{"title":"[Novel Therapeutic Strategies for Alzheimer's Disease].","authors":"Taisuke Tomita","doi":"10.11477/mf.1416202732","DOIUrl":null,"url":null,"abstract":"<p><p>The molecular pathogenesis of Alzheimer's disease (AD) has been elucidated through the biochemical analysis of senile plaques, neurofibrillary tangles, and pathological features of the brains of patients with AD. Genetic analysis, initiated with familial AD investigation, has revealed that Aβ aggregation and accumulation are crucial processes in AD pathogenesis. The success of lecanemab against aggregated Aβ is the result of these efforts. Meanwhile, research on tau as a causative molecule in AD and various other tauopathies is advancing gradually. Furthermore, genetic analysis has revealed that the inflammatory response of glial cells modifies AD pathophysiology; a novel therapeutic strategy for inflammation control is thus currently under consideration. This article summarizes the latest discoveries related to these new therapeutic strategies for AD.</p>","PeriodicalId":52507,"journal":{"name":"Brain and Nerve","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain and Nerve","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11477/mf.1416202732","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
The molecular pathogenesis of Alzheimer's disease (AD) has been elucidated through the biochemical analysis of senile plaques, neurofibrillary tangles, and pathological features of the brains of patients with AD. Genetic analysis, initiated with familial AD investigation, has revealed that Aβ aggregation and accumulation are crucial processes in AD pathogenesis. The success of lecanemab against aggregated Aβ is the result of these efforts. Meanwhile, research on tau as a causative molecule in AD and various other tauopathies is advancing gradually. Furthermore, genetic analysis has revealed that the inflammatory response of glial cells modifies AD pathophysiology; a novel therapeutic strategy for inflammation control is thus currently under consideration. This article summarizes the latest discoveries related to these new therapeutic strategies for AD.
通过对老年痴呆症（AD）患者大脑中的老年斑、神经纤维缠结和病理特征进行生化分析，阐明了阿尔茨海默病（AD）的分子发病机制。从家族性渐变性痴呆症调查开始的遗传分析表明，Aβ的聚集和积聚是渐变性痴呆症发病的关键过程。lecanemab 对抗聚集的 Aβ 的成功就是这些努力的结果。与此同时，关于 tau 作为 AD 及其他各种 tau 病致病分子的研究也在逐步推进。此外，遗传分析还揭示了神经胶质细胞的炎症反应会改变AD的病理生理学；因此，目前正在考虑一种控制炎症的新型治疗策略。本文总结了与这些新的AD治疗策略相关的最新发现。
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