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English Abstract
Journal Article
[Reduced neuronal nitric oxide synthetase and c-protein kinase levels in Alzheimer's disease].
Revista de Neurologia 2000 Februrary 17
INTRODUCTION: Alzheimer's disease is characterized by a general and progressive dementia and by the presence of beta-amiloide deposits.
OBJECTIVE: The levels of neuronal nitric oxide synthase (NOS) and protein kinase C (PKC), and the relationship between these proteins, the free-radical theory and the high level of beta-amiloide in Alzheimer's disease, have been studied.
MATERIAL AND METHODS: The study has been performed in samples of Alzheimer's disease (superior, medial and inferior regions of temporalis gyrus) from control individuals and patients. The tissue was homogenized and the proteins were analyzed using monoclonal antibodies for NOS and PKC.
RESULTS: Lower levels of neuronal constitutive NOS (37% +/- 2.5 and 52% +/- 3.0) in Alzheimer's disease derived superior and inferior temporalis gyrus, respectively, were observed. No changes were found in superior temporalis gyrus in PKC isoforms levels, involved in the processing for the beta-amiloide precursor protein. In the medial and inferior regions the PKC level was 5% +/- 0.5 to 22% +/- 3.0.
CONCLUSIONS: These results could be related with an imbalance in the superoxide/nitric oxide ratio as a consequence of the non-inhibition of lipoxygenase, and with a neurotransmission dysfunction due, all this, to the decrease of nitric oxide levels. On the other hand, a relationship could be proposed between the high concentrations of beta-amiloide and the decrease in PKC levels in Alzheimer's disease.
OBJECTIVE: The levels of neuronal nitric oxide synthase (NOS) and protein kinase C (PKC), and the relationship between these proteins, the free-radical theory and the high level of beta-amiloide in Alzheimer's disease, have been studied.
MATERIAL AND METHODS: The study has been performed in samples of Alzheimer's disease (superior, medial and inferior regions of temporalis gyrus) from control individuals and patients. The tissue was homogenized and the proteins were analyzed using monoclonal antibodies for NOS and PKC.
RESULTS: Lower levels of neuronal constitutive NOS (37% +/- 2.5 and 52% +/- 3.0) in Alzheimer's disease derived superior and inferior temporalis gyrus, respectively, were observed. No changes were found in superior temporalis gyrus in PKC isoforms levels, involved in the processing for the beta-amiloide precursor protein. In the medial and inferior regions the PKC level was 5% +/- 0.5 to 22% +/- 3.0.
CONCLUSIONS: These results could be related with an imbalance in the superoxide/nitric oxide ratio as a consequence of the non-inhibition of lipoxygenase, and with a neurotransmission dysfunction due, all this, to the decrease of nitric oxide levels. On the other hand, a relationship could be proposed between the high concentrations of beta-amiloide and the decrease in PKC levels in Alzheimer's disease.
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