疾病
认知功能衰退
淀粉样蛋白(真菌学)
阿尔茨海默病
神经科学
心理学
τ蛋白
透视图(图形)
老年学
痴呆
医学
病理
人工智能
计算机科学
出处
期刊:Nature Aging
日期:2024-04-19
卷期号:4 (4): 453-463
被引量:1
标识
DOI:10.1038/s43587-024-00611-5
摘要
Slowing neurodegenerative disorders of late life has lagged behind progress on other chronic diseases. But advances in two areas, biochemical pathology and human genetics, have now identified early pathogenic events, enabling molecular hypotheses and disease-modifying treatments. A salient example is the discovery that antibodies to amyloid ß-protein, long debated as a causative factor in Alzheimer's disease (AD), clear amyloid plaques, decrease levels of abnormal tau proteins and slow cognitive decline. Approval of amyloid antibodies as the first disease-modifying treatments means a gradually rising fraction of the world's estimated 60 million people with symptomatic disease may decline less or even stabilize. Society is entering an era in which the unchecked devastation of AD is no longer inevitable. This Perspective considers the impact of slowing AD and other neurodegenerative disorders on the trajectory of aging, allowing people to survive into late life with less functional decline. The implications of this moment for medicine and society are profound. The advent of plaque-clearing antibodies to the amyloid-β as the first disease-modifying treatment for Alzheimer's disease will change the course of this disease, the most common type of dementia. Related progress will gradually alter the trajectory of human aging.
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