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Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging | OMICS International | Abstract
ISSN: 2329-6895

Journal of Neurological Disorders
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Review Article

Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging

Zhi Huang, Grace Ha and John Petitto*
Departments of Neuroscience and Psychiatry, McKnight Brain Institute, University of Florida, Gainesville, FL, USA
Corresponding Author : John Petitto
McKnight Brain Institute
UF, 100 South Newell Drive Gainesville, FL 32611, USA
Tel: 352-294-0416
E-mail: [email protected]
Received March 07, 2014; Accepted June 30, 2014; Published July 04, 2014
Citation: Huang Z, Ha G, Petitto J (2014) Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging. J Neurol Disord 2:170. doi: 10.4172/2329-6895.1000170
Copyright: © 2014 Huang Z, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Emerging evidence indicates that neuroimmunological changes in the brain can modify intrinsic brain processes that are involved in regulating neuroplasticity. Increasing evidence suggests that in some forms of motor neuron injury, many neurons do not die, but reside in an atrophic state for an extended period of time. In mice, facial motor neurons in the brain undergo a protracted period of degeneration or atrophy following resection of their peripheral axons. Reinjuring the proximal nerve stump of the chronically resected facial nerve stimulates a robust reversal of motor neuron atrophy which results in marked increases in both the number and size of injured motor neurons in the facial motor nucleus. In this brief review, we describe research from our lab which indicates that the reversal of atrophy in this injury model is dependent on normal cellular immunity. The role of T cells in this unique form of neuroplasticity following injury and in brain aging, are discussed. The potential role of yet undiscover intrinsic actions of recombination activating genes in the brain are considered. Further research using the facial nerve reinjury model could identify molecular signals involved in neuroplasticity, and lead to new ways to stimulate neuroregenerative processes in neurotrauma and other forms of brain insult and disease.