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Striatal Expression of Glutamic Acid Decarboxylase Gene in Alzheimer's Disease
Author(s) -
Boissière Florence,
Faucheux Baptiste,
Duyckaerts Charles,
Hauw JeanJacques,
Agid Yves,
Hirsch Etienne C.
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.71020767.x
Subject(s) - striatum , glutamate decarboxylase , gabaergic , putamen , in situ hybridization , caudate nucleus , biology , neuroscience , medicine , endocrinology , messenger rna , dopamine , inhibitory postsynaptic potential , gene , biochemistry , enzyme
To examine potential alteration of GABAergic striatal neurons in Alzheimer's disease, we used quantitative in situ hybridization to analyze the messenger RNA coding for M r 67,000 glutamic acid decarboxylase (GAD 67 mRNA) in the striatum of five patients with Alzheimer's disease (AD) and nine matched control subjects. We found a 51–57% increase in the optical density of hybridization signal in the caudate nucleus and putamen, corresponding to a 30–42% increase in the number of neurons expressing a detectable amount of GAD 67 mRNA. By contrast, no alteration was observed in the ventral striatum. The expression of GAD 67 mRNA per neuron was similar in AD and control subjects both in the dorsal and ventral striatum. Taken together, our data indicate that, in AD, GABAergic neurotransmission is increased in the dorsal striatum but not in the ventral striatum. We suggest that this increased GABAergic neurotransmission may explain extrapyramidal signs often observed in AD.