Anti-Glutamic Acid Decarboxylase 65 (GAD65)-Associated Syndromes

2020 ◽  
pp. 55-71
Author(s):  
Pichet Termsarasab ◽  
Thananan Thammongkolchai ◽  
Bashar Katirji
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase ◽  
Glutamic Acid Decarboxylase 65

scholarly journals Assessment of CD4+ T Cell Responses to Glutamic Acid Decarboxylase 65 Using DQ8 Tetramers Reveals a Pathogenic Role of GAD65 121–140 and GAD65 250–266 in T1D Development

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112882 ◽  
Author(s):  
I-Ting Chow ◽  
Junbao Yang ◽  
Theresa J. Gates ◽  
Eddie A. James ◽  
Duy T. Mai ◽  
...  
Keyword(s):  
T Cell ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Acid Decarboxylase ◽  
Pathogenic Role ◽  
Cell Responses ◽  
Glutamic Acid Decarboxylase 65

scholarly journals Exercise training modulates glutamic acid decarboxylase-65/67 expression through TrkB signaling to ameliorate neuropathic pain in rats with spinal cord injury

2020 ◽  
Vol 16 ◽  
pp. 174480692092451
Author(s):  
Xiangzhe Li ◽  
Qinghua Wang ◽  
Jie Ding ◽  
Sheng Wang ◽  
Chuanming Dong ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Exercise Training ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase ◽  
Cord Injury ◽  
Tropomyosin Related Kinase B ◽  
Glutamic Acid Decarboxylase 65

Neuropathic pain is one of the most frequently stated complications after spinal cord injury. In post-spinal cord injury, the decrease of gamma aminobutyric acid synthesis within the distal spinal cord is one of the main causes of neuropathic pain. The predominant research question of this study was whether exercise training may promote the expression of glutamic acid decarboxylase-65 and glutamic acid decarboxylase-67, which are key enzymes of gamma aminobutyric acid synthesis, within the distal spinal cord through tropomyosin-related kinase B signaling, as its synthesis assists to relieve neuropathic pain after spinal cord injury. Animal experiment was conducted, and all rats were allocated into five groups: Sham group, SCI/PBS group, SCI-TT/PBS group, SCI/tropomyosin-related kinase B-IgG group, and SCI-TT/tropomyosin-related kinase B-IgG group, and then T10 contusion SCI model was performed as well as the tropomyosin-related kinase B-IgG was used to block the tropomyosin-related kinase B activation. Mechanical withdrawal thresholds and thermal withdrawal latencies were used for assessing pain-related behaviors. Western blot analysis was used to detect the expression of brain-derived neurotrophic factor, tropomyosin-related kinase B, CREB, p-REB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord. Immunohistochemistry was used to analyze the distribution of CREB, p-CREB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord dorsal horn. The results showed that exercise training could significantly mitigate the mechanical allodynia and thermal hyperalgesia in post-spinal cord injury and increase the synthesis of brain-derived neurotrophic factor, tropomyosin-related kinase B, CREB, p-CREB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord. After the tropomyosin-related kinase B signaling was blocked, the analgesic effect of exercise training was inhibited, and in the SCI-TT/tropomyosin-related kinase B-IgG group, the synthesis of CREB, p-CREB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord were also significantly reduced compared with the SCI-TT/PBS group. This study shows that exercise training may increase the glutamic acid decarboxylase-65 and glutamic acid decarboxylase-67 expression within the spinal cord dorsal horn through the tropomyosin-related kinase B signaling, and this mechanism may play a vital role in relieving the neuropathic pain of rats caused by incomplete SCI.

Immunotherapy of Autoimmune Diabetes by Nasal Administration of Tandem Glutamic Acid Decarboxylase 65 Peptides

2009 ◽  
Vol 38 (8) ◽  
pp. 690-703 ◽  
Author(s):  
Huaqian Wang ◽  
Jie Yang ◽  
Liang Jin ◽  
Jiao Feng ◽  
Yong Lu ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Autoimmune Diabetes ◽  
Nasal Administration ◽  
Acid Decarboxylase ◽  
Glutamic Acid Decarboxylase 65

scholarly journals A Glutamic Acid Decarboxylase 65-Specific Th2 Cell Clone Immunoregulates Autoimmune Diabetes in Nonobese Diabetic Mice

2001 ◽  
Vol 166 (11) ◽  
pp. 6925-6936 ◽  
Author(s):  
Roland Tisch ◽  
Bo Wang ◽  
Mark A. Atkinson ◽  
David V. Serreze ◽  
Randall Friedline
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Cell Clone ◽  
Autoimmune Diabetes ◽  
Acid Decarboxylase ◽  
Diabetic Mice ◽  
Nonobese Diabetic ◽  
Th2 Cell ◽  
Nonobese Diabetic Mice ◽  
Glutamic Acid Decarboxylase 65

scholarly journals Characteristics ofin-vitrophenotypes of glutamic acid decarboxylase 65 autoantibodies in high-titre individuals

2013 ◽  
Vol 171 (3) ◽  
pp. 247-254 ◽  
Author(s):  
M. Chéramy ◽  
C. S. Hampe ◽  
J. Ludvigsson ◽  
R. Casas
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
High Titre ◽  
Acid Decarboxylase ◽  
Glutamic Acid Decarboxylase 65

A Highly Sensitive Immunoassay Resistant to Autoantibody Interference for Detection of the Diabetes-Associated Autoantigen Glutamic Acid Decarboxylase 65 in Blood and Other Biological Samples

2006 ◽  
Vol 8 (2) ◽  
pp. 207-218 ◽  
Author(s):  
Megan A. Waldrop ◽  
Arthur T. Suckow ◽  
Tyler R. Hall ◽  
Chris S. Hampe ◽  
Santica M. Marcovina ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Biological Samples ◽  
Acid Decarboxylase ◽  
Highly Sensitive ◽  
Glutamic Acid Decarboxylase 65

scholarly journals MHC Class I-Restricted Determinants on the Glutamic Acid Decarboxylase 65 Molecule Induce Spontaneous CTL Activity

2001 ◽  
Vol 167 (3) ◽  
pp. 1748-1757 ◽  
Author(s):  
Anthony Quinn ◽  
Marcia F. McInerney ◽  
Eli E. Sercarz
Keyword(s):  
Glutamic Acid ◽  
Mhc Class I ◽  
Glutamic Acid Decarboxylase ◽  
Class I ◽  
Acid Decarboxylase ◽  
Glutamic Acid Decarboxylase 65 ◽  
Ctl Activity
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