Accumulation of amyloid precursor protein and beta-protein immunoreactivities in axons injured by cerebral infarct.
To determine the distribution of amyloid precursor protein (APP), monoclonal antibodies against APP45-62 (APP1-28-9) and beta1-17 (4A18 and 4A61) were produced. In the sections of Alzheimer's disease (AD) brain, APP1-28-9 was reactive with neurites around senile plaques and a few neurons but not with amyloid cores. This antibody also immunostained the axons in the ischemic lesions of brain tissues from cases with cerebral infarct. 4A18 and 4A61 were reactive with amyloid plaques but not with neurites and neurons. The latter two antibodies also immunostained axons in ischemic lesions. These findings suggest that APP, transported by the fast axonal flows, accumulated in the injured axons in the central nervous system. The beta immunoreactivity appearing in those axons may provide a clue to the mechanism of amyloidogenesis.
Nukina
N
N
Department of Neurology, University of Tokyo, Japan.
Kanazawa
I
I
Mannen
T
T
Uchida
Y
Y
D000544:Alzheimer Disease / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000911:Antibodies, Monoclonal; D001369:Axons / Q000378:metabolism; D002544:Cerebral Infarction / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D016501:Neurites / Q000378:metabolism
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D000911:Antibodies, Monoclonal