NEUROBIOLOGIA	Respuesta del sistema nervioso central a lesiones traumáticas: papel de las proteínas antioxidantes metalotioneínas
	© Juan Hidalgo , 2004   Juan.Hidalgo@uab.es

[RESUMEN]ABSTRACT

  Traumatic injury of the Central Nervous System (CNS) of an adult mammal may cause generalized functional losses that often result in permanent neurologic deficits. The clinical severity observed is caused by the poor capacity of the CNS for repairing itself following a traumatic lesion, in contrast to peripheral tissues. This is particularly evident regarding neuronal proliferation and restoration of the circuitry. However, actually the CNS responds prominently to a large variety of traumatic lesions. Neurons, the main cells of the CNS, but also glial cells (mainly microglia and astrocytes), produce many factors (neurotrophins, growth factors, citokines, etc.) that form a complex regulatory net of neuronal survival, glial activation and recruitment of inflammatory cells, and that attempt to reduce the consequences of the lesion. To determine the causes of the poor capacity of the CNS for repair despite these robust responses is of great importance. Several evidences show that oxidative stress, an imbalance between the production of free radicals and the antioxidant mechanisms of the cell, could have a special relevance in the pathophysiology of the traumatic CNS injuries, and likely of neurodegenerative diseases such as Alzheimer disease. My group of research has investigated, among other aspects of the inflammatory response, of the role of the antioxidant proteins metallothioneins (MT) in the response of the CNS to a number of injury models in mice.