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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
08:57

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin

Published on: March 26, 2015

Myelin and Oligodendrocyte Dysfunction in Demyelinating and Neurodegenerative Disorders: Signaling Pathways and

Shivang Shukla1, Vivek Srivastava2, Harshita Gaur2

  • 1Department of Pharmacy, Faculty of Medical, Paramedical, Health and Allied Sciences, Jagannath University, Chaksu Campus, Jaipur, 303901, India.

CNS & Neurological Disorders Drug Targets
|August 19, 2026
PubMed
Abstract

Insights

Oligodendrocyte (OL) dysfunction and myelin damage are implicated in neurodegenerative diseases like Alzheimer's, Parkinson's, and multiple sclerosis. Targeting myelination pathways offers potential therapeutic strategies for these conditions.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Oligodendrocytes (OLs) are crucial for myelin synthesis, vital for Central Nervous System (CNS) function.
  • Myelin abnormalities are implicated in Alzheimer's Disease (AD), Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS).
  • MS involves autoimmune demyelination, while AD and ALS feature neurodegeneration and myelin damage.

Purpose of the Study:

  • To critically discuss myelin and OL dysfunction in AD, MS, and ALS.
  • To explore signaling pathways and treatment strategies for myelination and remyelination.

Main Methods:

  • A narrative literature search was conducted across major scientific databases (Scopus, Google Scholar, Web of Science, PubMed).
  • The search focused on research concerning myelination, remyelination, OLs, signaling pathways, and therapeutic interventions.

Main Results:

  • MS pathogenesis involves inflammation-induced demyelination and OL dysfunction.
  • ALS pathogenesis is linked to oxidative and mitochondrial dysfunction, while AD involves disrupted neuronal support and myelin damage.
  • Key pathways for OL formation and myelin repair include Wnt/β-catenin, AKT/mTOR, and ERK/MAPK; drugs like edaravone, ocrelizumab, and siponimod show promise for myelin repair.

Conclusions:

  • While MS, AD, and ALS share similarities in OL dysfunction and demyelination, each disease has a unique molecular basis.
  • Targeting shared myelination and remyelination signaling pathways presents a potential therapeutic avenue.
  • Disease variability necessitates tailored therapeutic approaches for optimal outcomes.
Keywords:
Myelinmultiple sclerosisneurodegenerative diseasesoligodendrocyteoxidative stresssignaling pathways.

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