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Emerging Neuroprotective and Regenerative Strategies for the Treatment of Demyelinating Disorders of the Central Nervous

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: 20 March 2025 | Viewed by 1339

Special Issue Editor

Special Issue Information

Dear Colleagues,

Demyelinating disorders that specifically affect the brain and/or spine in the central nervous system (CNS) are common neurological conditions and can be separated into primary and secondary idiopathic inflammatory-demyelinating diseases (IIDDs). Both groups of IIDDs are characterised by damage to the myelin sheaths covering axons, with the main difference being that in secondary IIDDs, the aetiology is usually well defined (e.g., post-infectious, ischemic, metabolic, or toxic), so therapies targeting the underlying cause can (in most cases) successfully reverse disease progression. In contrast, there is no known cause for primary IIDDs, although growing evidence suggests the contribution of several risk factors (i.e., genetics, environment, life style, diet, etc.) in disease pathogenesis. To date, there is no definitive cure for primary IIDDs; however, there are several disease-modifying therapies able to alter disease progression in some patients and an increasing number of promising therapeutic strategies are currently under scrutiny in preclinical models and in clinical trials. Such emerging therapeutics primarily aim to increase neuroprotection, enhance nerve conduction and/or promote myelin regeneration.

The main scope of the Special Issue is to shed light on the most recent advances on such novel therapeutic strategies for IIDDs, as well as rare demyelinating conditions of the CNS. Special emphasis will be given to contributions focusing on the identification and preclinical validation of targets of potential clinical significance in demyelinating disorders of the CNS, as well as review articles providing updates on emerging treatment options for such devastating pathologies.

Dr. Alessandro Castorina
Guest Editor

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Keywords

  • neuroprotection
  • demyelinating disorders
  • multiple sclerosis
  • optic neuritis
  • transverse myelitis
  • Aicardi–Goutières syndrome
  • acute disseminated encephalomyelitis
  • neuromyelitis optica
  • HTLV-I associated myelopathy
  • Balo’s disease
  • Schilder’s disease

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Published Papers (1 paper)

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24 pages, 16101 KiB  
Article
Differential Expression of PACAP/VIP Receptors in the Post-Mortem CNS White Matter of Multiple Sclerosis Donors
by Margo Iris Jansen, Giuseppe Musumeci and Alessandro Castorina
Int. J. Mol. Sci. 2024, 25(16), 8850; https://doi.org/10.3390/ijms25168850 - 14 Aug 2024
Viewed by 858
Abstract
Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two neuroprotective and anti-inflammatory molecules of the central nervous system (CNS). Both bind to three G protein-coupled receptors, namely PAC1, VPAC1 and VPAC2, to elicit their beneficial effects in various CNS diseases, [...] Read more.
Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two neuroprotective and anti-inflammatory molecules of the central nervous system (CNS). Both bind to three G protein-coupled receptors, namely PAC1, VPAC1 and VPAC2, to elicit their beneficial effects in various CNS diseases, including multiple sclerosis (MS). In this study, we assessed the expression and distribution of PACAP/VIP receptors in the normal-appearing white matter (NAWM) of MS donors with a clinical history of either relapsing–remitting MS (RRMS), primary MS (PPMS), secondary progressive MS (SPMS) or in aged-matched non-MS controls. Gene expression studies revealed MS-subtype specific changes in PACAP and VIP and in the receptors’ levels in the NAWM, which were partly corroborated by immunohistochemical analyses. Most PAC1 immunoreactivity was restricted to myelin-producing cells, whereas VPAC1 reactivity was diffused within the neuropil and in axonal bundles, and VPAC2 in small vessel walls. Within and around lesioned areas, glial cells were the predominant populations showing reactivity for the different PACAP/VIP receptors, with distinctive patterns across MS subtypes. Together, these data identify the differential expression patterns of PACAP/VIP receptors among the different MS clinical entities. These results may offer opportunities for the development of personalized therapeutic approaches to treating MS and/or other demyelinating disorders. Full article
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