van Marum Robert J
Geriatric Department, B05.256, University Medical Center Utrecht, PO Box 855000, 3500 GA Utrecht, The Netherlands.
Fundam Clin Pharmacol. 2008 Jun;22(3):265-74. doi: 10.1111/j.1472-8206.2008.00578.x.
Dementia is increasingly being recognized as one of the most important medical problems in the elderly. As most pharmacological research within the field of dementia is focused on Alzheimer's dementia (AD), this review will focus on pharmacological interventions in AD. Most disease-modifying therapies are based on the amyloid hypothesis. In this hypothesis, the pathological accumulation of Abeta in the brain leads to oxidative stress, neuronal destruction and finally the clinical syndrome of AD. Following this hypothesis, secondary prevention of AD can be made by: decreasing the production of Abeta, stimulation of clearance of Abeta formed or prevention of aggregation of Abeta into amyloid plaques. First a short overview on current approved therapies for AD is given. The main part of the review will focus on potential disease-modifying therapies for AD that are currently being studied in phase I to phase III trials.
痴呆症日益被视为老年人最重要的医学问题之一。由于痴呆症领域的大多数药理学研究都集中在阿尔茨海默病(AD)上,本综述将聚焦于AD的药物干预。大多数疾病修饰疗法都基于淀粉样蛋白假说。在该假说中,大脑中β淀粉样蛋白(Aβ)的病理性积累会导致氧化应激、神经元破坏,最终引发AD的临床综合征。按照这一假说,AD的二级预防可通过以下方式实现:减少Aβ的产生、促进已形成的Aβ的清除或防止Aβ聚集成淀粉样斑块。首先对目前已批准的AD疗法进行简要概述。综述的主要部分将聚焦于目前正在进行I期至III期试验研究的AD潜在疾病修饰疗法。