講演者：　岩田 修永　（長崎大学 医歯薬総合研究科 生命薬科学専攻 分子創薬科学講座 ゲノム創薬学分野　教授）

演題：A disease mechanism-based therapy for Alzheimer’s disease

日時： 9月7日（水） 12:00-13:00
会場： 発生医学研究所1階　カンファレンス室

Abstract：

Aggregation and deposition of amyloid-β peptide (Aβ) in the brain are triggering events of the long-term pathological cascade of Alzheimer’s disease (AD), and are closely associated with the metabolic balance between Aβ anabolic and catabolic activities. As almost all familial AD mutations cause an increase in the anabolism of a particular form of Aβ, Aβ_1-42, leading to Aβ deposition and accelerating AD pathology, a chronic reduction in the catabolic activity would also promote Aβ deposition. Neprilysin is a rate-limiting peptidase involved in brain Aβ catabolism. Mounting evidence that expression levels of neprilysin are decreased in the hippocampus and cerebral cortex of AD patients from the early stages of disease development and also with aging in humans, suggests a close association of neprilysin with the etiology and pathogenesis of AD. Thus, a subtle but long-term decline in neprilysin activity appears to be at least partly responsible for the memory-related symptoms of AD, and up-regulation of neprilysin would be a promising strategy for disease-modifying therapy of AD. In this lecture, I will talk about several approaches to up-regulate neuronal neprilysin activity in the brain.

References:
1) Iwata N. et al., Nat. Med., 6, 143-150 (2000).

2) Iwata N. et al., Science, 292, 1550-1552 (2001).

3) Iwata N. et al., Pharmacol. Ther., 108, 129-148 (2001).

4) Saito T. et al., Nat. Med., 11, 434-439 (2005).

5) Iwata N. et al., Sci. Rep., 3, 1472 (2013).

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担当分野：　微生物薬学分野　大槻純男