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Clinical trials for Alzheimer disease and perspectives
https://doi.org/10.69202/0000000304
https://doi.org/10.69202/0000000304c2a01a7f-4e8f-4cd0-9994-d5dae659560b
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
C 1-012-019 (279.4 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2021-08-10 | |||||
| タイトル | ||||||
| タイトル | Clinical trials for Alzheimer disease and perspectives | |||||
| 言語 | en | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Alzheimer disease | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | amyloid β-protein | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | γ-secretase inhibitors | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | BACE inhibitors | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | anti-Aβ antibodies | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_1843 | |||||
| 資源タイプ | other | |||||
| ID登録 | ||||||
| ID登録 | 10.69202/0000000304 | |||||
| ID登録タイプ | JaLC | |||||
| 内容種別 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Review Article | |||||
| 言語 | en | |||||
| 著者 |
Shinji TAGAMI
× Shinji TAGAMI× Masatoshi TAKEDA× Masayasu OKOCHI |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | 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. | |||||
| 言語 | en | |||||
| 書誌情報 |
en : COGNITION & REHABILITATION 巻 1, 号 1, p. 12-19, 発行日 2020-12 |
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| 出版者 | ||||||
| 出版者 | 大阪河﨑リハビリテーション大学 | |||||
| 言語 | ja | |||||
| ISSN | ||||||
| 収録物識別子タイプ | PISSN | |||||
| 収録物識別子 | 2436-1097 | |||||
