Advances in neuroregulation and neuroprotection by Collin, Catherine

By Collin, Catherine

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Besides, NO exposure causes cobalamin deficiency resulting from its inactivity which is known to produce impaired neurological functions (Stollhoff et al, 1987; Hall, 1990). Congenital defects of cobalamine metabolism and nutritional deficiencies have been reported to produce abnormal CNS and peripheral neuronal function in humans (Hall, 1990). The present study deals with CSF analysis of homocysteine and cobalamine in PD patients in on-off pathological conditions. These levels are reported with the assumption that CSF concentrations reflect brain or spinal cord concentrations and perhaps synaptic activity, since CSF is in constant exchange with the extracellular fluid of the CNS.

The results indicate that the immunomodulatory effect of the two hormones depends on the conditions of the study. Thus, melatonin led to increased phagocytic capacity in macrophages from both the basal and the stressed animals, while corticosterone only had an immunostimulatory effect with macrophages from the unstressed animals. With both hormones acting together, the macrophage phagocytic activity was stimulated at all the concentrations used and independently of whether or not the corresponding animals had been stressed, although the greatest activation was seen in the basal animal phagocytes incubated with the higher corticosterone concentration.

M. and Strake-Reed, P. E. (1991). Excess brain protein oxidation and enzyme dysfunction in normal aging and Alzehamier's disease, Proc. Natl. Acad. Sci. (USA) 88, 1054010543. Stollhoff, K. and Schulte, F. J. (1987). Vitamin B12 and brain development, Eur. J. Paediatr. 146, 201-205. Tatton, W. , et al. (2003). Apoptosis in Parkinson's disease: Signal for neuronal degradation, Ann. Neurol. 53 (Suppl. 3), S61-S72. , Rajput, A. , et al (1990). Age, environments and the number of substancia nigra neurons, Adv.

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