A. Ikemoto et al., Increased expression of growth-associated protein 43 on the surface of theanterior horn cells in amyotrophic lateral sclerosis, ACT NEUROP, 98(4), 1999, pp. 367-373
This study examined axonal terminal alterations in the anterior horn of amy
otrophic lateral sclerosis (ALS) patients. An antibody against growth-assoc
iated protein 43 (GAP43), a phosphoprotein which is expressed in elongating
terminals of neurites, was employed for immunohistochemical staining. Lumb
ar spinal cords taken at autopsy from five ALS patients and from six contro
l adults were examined. In control patients, there were numerous GAP43-posi
tive granules diffusely dispersed throughout the anterior horn neuropil, an
d individual large anterior horn cells (AHCs) showed numerous tiny immunore
active granules and small dots on the surface. A small number of AHCs showe
d dense accumulation of GAP43 immunoreactivity on the surface of the cell b
ody and proximal processes. In all ALS patients, similar accumulation of GA
P43 immunoreactivity was seen on the surface of a large number of remaining
AHCs. Statistical analysis revealed a significant increase in number of AH
Cs with such accumulation in ALS patients. These results suggest that durin
g the ALS disease process there may be plastic alterations or a compensator
y mechanism of the axonal terminals located on the surface of some AHCs for
ongoing anterior horn presynaptic terminal degeneration.