism towards reliance on the cannabinoid system. Understanding this mechanistic shift may help optimize EA treatment strategies and improve pain management outcomes. Full article
(This article belongs to the Special Issue Research Advances in Neurodegeneration and Neuropathy)
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17 pages, 6541 KiB  
Article
Protective Effect of Electroacupuncture on Chemotherapy-Induced Salivary Gland Hypofunction in a Mouse Model
by Thanh-Hien Vu Nguyen, Kuo-Chou Chiu, Yin-Hwa Shih, Chung-Ji Liu, Tran Van Bao Quach, Shih-Min Hsia, Yi-Hung Chen and Tzong-Ming Shieh
Int. J. Mol. Sci. 2023, 24(14), 11654; https://doi.org/10.3390/ijms241411654 - 19 Jul 2023
Cited by 2 | Viewed by 2268
Abstract
Radiotherapy and chemotherapy can impair salivary gland (SG) function, which causes xerostomia and exacerbate other side effects of chemotherapy and oral infection, reducing patients’ quality of life. This animal study aimed to assess the efficacy of electroacupuncture (EA) as a means of preventing [...] Read more.
Radiotherapy and chemotherapy can impair salivary gland (SG) function, which causes xerostomia and exacerbate other side effects of chemotherapy and oral infection, reducing patients’ quality of life. This animal study aimed to assess the efficacy of electroacupuncture (EA) as a means of preventing xerostomia induced by 5−fluorouracil (5−FU). A xerostomia mouse model was induced via four tail vein injections of 5−FU (80 mg/kg/dose). EA was performed at LI4 and LI11 for 7 days. The pilocarpine-stimulated salivary flow rate (SFR) and salivary glands weight (SGW) were recorded. Salivary immunoglobulin A (SIgA) and lysozyme were determined via enzyme-linked immunosorbent assay (ELISA). SG was collected for hematoxylin and eosin staining to measure acini number and acinar cell size. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and aquaporin 5 (AQP5) mRNA expressions in SG were quantified via RT-qPCR. 5−FU caused significant decreases in SFR, SGW, SIgA, lysozyme, AQP5 expression, and acini number, while TNF-α and IL-1β expressions and acinar cell size were significantly increased. EA treatment can prevent 5−FU damage to the salivary gland, while pilocarpine treatment can only elevate SFR and AQP5 expression. These findings provide significant evidence to support the use of EA as an alternative treatment for chemotherapy-induced salivary gland hypofunction and xerostomia. Full article
(This article belongs to the Special Issue Research Advances in Neurodegeneration and Neuropathy)
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