Axonal degeneration promotes abnormal accumulation of amyloid β-protein in ascending gracile tract of gracile axonal dystrophy (GAD) mouse

The GAD mouse is a spontaneous neurological mutant with axonal dystrophy in the gracile tract of the medulla oblongata and spinal cord. The immunoreactivity of amyloid precursor protein (APP-IR) and amyloid β-protein (AβP-IR) was examined in the gracile tract and the dorsal root ganglia of normal an...

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Bibliographic Details
Published in:Brain research 1995-10, Vol.695 (2), p.173-178
Main Authors: Ichihara, Nobutsune, Wu, Jiang, Hua Chui, De, Yamazaki, Kazuto, Wakabayashi, Tsuneo, Kikuchi, Tateki
Format: Article
Language:English
Subjects:
Amyloid beta-Protein Precursor - metabolism
Amyloid precursor protein
Amyloid β-protein
Animal model
Animals
Axonal degeneration
Axons - physiology
Biological and medical sciences
Development. Senescence. Regeneration. Transplantation
Fundamental and applied biological sciences. Psychology
Ganglia, Spinal - metabolism
Ganglia, Spinal - pathology
Immunohistochemistry
Medulla Oblongata - metabolism
Medulla Oblongata - pathology
Mice
Mice, Inbred C57BL
Mice, Neurologic Mutants
Mutant mouse
Nerve Degeneration - physiology
Neural Pathways - metabolism
Neural Pathways - pathology
Neuromuscular Diseases - genetics
Neuromuscular Diseases - metabolism
Spinal Cord - metabolism
Spinal Cord - pathology
Vertebrates: nervous system and sense organs
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Summary:The GAD mouse is a spontaneous neurological mutant with axonal dystrophy in the gracile tract of the medulla oblongata and spinal cord. The immunoreactivity of amyloid precursor protein (APP-IR) and amyloid β-protein (AβP-IR) was examined in the gracile tract and the dorsal root ganglia of normal and GAD mice. The mice were studied at 4, 9, 18, and 32 weeks of age. These periods correspond clinically to the initial, progressive, critical, and terminal stages of the disease, respectively. The APR-IR in both axons and glial cells was already accentuated to a higher level as early as 4 weeks of age in the gracile nucleus of GAD mouse. Similarly there was increase in APR-IR of GAD mouse in the dorsal root ganglia. Almost all of the primary neurons in the dorsal root ganglia at the lumbar cord level of GAD mouse revealed stronger APP-IR than those of normal mouse throughout all stages. The cells showing immunoreactivity for amyloid β-protein became positive in axons and glial cells in the gracile nucleus by approximately the 9th week, and followed by an increase of AβP-IR in order of the cervical, thoracic and lumbar spinal cords. These results suggest that the initial feature in GAD mouse is an accumulation of amyloid precursor protein induced by axonal dystrophy which then leads to a deposition of amyloid β-protein within the cytoplasm of both axons and glial cells in the gracile tract.
ISSN:0006-8993
1872-6240
DOI:10.1016/0006-8993(95)00729-A