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タイトル	en Clinical trials for Alzheimer disease and perspectives
作成者	en Shinji TAGAMI en Masatoshi TAKEDA en Masayasu OKOCHI
主題	Other en Alzheimer disease Other en amyloid β-protein Other en γ-secretase inhibitors Other en BACE inhibitors Other en anti-Aβ antibodies
内容注記	Abstract en Alzheimer disease (AD) is the most common type of dementia and may account for 60 - 70% of dementia cases. Senile plaques are a hallmark of AD, and their major constituent is amyloid β-protein (Aβ) 42. Aβ is produced via endoproteolysis by beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), which cleaves β-amyloid precursor protein at the extracellular domain, followed by cleavages by presenilin/γ-secretase. Aβ accumulation in the brain is thought to occur decades before disease onset, and pathological changes such as synaptic dysfunction and tau accumulation gradually proceed. Most candidates for disease-modifying therapy (DMT) for AD have targeted either inhibition of Aβ generation with secretase inhibitors or removal of produced and aggregated Aβ with anti-Aβ antibodies. None of them has been approved for clinical practice. Moreover, application of BACE inhibitors and γ-secretase inhibitors in several clinical studies caused paradoxical cognitive impairment. However, early AD patients treated with aducanumab, a monoclonal anti-Aβ antibody, showed a significant reduction in cognitive decline and its clinical use is awaiting approval by the FDA in 2020. In this review, we present a brief summary of DMTs that target Aβ and perspectives for future AD therapy. Other en Review Article
出版者	ja 大阪河﨑リハビリテーション大学
日付	Issued2020-12
言語	und
資源タイプ	other
資源識別子	DOI https://doi.org/10.69202/0000000304 , URI https://kawasakigakuen.repo.nii.ac.jp/records/304
ID	JaLC 10.69202/0000000304
収録誌情報	PISSN 2436-1097 en COGNITION & REHABILITATION 巻1 号1 開始ページ12 終了ページ19
ファイル	C 1-012-019 279.4 kB (application/pdf) Available2021-08-10
コンテンツ更新日時	2024-09-29