[Mechanisms of secondary degeneration in the central nervous system during acute neural disorders and white matter damage].
BACKGROUND
Acute neurodegenerative diseases, including stroke and traumatic brain and spinal cord injury, possess an elevated worldwide incidence. Two distinct lesive patterns can be identified after these destructive events: primary damage, an early consequence of the primary pathological event, and secondary neural degeneration (SND), a group of pathological events inducing late degeneration in cells not or even only partially affected by the primary damage. This pathological mechanism is an important contributing factor for functional deficits and target for therapeutic approaches. Several factors are involved on the SND etiology, including excitotoxicity, inflammation, and oxidative stress.


OBJECTIVE
To review the main mechanisms underlying the SND occurring after acute neural disorders.


METHODS
The more recent findings about the eliciting processes of SND degeneration are discussed, as well as their significance to degeneration of white matter tracts.


CONCLUSIONS
The characterization of the events underlying SND is of fundamental importance for the development of new therapeutic approaches effective enough to decrease the functional deficits, contributing to the improvement of the quality of life of people suffering neurological diseases. These therapeutic approaches must be validated in experimental models of both brain and spinal cord diseases, which effectively simulate human neural disorders protecting both gray and white matters for a better neuroprotective efficacy.
Guimarães
J S
JS
Laboratorio de Neurobiología Celular, Instituto Internacional de Neurociencia Edmon y Lily Safra de Natal (IINN-ELS), Natal, RN, Brazil.
Freire
M A M
MA
Lima
R R
RR
Souza-Rodrigues
R D
RD
Costa
A M R
AM
dos Santos
C D
CD
Picanço-Diniz
C W
CW
Gomes-Leal
W
W
D002490:Central Nervous System / Q000033:anatomy & histology / Q000473:pathology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D019636:Neurodegenerative Diseases / Q000150:complications / Q000453:epidemiology / Q000473:pathology* / Q000503:physiopathology*; D018384:Oxidative Stress
D018698:Glutamic Acid