Amyotrophic Lateral Sclerosis is a devastating neurodegenerative disease that affects motor neurons. Many theories about mechanisms contributing in its pathogenesis have been suggested. There is also evidence for alterations in synaptic plasticity during the progress of ALS. In particular, the expression of axonal growth promoting molecules like GAP-43, responsible for axonal regeneration, have been suggested to be sustained during the disease. On the other hand, axonal inhibitory molecules like Nogo-A seem to play an important part in compensating this regeneration attempt. In order to investigate the role of these two participating proteins during the preclinical and clinical stages of ALS, the spinal cord of SOD1 mice, the animal model mimicking one genetic form of ALS, have been examined. Using immunocytochemistry, immunoreactivity of Nogo-A and GAP-43 was shown in spinal cord sections of 6, 13 and 18 weeks of age. Our results suggest that Nogo-A has increased irnrnunoreactivity in the oligodentrocytes in the ventral horns in grey matter of the spinal cord of the clinical Tg SOD1 mice and in the ventral white matter during preclinical and clinical stages. Increased immunoreatcivity was also found in the ventral horn neurons of the 13 weeks Tg mice compared to the other stages. GAP-43 has also shown greater immunoreactivity in Tg mice relating to the controls. These results suggest that a regeneration attempt is likely to happen during ALS but is maybe compensated by the inhibition of axonal growth at the later stages
