Tobias Gerhard, PhD, Center for Health Services Research on Pharmacotherapy, Chronic Disease Management, and Outcomes, Institute for Health, Health Care Policy and Aging Research, Rutgers, The State University of New Jersey, New Brunswick and Department of Pharmacy Practice and Administration, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey; D. P. Devanand, MD, Department of Psychiatry, College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute, New York; Cecilia Huang, PhD, Stephen Crystal, PhD, Center for Health Services Research on Pharmacotherapy, Chronic Disease Management, and Outcomes, Institute for Health, Health Care Policy and Aging Research, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Mark Olfson, MD, MPH, Department of Psychiatry, College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute, New York, USA
Tobias Gerhard, PhD, Center for Health Services Research on Pharmacotherapy, Chronic Disease Management, and Outcomes, Institute for Health, Health Care Policy and Aging Research, Rutgers, The State University of New Jersey, New Brunswick and Department of Pharmacy Practice and Administration, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, New Jersey; D. P. Devanand, MD, Department of Psychiatry, College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute, New York; Cecilia Huang, PhD, Stephen Crystal, PhD, Center for Health Services Research on Pharmacotherapy, Chronic Disease Management, and Outcomes, Institute for Health, Health Care Policy and Aging Research, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Mark Olfson, MD, MPH, Department of Psychiatry, College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute, New York, USA.
Br J Psychiatry. 2015 Jul;207(1):46-51. doi: 10.1192/bjp.bp.114.154047. Epub 2015 Jan 22.
BackgroundLithium inhibits glycogen synthase kinase-3, an enzyme implicated in the pathogenesis of dementia.AimsTo examine the association of lithium and dementia risk in a large claims-based US cohort of publicly insured older adults with bipolar disorder.MethodThe cohort included individuals ≥50 years diagnosed with bipolar disorder who did not receive dementia-related services during the prior year. Each follow-up day was classified by past-year cumulative duration of lithium use (0, 1-60, 61-300 and 301-365 days). Dementia diagnosis was the study outcome. Anticonvulsants commonly used as mood stabilisers served as a negative control.ResultsCompared with non-use, 301-365 days of lithium exposure was associated with significantly reduced dementia risk (hazard ratio (HR) = 0.77, 95% CI 0.60-0.99). No corresponding association was observed for shorter lithium exposures (HR = 1.04, 95% CI 0.83-1.31 for 61-300 days; HR = 1.07, 95% CI 0.67-1.71 for 1-60 days) or for any exposure to anticonvulsants.ConclusionsContinuous lithium treatment may reduce dementia risk in older adults with bipolar disorder.
锂能抑制糖原合成酶激酶-3,这种酶与痴呆的发病机制有关。
在一个大型基于理赔的美国有公共保险的老年双相情感障碍患者队列中,检查锂与痴呆风险的相关性。
该队列包括年龄≥50 岁且在过去一年中未接受与痴呆相关服务的被诊断为双相情感障碍的个体。每个随访日根据过去一年锂使用的累积持续时间(0、1-60、61-300 和 301-365 天)进行分类。痴呆诊断是研究结果。作为情绪稳定剂常用的抗惊厥药作为阴性对照。
与非使用者相比,301-365 天的锂暴露与痴呆风险显著降低相关(风险比(HR)=0.77,95%CI 0.60-0.99)。对于较短的锂暴露,未观察到相应的关联(HR=1.04,95%CI 0.83-1.31 用于 61-300 天;HR=1.07,95%CI 0.67-1.71 用于 1-60 天)或任何抗惊厥药暴露。
连续锂治疗可能降低老年双相情感障碍患者的痴呆风险。