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Peripheral Neuropathies: Molecular Research and Novel Therapy
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Peripheral Neuropathies: Molecular Research and Novel Therapy

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: 30 July 2024 | Viewed by 2558

Special Issue Editor

Dr. Kazunori Sango

E-Mail Website
Guest Editor
Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan
Interests: diabetic neuropathy; drug-induced neuropathies; dorsal root ganglia; axon-Schwann cell interplay; demyelination
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The quality of life of those with peripheral neuropathies is undermined by their various symptoms, such as pain and numbness of the extremities, muscle weakness, autonomic disorders, etc. The neuropathies are caused by gene mutations, immune system disorders, metabolic abnormalities, cancers and anti-cancer drugs, and other systemic diseases; however, the onset and progression mechanisms remain largely unclear and the efficacious remedies against them have not yet been developed. This Special Issue provides a platform for researchers pursuing the molecular pathogenesis of peripheral neuropathies and novel therapeutic approaches toward them. Detailed information is paid to the findings of recent research on inherited neuropathy (e.g., Charcot–Marie–Tooth Disease, hereditary ATTR amyloidosis, and Fabry disease), diabetic polyneuropathy, immune-mediated neuropathy (e.g., Guillain–Barré Syndrome, chronic inflammatory demyelinating polyneuropathy, and autoimmune autonomic ganglionopathy), and drug-induced neuropathy (e.g., anti-cancer drugs including immune checkpoint inhibitors, amiodarone, and tumor necrosis factor-a antagonists). Basic studies regarding axonal degeneration, demyelination, and neuron-Schwann cell interplay under physiological and pathophysiological conditions are also welcome for submission.

Dr. Kazunori Sango
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

  • axonal degeneration
  • demyelination
  • Schwann cells
  • dorsal root ganglia
  • diabetic neuropathy
  • chemotherapy-induced peripheral neuropathies
  • immune-mediated neuropathies
  • immune checkpoint inhibitors
  • Charcot-Marie-tooth disease
  • autonomic neuropathies

Published Papers (2 papers)

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Research

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13 pages, 1377 KiB  
Article
Mitochondrial DNA and Electron Transport Chain Protein Levels Are Altered in Peripheral Nerve Tissues from Donors with HIV Sensory Neuropathy: A Pilot Study
by Ali Boustani, Jacqueline R. Kulbe, Mohammadsobhan Sheikh Andalibi, Josué Pérez-Santiago, Sanjay R. Mehta, Ronald J. Ellis and Jerel Adam Fields
Int. J. Mol. Sci. 2024, 25(9), 4732; https://doi.org/10.3390/ijms25094732 - 26 Apr 2024
Viewed by 203
Abstract
Distal sensory polyneuropathy (DSP) and distal neuropathic pain (DNP) remain significant challenges for older people with HIV (PWH), necessitating enhanced clinical attention. HIV and certain antiretroviral therapies (ARTs) can compromise mitochondrial function and impact mitochondrial DNA (mtDNA) replication, which is linked to DSP [...] Read more.
Distal sensory polyneuropathy (DSP) and distal neuropathic pain (DNP) remain significant challenges for older people with HIV (PWH), necessitating enhanced clinical attention. HIV and certain antiretroviral therapies (ARTs) can compromise mitochondrial function and impact mitochondrial DNA (mtDNA) replication, which is linked to DSP in ART-treated PWH. This study investigated mtDNA, mitochondrial fission and fusion proteins, and mitochondrial electron transport chain protein changes in the dorsal root ganglions (DRGs) and sural nerves (SuNs) of 11 autopsied PWH. In antemortem standardized assessments, six had no or one sign of DSP, while five exhibited two or more DSP signs. Digital droplet polymerase chain reaction was used to measure mtDNA quantity and the common deletions in isolated DNA. We found lower mtDNA copy numbers in DSP+ donors. SuNs exhibited a higher proportion of mtDNA common deletion than DRGs in both groups. Mitochondrial electron transport chain (ETC) proteins were altered in the DRGs of DSP+ compared to DSP− donors, particularly Complex I. These findings suggest that reduced mtDNA quantity and increased common deletion abundance may contribute to DSP in PWH, indicating diminished mitochondrial activity in the sensory neurons. Accumulated ETC proteins in the DRG imply impaired mitochondrial transport to the sensory neuron’s distal portion. Identifying molecules to safeguard mitochondrial integrity could aid in treating or preventing HIV-associated peripheral neuropathy. Full article
(This article belongs to the Special Issue Peripheral Neuropathies: Molecular Research and Novel Therapy)
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Review

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18 pages, 1088 KiB  
Review
Autoimmune Autonomic Neuropathy: From Pathogenesis to Diagnosis
by Shunya Nakane, Haruki Koike, Tomohiro Hayashi and Yuji Nakatsuji
Int. J. Mol. Sci. 2024, 25(4), 2296; https://doi.org/10.3390/ijms25042296 - 15 Feb 2024
Viewed by 1458
Abstract
Autoimmune autonomic ganglionopathy (AAG) is a disease of autonomic failure caused by ganglionic acetylcholine receptor (gAChR) autoantibodies. Although the detection of autoantibodies is important for distinguishing the disease from other neuropathies that present with autonomic dysfunction, other factors are important for accurate diagnosis. [...] Read more.
Autoimmune autonomic ganglionopathy (AAG) is a disease of autonomic failure caused by ganglionic acetylcholine receptor (gAChR) autoantibodies. Although the detection of autoantibodies is important for distinguishing the disease from other neuropathies that present with autonomic dysfunction, other factors are important for accurate diagnosis. Here, we provide a comprehensive review of the clinical features of AAG, highlighting differences in clinical course, clinical presentation, and laboratory findings from other neuropathies presenting with autonomic symptoms. The first step in diagnosing AAG is careful history taking, which should reveal whether the mode of onset is acute or chronic, followed by an examination of the time course of disease progression, including the presentation of autonomic and extra-autonomic symptoms. AAG is a neuropathy that should be differentiated from other neuropathies when the patient presents with autonomic dysfunction. Immune-mediated neuropathies, such as acute autonomic sensory neuropathy, are sometimes difficult to differentiate, and therefore, differences in clinical and laboratory findings should be well understood. Other non-neuropathic conditions, such as postural orthostatic tachycardia syndrome, chronic fatigue syndrome, and long COVID, also present with symptoms similar to those of AAG. Although often challenging, efforts should be made to differentiate among the disease candidates. Full article
(This article belongs to the Special Issue Peripheral Neuropathies: Molecular Research and Novel Therapy)
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