L-Glutamic Acid Decarboxylase in Parkinson's Disease: Effect of L-Dopa Therapy

Nature ◽  
1973 ◽  
Vol 243 (5409) ◽  
pp. 521-523 ◽  
Author(s):  
K. G. LLOYD ◽  
O. HORNYKIEWICZ
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase ◽  
Disease Effect

Glutamic acid decarboxylase in Parkinson's disease and epilepsy

Neurology ◽  
1971 ◽  
Vol 21 (10) ◽  
pp. 1000-1000 ◽  
Author(s):  
P. L. McGeer ◽  
E. G. McGeer ◽  
J. A. Wada
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase

Normal glutamic decarboxylase activity in rat striatum and retina following administration of L-DOPA

1976 ◽  
Vol 54 (2) ◽  
pp. 79-82 ◽  
Author(s):  
G. Tunnicliff ◽  
R. F. Butterworth ◽  
Y. Tsukada ◽  
A. Barbeau
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Rat Striatum ◽  
Acid Decarboxylase ◽  
Decarboxylase Activity ◽  
Gad Activity

Recent reports of the in vivo action of L-dihydroxyphenylalanine (L-DOPA) on glutamic acid decarboxylase (GAD) activity are contradictory. This investigation was undertaken to clarify the situation. Both acute (100 mg/kg and 1 g/kg) and chronic (1 g/kg) administration of L-DOPA to rats failed to produce any alteration in the activity of striatal or retinal GAD activity. These results are discussed in the light of a report relating L-DOPA therapy to modification of GAD activity in Parkinson's disease.

Brain Glutamic Acid Decarboxylase Activity in Parkinson’s Disease

1974 ◽  
Vol 12 (1) ◽  
pp. 13-19 ◽  
Author(s):  
U.K. Rinne ◽  
H. Laaksonen ◽  
P. Riekkinen ◽  
V. Sonninen
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase ◽  
Decarboxylase Activity

scholarly journals Decreased glutamic acid decarboxylase mRNA expression in prefrontal cortex in Parkinson's disease

2010 ◽  
Vol 226 (1) ◽  
pp. 207-217 ◽  
Author(s):  
Amélie C. Lanoue ◽  
Alexandra Dumitriu ◽  
Richard H. Myers ◽  
Jean-Jacques Soghomonian
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Prefrontal Cortex ◽  
Glutamic Acid ◽  
Mrna Expression ◽  
Glutamic Acid Decarboxylase ◽  
Acid Decarboxylase

scholarly journals Subthalamic hGAD65 Gene Therapy and Striatum TH Gene Transfer in a Parkinson’s Disease Rat Model

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Deyu Zheng ◽  
Xiaohua Jiang ◽  
Junpeng Zhao ◽  
Deyi Duan ◽  
Huanying Zhao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Gene Therapy ◽  
Parkinson's Disease ◽  
Gene Transfer ◽  
Gene Delivery ◽  
Glutamic Acid ◽  
Rat Model ◽  
Combination Method ◽  
Combination Group ◽  
Acid Decarboxylase

The aim of the present study is to detect a combination method to utilize gene therapy for the treatment of Parkinson’s disease (PD). Here, a PD rat model is used for thein vivogene therapy of a recombinant adeno-associated virus (AAV2) containing a human glutamic acid decarboxylase 65 (rAAV2-hGAD65) gene delivered to the subthalamic nucleus (STN). This is combined with theex vivogene delivery of tyrosine hydroxylase (TH) by fibroblasts injected into the striatum. After the treatment, the rotation behavior was improved with the greatest efficacy in the combination group. The results of immunohistochemistry showed that hGAD65 gene delivery by AAV2 successfully led to phenotypic changes of neurons in STN. And the levels of glutamic acid and GABA in the internal segment of the globus pallidus (GPi) and substantia nigra pars reticulata (SNr) were obviously lower than the control groups. However, hGAD65 gene transfer did not effectively protect surviving dopaminergic neurons in the SNc and VTA. This study suggests that subthalamic hGAD65 gene therapy and combined with TH gene therapy can alleviate symptoms of the PD model rats, independent of the protection the DA neurons from death.

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