Nervous System Inflammation

A topical collection in Biomedicines (ISSN 2227-9059). This collection belongs to the section "Neurobiology and Clinical Neuroscience".

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Collection Editor
Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA
Interests: demyelinating disorders; multiple sclerosis; epidemiology and genetic aspects; therapeutic trials
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Topical Collection Information

Dear Colleagues,

The concept of nervous system inflammation has ample connotations ranging from infectious and post-infectious processes to demyelinating disorders. Autoimmune mechanisms play a fundamental role in many of these pathologies, affecting CNS structures and the peripheral nervous system. Dysfunction of the innate and the adaptive immune systems participates mechanistically, while non-resolving, chronic or pervasive inflammation in the CNS may result in degeneration and loss of structure. The pathophysiology involved in many of these disorders leads to the theoretical utilization of diverse immunotherapies. Viral encephalitis (e.g., herpes human virus and ECHO) and other infections are sporadic, some acquiring a seasonal or regional apparition, while more common disorders such as multiple sclerosis (MS) and less common demyelinating diseases such as neuromyelitis optica spectrum disorders (NMOSD), myelin oligodendrocyte glycoprotein antibody disease (MOGAD), and acute disseminated encephalomyelitis (ADEM), this latter usually a post-infectious development, have a more consistent epidemiologic pattern. Serious, albeit rare neuroimmune conditions include paraneoplastic and autoimmune encephalitis, autoimmune epilepsies, and “idiopathic” transverse myelitis. Detecting neuronal cell surface antibodies is emphasized in inflammatory cerebral cases. CNS vasculitis, neurorheumatological disorders (e.g., Behçet’s disease, Sjögren’s syndrome, systemic lupus erythematosus), and neurosarcoidosis are considered in this topic. Specific investigations and careful differentiation of MRI patterns are of primary importance in the proper identification of these syndromes. Autoimmune polyradiculoneuropathies classically represented as Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are prime examples of inflammatory diseases of the peripheral nervous system. Cerebrospinal fluid analysis, electrophysiological studies, highly sensitive nerve biopsy techniques, and autonomic dysfunction testing all are fundamental for the proper diagnosis and management of peripheral nervous system disease. Contributions to this Topical Collection will enrich knowledge and procure more options of management for the people afflicted by these diseases.

Prof. Víctor M. Rivera
Collection Editor

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  • inflammation
  • post-infectious disease
  • demyelinating disorder
  • viral encephalitis
  • MS
  • ADEM
  • paraneoplastic encephalitis
  • autoimmune encephalitis
  • immunotherapies
  • Guillain-Barré síndrome
  • CIDP

Published Papers (1 paper)


41 pages, 1111 KiB  
Newly Identified Deficiencies in the Multiple Sclerosis Central Nervous System and Their Impact on the Remyelination Failure
by Giuseppe Scalabrino
Biomedicines 2022, 10(4), 815; - 30 Mar 2022
Cited by 4 | Viewed by 3621
The pathogenesis of multiple sclerosis (MS) remains enigmatic and controversial. Myelin sheaths in the central nervous system (CNS) insulate axons and allow saltatory nerve conduction. MS brings about the destruction of myelin sheaths and the myelin-producing oligodendrocytes (ODCs). The conundrum of remyelination failure [...] Read more.
The pathogenesis of multiple sclerosis (MS) remains enigmatic and controversial. Myelin sheaths in the central nervous system (CNS) insulate axons and allow saltatory nerve conduction. MS brings about the destruction of myelin sheaths and the myelin-producing oligodendrocytes (ODCs). The conundrum of remyelination failure is, therefore, crucial in MS. In this review, the roles of epidermal growth factor (EGF), normal prions, and cobalamin in CNS myelinogenesis are briefly summarized. Thereafter, some findings of other authors and ourselves on MS and MS-like models are recapitulated, because they have shown that: (a) EGF is significantly decreased in the CNS of living or deceased MS patients; (b) its repeated administration to mice in various MS-models prevents demyelination and inflammatory reaction; (c) as was the case for EGF, normal prion levels are decreased in the MS CNS, with a strong correspondence between liquid and tissue levels; and (d) MS cobalamin levels are increased in the cerebrospinal fluid, but decreased in the spinal cord. In fact, no remyelination can occur in MS if these molecules (essential for any form of CNS myelination) are lacking. Lastly, other non-immunological MS abnormalities are reviewed. Together, these results have led to a critical reassessment of MS pathogenesis, partly because EGF has little or no role in immunology. Full article
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