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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Increase of monoamine oxidase-B activity in the brain of scrapie-infected hamsters.
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Increase of monoamine oxidase-B activity in the brain of scrapie-infected hamsters.

机译：瘙痒病感染的仓鼠大脑中单胺氧化酶B活性的增加。

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In the present study, the purpose is to determine activities of monoamine oxidases (MAO) in the brain of 263K scrapie-infected hamsters during the development of this experimental prion disease. Indeed, MAO activity modifications which have already been related in aging and neurodegenerations is suspected to be involved in the neuron loss process by elevated hydrogen peroxide formation. Monoamine oxidase type A (MAO-A) and B (MAO-B) activities were followed in the brain at different stages of the disease. MAO-A activity did not change significantly during the evolution of the disease. However, concerning the MAO-B activity, a significant increase was observed from 50 days post-infection and through the course of the disease and reached 42.9+/-5.3% at its ultimate stage. Regarding these results, MAO-B could be a potential therapeutic target then we have performed a pre-clinical treatment with irreversible (Selegiline or l-deprenyltrade mark) or and reversible (MS-9510) MAO-B inhibitors used alone or in association with an anti-scrapie drug such as MS-8209, an amphotericin B derivative. Our results show that none of the MAO-B inhibitors used was able to delay the onset of the disease. Neither these MAO-B inhibitors nor R-NMDA inhibitors (MK-801) can enhance the effects of MS-8209. The present findings clearly indicate a significant increase of cerebral MAO-B activity in scrapie-infected hamsters. Furthermore, inhibitors of MAO-B do not have any curative or palliative effect on this experimental model indicating that the raise of this activity is probably more a consequence rather than a causal event of the neurodegenerative process.
机译：在本研究中，目的是确定在实验性pr病毒病发展过程中263K瘙痒病感染的仓鼠大脑中单胺氧化酶（MAO）的活性。确实，已经怀疑与衰老和神经退行性相关的MAO活性改变是由于过氧化氢形成的增加而参与了神经元的丧失过程。在疾病的不同阶段，在大脑中跟踪了A型单胺氧化酶（MAO-A）和B型（MAO-B）的活动。在疾病的发展过程中，MAO-A活性没有明显改变。然而，关于MAO-B活性，从感染后50天到整个病程中观察到显着增加，并且在其最终阶段达到42.9 +/- 5.3％。关于这些结果，MAO-B可能是潜在的治疗靶标，然后我们进行了不可逆的（司来吉兰或1-去异戊二烯商标）或可逆的（MS-9510）MAO-B抑制剂单独或与之联合使用的临床前治疗一种抗刮擦药物，例如两性霉素B衍生物MS-8209。我们的结果表明，所使用的MAO-B抑制剂均不能延缓疾病的发作。这些MAO-B抑制剂和R-NMDA抑制剂（MK-801）均不能增强MS-8209的作用。目前的发现清楚地表明在瘙痒病感染的仓鼠中脑MAO-B活性显着增加。此外，MAO-B抑制剂对该实验模型没有任何治愈或缓解作用，表明该活性的升高可能更多是神经退行性过程的结果而不是因果关系。

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