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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting motor neurons in the spinal cord, brain stem, and cortex. Cultures of fetal rat spinal cord cells were used to test sera from ALS patients (ALS sera) on their ability to influence the expression of the neuron-specific phosphoprotein B-50/GAP-43. Neurons were treated with ALS sera, sera of age-matched controls (CON sera), or sera of patients with autonomic neuropathy (AUTO sera) and fixed after 24 or 96 h. The levels of B-50 and neurofilament (NF) protein were assayed with an enzyme-linked immunoadsorbent assay (ELISA). No toxic effects of the ALS sera were observed. It appeared that after 24 h, both B-50 and NF levels were elevated in the ALS sera-treated cells by 12 and 11%, respectively. After 96 h, the B-50 level was 19% higher than in CON sera-treated neurons, and the NF level was 29% higher. AUTO sera did not differ from CON sera. The stimulating effect of ALS sera was absent if the sera were heated at 56 degrees C for 30 min. We conclude that ALS serum induces the expression of B-50 and the subsequent axonal outgrowth and maturation in vitro. This induction might be a reflection in vitro of the processes underlying the collateral sprouting responses observed in ALS patients.

Serum from patients with amyotrophic lateral sclerosis induces the expression of B-50/GAP-43 and neurofilament in cultured rat fetal spinal neurons