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Studies using ADNI cross-sectional and longitudinal data from multiple modalities have reported that:
面向ADNI多模态的横向与纵向数据的研究表明:
AD pathology is already present in people with no outward sign of memory loss and these cognitively normal people may already have subtle brain atrophy
即使没有显著的记忆损失,一些人的脑部也可能存在AD(阿尔茨海默症)的病灶。除此之外,认知正常的人的脑部可能已经有微小的脑萎缩
There are typical patterns of amyloid deposition, declines in glucose metabolism, and structural brain changes that occur in AD
AD患者的淀粉样蛋白沉积物、血糖代谢的下降与脑部结构变化均呈现特殊的模式
Cognitive decline is more closely linked to tau then Aß deposition
与Aß沉积物相比,认知下降与tau的关联更近
PS:ß-淀粉样蛋白(amyloid-ß,Aß)是由淀粉样前体蛋白经ß-和γ-分泌酶的蛋白水解作用产生的含有39~42个氨基酸的多肽。它可由多种细胞产生,循环于血液、脑脊液和脑间质液中,大多与伴侣蛋白分子结合,少数以游离状态存在。人体内Aß最常见的亚型是Aß1~40和Aß1~42. Aß1~42具有更强的毒性,且更容易聚集,从而形成Aß沉淀的核心,引发神经毒性作用。
Aß沉积不仅与神经元的退行性病变有关,且可以激活一系列病理事件,包括星形胶质细胞和小胶质细胞的激活、血脑屏障的破坏和微循环的变化等 (https://baike.baidu.com/item/%CE%B2-%E6%B7%80%E7%B2%89%E6%A0%B7%E8%9B%8B%E7%99%BD/1212967?fr=aladdin)
Researchers have discovered a link between two proteins related to AD, tau and amyloid beta, finding that people with more amyloid in their brains also produce more tau. (https://www.futurity.org/tau-amyloid-link-alzheimers-1712012/)
AD is characterized by the progressive disruption of the brain connectome. As the disease progresses, there are fewer connections between essential brain regions.
AD患者以脑部连接的发展中断为特征。随着疾病恶化,重要脑区的连接更少。
Many genes in addition to APOE4 underlie AD. ADNI data has helped to identify or confirm 10 of the approximately 20 genes currently identified
除了APOE4,更多的基因与AD有关。ADNI数据帮助我们识别或者确认:在已识别的近20个基因中,10个与AD有关。
Cerebrovascular disease can accelerate disease progression in AD
脑血管疾病会加剧阿尔茨海默症的恶化
Both the cognitively normal and MCI groups are pathologically heterogeneous. Some people show no signs of AD, some show signs of progressing to AD quickly, and others show signs of progressing to dementias other than AD
认知正常组与轻度认知障碍组的病理呈现多样性。一些人没有展现AD迹象,一些人展现快速恶化为AD的迹象,另一些人呈现恶化为老年痴呆、而非阿尔茨海默症的迹象
From: http://adni.loni.usc.edu/study-design/#background-container
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