Sleep as a window to understand and regulate Alzheimer's disease:emerging roles of thalamic reticular nucleus  

作　　者：Haoqi Sun Shiqian Shen Robert J.Thomas M.Brandon Westover Can Zhang 

机构地区：[1]Department of Neurology,Beth Israel Deaconess Medical Center,Harvard Medical School,Boston,MA,USA [2]Center for Translational Pain Research,Department of Anesthesia,Critical Care and Pain Medicine,Massachusetis General Hospital,Harvard Medical School,Boston,MA,USA [3]Division of Pulmonary,Critical Care and Sleep Medicine,Department of Medicine,Beth Israel Deaconess Medical Center,Harvard Medical School,Boston,MA,USA [4]Genetics and Aging Research Unit,McCance Center for Brain Health,Mass General Institute for Neurodegenerative Disease,Department of Neurology,Massachusetts General Hospital,Harvard Medical School,Boston,MA,USA

出　　处：《Neural Regeneration Research》2025年第6期1711-1712,共2页中国神经再生研究（英文版）

基　　金：supported by the Massachusetts General Hospital Scientific Projects to Accelerate Research and Collaboration (SPARC) award;Cure Alzheimer’s Fund (to CZ);the National Institutes of Health (NIH),including R01NS102190,RF1NS120947,and R01HL161253 (to MBW),RF1NS120947 (to RJT)。

摘　　要：Introduction:Alzheimer 's disease(AD) is a common neurodegenerative disorder and the primary cause of dementia. Considerable evidence supports the “amyloid hypothesis,” stating that the pathogenesis of AD is primarily caused by the deposition of amyloid-β(Aβ), which drives tau phosphorylation, neuroinflammation, and neurodegeneration in the brain. The amyloid hypothesis is strengthened by the significant and moderate benefit of lecanemab, a humanized antibody through an anti-amyloid mechanism,showing slowed clinical decline(van Dyck et al.,2023). The recent positive results of anti-amyloid trials have brought back focus on the amyloid hypothesis through biochemical, genetic, and pharmacological approaches(Zhang, 2023).

关 键 词：ALZHEIMER inflammation HYPOTHESIS 

分 类 号：R749.16[医药卫生—神经病学与精神病学]