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Inflammation in white matter: clinical and pathophysiological aspects

David Pleasure1, Athena Soulika, Sunit K Singh

  • 1Deparment of Neurology, UC Davis School of Medicine, and Shriners Hospitals for Children Northern California, Sacramento, California 95817, USA. david.pleasure@ucdmc.ucdavis.edu

Mental Retardation and Developmental Disabilities Research Reviews
|June 30, 2006
PubMed

Insights

Immune-mediated white matter damage in the central nervous system (CNS) affects premature infants and adults, causing neurological deficits. Understanding genetic predispositions and immune responses is crucial for treating conditions like periventricular leukomalacia and multiple sclerosis.

Area of Science:

  • Neuroimmunology
  • Developmental Neuroscience
  • Neurology

Background:

  • The central nervous system (CNS) is considered immunoprivileged, yet immune-mediated white matter damage occurs in both perinatal and adult stages.
  • Periventricular leukomalacia (PVL), an inflammatory white matter disease in premature infants, leads to cerebral palsy (CP) via hypoxic/ischemic and innate immune damage to oligodendroglia and axons.
  • Multiple sclerosis (MS), an adult inflammatory white matter disease, causes progressive neurological disability through destruction of mature oligodendroglia and axons, influenced by genetic factors and adaptive immunity.

Purpose of the Study:

  • To explore the potential genetic predisposition in periventricular leukomalacia (PVL) and its neurological outcomes.
  • To compare the immune mechanisms underlying PVL in infants and multiple sclerosis (MS) in adults.
  • To highlight the role of both innate and adaptive immunity in CNS white matter diseases.

Main Methods:

  • Review of clinical and experimental studies on PVL pathogenesis.
  • Analysis of genetic and immunological factors in multiple sclerosis (MS).
  • Comparative analysis of immune-mediated white matter damage in perinatal and adult CNS diseases.

Main Results:

  • Hypoxic/ischemic and innate immune factors contribute to PVL, affecting immature oligodendroglia and axons.
  • Genetic polymorphisms and adaptive immune responses to myelin antigens are key in MS.
  • No data currently exist on genetic predisposition for PVL or its sequelae.

Conclusions:

  • Immune-mediated white matter damage is a significant factor in both infant (PVL) and adult (MS) neurological disorders.
  • Understanding the distinct and overlapping immune mechanisms is vital for developing targeted therapies.
  • Further research is needed to investigate genetic predispositions in PVL to mitigate long-term neurological deficits.

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