Scholarlink

Multiple sclerosis is a multifaceted and progressive neurological disorder marked by persistent inflammation, demyelination, and axonal injury. Due to autoreactive Th1 and Th17 lymphocytes infiltration into the central nervous system, which disrupts the blood–brain barrier and initiates inflammatory assaults on oligodendrocytes and neuronal axons. Defective autophagy in microglia and neurons impairs the clearance of myelin fragments and damaged organelles, thereby maintaining a chronic inflammatory environment. Mitochondrial impairment and oxidative stress further destabilize neuronal function in repressing autophagy-associated genes and promoting inflammasome activation. Due to the limitations of single-target immunomodulatory therapies in halting disease progression, this chapter proposes combinatorial strategies. The potential of gene therapies in modulating transcription factors, as well as nanoparticle-facilitated delivery of autophagy-enhancing compounds, is also discussed. This chapter emphasizes the importance of targeting both inflammatory and cellular clearance pathways and advocates for a systems-level therapeutic model, guided by biomarkers and precision medicine, to counter neurodegeneration in multiple sclerosis.

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Inflammatory Demyelination and Autophagic Dysfunction in Multiple Sclerosis

  • 章节

  • 发表日期：

    2026年

查看全文
  • Praveen Halagali,
  • Salini P. Nair,
  • S. N. Manjula,
  • Himanshu Sharma,
  • Vamshi Krishna Tippavajhala

摘要

Multiple sclerosis is a multifaceted and progressive neurological disorder marked by persistent inflammation, demyelination, and axonal injury. Due to autoreactive Th1 and Th17 lymphocytes infiltration into the central nervous system, which disrupts the blood–brain barrier and initiates inflammatory assaults on oligodendrocytes and neuronal axons. Defective autophagy in microglia and neurons impairs the clearance of myelin fragments and damaged organelles, thereby maintaining a chronic inflammatory environment. Mitochondrial impairment and oxidative stress further destabilize neuronal function in repressing autophagy-associated genes and promoting inflammasome activation. Due to the limitations of single-target immunomodulatory therapies in halting disease progression, this chapter proposes combinatorial strategies. The potential of gene therapies in modulating transcription factors, as well as nanoparticle-facilitated delivery of autophagy-enhancing compounds, is also discussed. This chapter emphasizes the importance of targeting both inflammatory and cellular clearance pathways and advocates for a systems-level therapeutic model, guided by biomarkers and precision medicine, to counter neurodegeneration in multiple sclerosis.