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Brain γ-Aminobutyric Acid Changes in Stiff-Person Syndrome
Author(s) -
Lucien M. Levy,
Igor Levy-Reis,
Mavis Fujii,
Marinos C. Dalakas
Publication year - 2005
Publication title -
archives of neurology
Language(s) - English
Resource type - Journals
eISSN - 1538-3687
pISSN - 0003-9942
DOI - 10.1001/archneur.62.6.970
Subject(s) - glutamate decarboxylase , gabaergic , gamma aminobutyric acid , medicine , cortex (anatomy) , autoantibody , endocrinology , glutamic acid , inhibitory postsynaptic potential , neuroscience , antibody , chemistry , psychology , biochemistry , immunology , amino acid , enzyme , receptor
Patients with stiff-person syndrome (SPS) have circulating antibodies against glutamic acid decarboxylase, the rate-limiting enzyme responsible for the synthesis of gamma-aminobutyric acid (GABA). Although the patients' symptoms of stiffness and unexpected spasms can be explained on the basis of reduced or impaired inhibitory neurotransmitters, such as GABA, it is unclear whether the level of GABA in the brains of these patients is reduced and, if so, whether the reduction is due to anti-glutamic acid decarboxylase antibodies.

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