[Neurodegeneration: aging and dementia. Etiopathogenic role of electron transport disorders. Therapeutic possibilities]

Orv Hetil. 1997 Feb 9;138(6):331-5.
[Article in Hungarian]

Abstract

The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems. The late onset diseases and slow neurodegeneration is connected with excitotoxins and alteration of mitochondrial electron transport chain. In elderly, congenital and acquired defects of mitochondrial complexes cause formation of free radicals. The overstimulation of excitatory amino acid receptors interfere with the cellular energy metabolism and also forming reactive oxygen species. The impaired energy metabolism make neuronal cells vulnerable to the excitotoxic damage. In these ways, excitotoxicity may be the final common pathway of neuronal death in a variety of neurodegenerative diseases. Potential therapeutic strategies would be use receptor antagonist or drugs to bypass energetic defects.

Publication types

  • Review

MeSH terms

  • Aged
  • Aging*
  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / physiopathology*
  • Calcium Channel Blockers / therapeutic use
  • Cerebellar Diseases / drug therapy
  • Cerebellar Diseases / physiopathology*
  • Dementia / drug therapy
  • Dementia / physiopathology*
  • Electron Transport
  • Female
  • Humans
  • Huntington Disease / drug therapy
  • Huntington Disease / physiopathology*
  • Lamotrigine
  • Male
  • Middle Aged
  • Monoamine Oxidase Inhibitors / therapeutic use
  • Neuroprotective Agents / therapeutic use
  • Parkinson Disease / drug therapy
  • Parkinson Disease / physiopathology*
  • Riluzole
  • Thiazoles / therapeutic use
  • Triazines / therapeutic use

Substances

  • Calcium Channel Blockers
  • Monoamine Oxidase Inhibitors
  • Neuroprotective Agents
  • Thiazoles
  • Triazines
  • Riluzole
  • Lamotrigine