Kage M, Ikemoto A, Akiguchi I, Kimura J, Matsumoto S, Kimura H, Tooyama I
Institute of Molecular Neurobiology, Shiga University of Medical Science, Otsu, Japan.
Neuroreport. 1998 May 11;9(7):1403-6. doi: 10.1097/00001756-199805110-00028.
Recent evidence suggests that the growth associated protein GAP-43 is involved in the pathology of amyotrophic lateral sclerosis (ALS). In order to assess the primary structure of the GAP-43 mRNA expressed in the spinal cord of ALS patients, the total coding region of the GAP-43 mRNA was amplified from postmortem human spinal cord specimens using the reverse transcriptase-polymerase chain reaction (RT-PCR) method. GAP-43 amplification products were clearly detected in all of the ALS cases but not in the normal controls. The GAP-43 mRNA and the deduced amino acid sequences from all ALS cases coincided completely with the sequence of human fetal GAP-43. These results suggest that the abnormal expression of GAP-43 mRNA underlying the pathogenesis of ALS is due to a quantitative increase, and that there are no qualitative abnormalities associated with a change in the amino acid sequences.
