Circulating NGF antibody alters the distribution of NG2 and CD56 positive cells in the brain of an animal model of inflammatory disorder.

Using an animal model of endogenous Nerve Growth Factor (NGF) deprivation, we have investigated the effect of this molecule on the distribution of NG2 and CD56-positive cells in the brain of normal and of Experimental Allergic Encephalomyelitis (EAE) rats. We found that the number of these cells is significantly altered in the SubVentricular Zone (SVZ) and in other brain regions. These findings indicate that NGF might be implicated in the regulation of the antigen expressed by oligodendrocyte progenitors (NG2) and of the neural cell adhesion molecule (CD56/NCAM). Both antigens are associated with mechanisms of brain repair thus providing additional evidence for a major role of NGF in the brain response to pathological conditions such as EAE. Acknowledgements.--We thank Prof. R. Levi-Montalcini for her stimulating discussions. We also thank Dr. L. Aloe for critical reading of the manuscript. This study was supported by Proj. Strategico CNR, by AISM and by Fondazione CARISBO, Bologna. Dr. V. Triaca is a recipient of a fellowship from the AISM.