Axonal degeneration of ascending sensory neurons in gracile axonal dystrophy mutant mouse

1990 ◽  
Vol 80 (2) ◽  
pp. 145-151 ◽  
Author(s):  
T. Kikuchi ◽  
M. Mukoyama ◽  
K. Yamazaki ◽  
H. Moriya
Keyword(s):  
Sensory Neurons ◽  
Axonal Degeneration ◽  
Mutant Mouse ◽  
Axonal Dystrophy ◽  
Gracile Axonal Dystrophy

Pathophysiological study of axonal degeneration in the gracile axonal dystrophy mutant mouse

1994 ◽  
Vol 19 ◽  
pp. S154
Author(s):  
Jun-Gyo Suh ◽  
Kohichi Tanaka ◽  
Hiroshi Yorifuji ◽  
Keiji Wada
Keyword(s):  
Axonal Degeneration ◽  
Mutant Mouse ◽  
Axonal Dystrophy ◽  
Gracile Axonal Dystrophy

Methylcobalamin (methyl-B12) promotes regeneration of motor nerve terminals degenerating in anterior gracile muscle of gracile axonal dystrophy (GAD) mutant mouse

1994 ◽  
Vol 170 (1) ◽  
pp. 195-197 ◽  
Author(s):  
Kazuto Yamazaki ◽  
Kenichiro Oda ◽  
Chiyoko Endo ◽  
Tateki Kikuchi ◽  
Tsuneo Wakabayashi
Keyword(s):  
Mutant Mouse ◽  
Motor Nerve ◽  
Nerve Terminals ◽  
Axonal Dystrophy ◽  
Motor Nerve Terminals ◽  
Gracile Axonal Dystrophy

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

1995 ◽  
Vol 695 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Nobutsune Ichihara ◽  
Jiang Wu ◽  
De Hua Chui ◽  
Kazuto Yamazaki ◽  
Tsuneo Wakabayashi ◽  
...  
Keyword(s):  
Axonal Degeneration ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Axonal Dystrophy ◽  
Β Protein ◽  
Abnormal Accumulation ◽  
Gracile Axonal Dystrophy

Fine structural changes of muscle spindles in the gracile axonal dystrophy mutant mouse

1996 ◽  
Vol 428-428 (4-5) ◽  
Author(s):  
A. Takagi ◽  
H. Kajihara ◽  
K. Oda ◽  
T. Kikuchi
Keyword(s):  
Structural Changes ◽  
Mutant Mouse ◽  
Muscle Spindles ◽  
Axonal Dystrophy ◽  
Gracile Axonal Dystrophy

Substance P-immunoreactive astrocytes in gracile sensory nervous tract of spinal cord in gracile axonal dystrophy mutant mouse

1993 ◽  
Vol 20 (1) ◽  
pp. 1-20 ◽  
Author(s):  
K. Yamazaki ◽  
H. Moriya ◽  
N. Ichihara ◽  
H. Mitsushio ◽  
S. Inagaki ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Mutant Mouse ◽  
Axonal Dystrophy ◽  
Gracile Axonal Dystrophy

scholarly journals Circular breakdown of neural networks due to loss of deubiquitinating enzyme (UCH-L1) in gracile axonal dystrophy (gad) mouse

2021 ◽  
Vol 8 (4) ◽  
pp. 311-324
Author(s):  
Tateki Kikuchi ◽  
Keyword(s):  
Nervous System ◽  
Axonal Degeneration ◽  
Muscular Atrophy ◽  
Amyloid Β ◽  
Dorsal Column ◽  
Pathological Examination ◽  
Amyloid Β Protein ◽  
Axonal Dystrophy ◽  
Gracile Nucleus ◽  
Gracile Axonal Dystrophy

<abstract> <p>Gracile axonal dystrophy (gad) mouse shows tremor, ataxia and muscular atrophy of hind limbs from about 80-days of age. These clinical features become progressively severe to death. Pathological examination reveals that main and early axonal degeneration exists in a long ascending nervous tract in dorsal column of the spinal cord: gracile nucleus and fascicules. Similar lesions are seen in axonal terminals of peripheral sensory (muscle spindles) and motor endplates. Most striking features of axonal dystrophy are “dying-back” axonal degeneration with partial swellings (“spheroids” in matured type) which come to be most frequently in gracile nucleus, followed by in order of gracile fasciculus of cervical, thoracic and lumber cord levels. Immunocytochemical increase of glial fibrillary acidic protein (GFAP) and substance P (SP) is seen in reactive astrocytes and degenerating axons. Likewise, amyloid precursor protein (APP) and amyloid β-protein (AβP) activity become positive in axons and astrocytes along ascending tract. Moreover, ubiquitin-positive dot-like structures accumulate in gracile nucleus, spinocerebellar tract, and cerebellum in <italic>gad</italic> mice after 9<sup>th</sup>-week old. Ubiquitinated structures are localized in spheroids with a larger diameter than normal. The <italic>gad</italic> mutation is caused by an in-frame deletion including exon 7 and 8 of <italic>UCH-L1</italic> gene, encoding the ubiquitin c-terminal hydrolase (UCH) isozyme (UCH-L1) selectively expressed in nervous system and testis/ovary. The <italic>gad</italic> allele encodes a truncated UCH-L1 lacking a segment of 42 amino acids containing catalytic site. The evaluation as mouse models for Parkinson's and Alzheimer's diseases and the collapse of synapse-axon circulation around central nervous system from peripheral nervous system are discussed.</p> </abstract>

scholarly journals PATHOPHYSIOLOGICAL STUDY OF AXONAL DEGENERATION IN THE GRACILE AXONAL DYSTROPHY (GAD) MUTANT MOUSE

1994 ◽  
Vol 15 (4) ◽  
pp. 241-246 ◽  
Author(s):  
JUN-GYO SUH ◽  
KENICHIRO ODA ◽  
KOHICHI TANAKA ◽  
HIROSHI YORIFUJI ◽  
TAKESHI TOMITA ◽  
...  
Keyword(s):  
Axonal Degeneration ◽  
Axonal Dystrophy ◽  
Gracile Axonal Dystrophy

Proteomic and histochemical analysis of proteins involved in the dying-back-type of axonal degeneration in the gracile axonal dystrophy (gad) mouse

2009 ◽  
Vol 54 (5-6) ◽  
pp. 330-338 ◽  
Author(s):  
Akiko Goto ◽  
Yu-Lai Wang ◽  
Tomohiro Kabuta ◽  
Rieko Setsuie ◽  
Hitoshi Osaka ◽  
...  
Keyword(s):  
Axonal Degeneration ◽  
Axonal Dystrophy ◽  
Histochemical Analysis ◽  
Gracile Axonal Dystrophy ◽  
Dying Back

scholarly journals Behavioral Study on the Gracile Axonal Dystrophy (GAD) Mutant Mouse

1992 ◽  
Vol 41 (4) ◽  
pp. 523-527 ◽  
Author(s):  
Kazuto YAMAZAKI ◽  
Takahiro NAKAZAWA ◽  
Manabu MATSUNAGA ◽  
Akira KUMAZAWA ◽  
Takeru KANEKO ◽  
...  
Keyword(s):  
Mutant Mouse ◽  
Behavioral Study ◽  
Axonal Dystrophy ◽  
Gracile Axonal Dystrophy
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