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On CNS repair and protection strategies: novel approaches with implications for spinal cord injury and Parkinson's disease

Lars Olsona,*, Henrich Chengb, Rolf H. Zetterströma, Ludmila Solominc, Lottie Janssonc, Lydia Giménez-Llorta Barry J. Hofferd, Thomas Perlmannc
aDepartment of Neuroscience, Karolinska Institute, S-17777 Stockholm, Sweden, bDepartment of Neurosurgery, Neurological Institute, Veterans General Hospital-Taipei, Taipei, Taiwan, cLudwig Institute for Cancer Research, Stockholm Branch, S-17177 Stockholm, Sweden, dDivision of Intramural Research, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA




Abstract
In the adult mammalian central nervous system lost nerve cells are not replaced and there is no regeneration of injured axons in white matter. Together, these two facts mean there are no spontaneous reparative mechanisms in operation. Instead, the adult central nervous system copes with the risks of injuries and diseases by protective encapsulation in bone, by a multitude of neuroprotective mechanisms, and finally by the fact that many important functions are represented by a much larger number of neurons than minimally needed. The long life expectancy of a human being nevertheless means that the risk that the central nervous system is affected by disease, injury or other forms of insults for which it cannot fully compensate is relatively high. Experimentally, two strategies are being pursued in order to develop ways of minimizing various forms of CNS damage, namely neuroprotective and reparative strategies. Here we present a possible reparative intervention applicable to spinal cord injury based on multiple white-to-gray matter peripheral nerve bridge grafts and work based on the specific role of Nurr1 for dopamine neuron development, suggesting that development of ligands to transcription factor might be a new inroad to neuroprotective treatments in Parkinson's disease.


Corresponding author: Lars.Olson@neuro.ki.se


Brain Research Reviews 26 (1998) 295-301
Copyright © 1998 Elsevier Science B. V. All rights reserved.

 

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