Young Min Choe1, Ki Woong Kim2, Jin Hyeong Jhoo3, Seung Ho Ryu4, Eun Hyun Seo5, Bo Kyung Sohn6, Min Soo Byun7, Jae-Hwa Bak7, Jong-Min Lee8, Hyuk Jin Yun8, Myeong-Il Han9, Jong Inn Woo7, Dong Young Lee7. 1. Department of Neuropsychiatry, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, Korea. 2. Department of Neuropsychiatry, Seoul National University Bundang Hospital, Seongnam, Korea. 3. Department of Neuropsychiatry, Kangwon National University Hospital, Chunchon, Korea. 4. Department of Neuropsychiatry, Konkuk University Hospital, Seoul, Korea. 5. Division of Natural Medical Sciences, College of Health Science Chosun University, Gwangju, Korea. 6. Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Korea. 7. Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Korea. 8. Department of Biomedical Engineering, Hanyang University, Seoul, Korea. 9. Department of Psychiatry, Maeumsarang Hospital, Wanju, Korea.
Abstract
OBJECTIVES: A series of preclinical studies have suggested that selective serotonin reuptake inhibitor antidepressants not only stimulate neurogenesis but also have neuroprotective effects. The present study primarily aimed to investigate whether escitalopram would decelerate the brain atrophy of patients with mild-to-moderate Alzheimer's disease (AD). We also assessed the effects of escitalopram on the cognitive function and neuropsychiatric symptoms of these participants. METHODS:Seventy-four probable AD patients without major depression were recruited from four dementia clinics of university hospitals and randomly assigned in a 1:1 ratio. Each group received 20 mg/day of escitalopram or placebo for 52 weeks. The primary outcome measures were the change rates of hippocampal and whole brain volume on magnetic resonance imaging for 52 weeks. The Alzheimer's Disease Assessment Scale-cognitive subscale, Mini-Mental State Examination, Neuropsychiatric Inventory, and Cornell Scale for Depression in Dementia (CSDD) were also applied. RESULTS: We did not find any significant differences in the changes of hippocampal or whole brain volume between the groups. Escitalopram showed significant beneficial effects on the CSDD score at 28 weeks compared with placebo (t = -2.17, df = 50.42, p = 0.035), but this finding did not persist throughout the study. CONCLUSION: The findings of the present study do not support the role of escitalopram as a progression-delaying treatment for AD. However, the negative results of the present trial should be interpreted cautiously because of the relatively small sample size. Further large-scale escitalopram trials targeting the earlier stages of AD, even prodromal AD, are still needed.
RCT Entities:
OBJECTIVES: A series of preclinical studies have suggested that selective serotonin reuptake inhibitor antidepressants not only stimulate neurogenesis but also have neuroprotective effects. The present study primarily aimed to investigate whether escitalopram would decelerate the brain atrophy of patients with mild-to-moderate Alzheimer's disease (AD). We also assessed the effects of escitalopram on the cognitive function and neuropsychiatric symptoms of these participants. METHODS: Seventy-four probable ADpatients without major depression were recruited from four dementia clinics of university hospitals and randomly assigned in a 1:1 ratio. Each group received 20 mg/day of escitalopram or placebo for 52 weeks. The primary outcome measures were the change rates of hippocampal and whole brain volume on magnetic resonance imaging for 52 weeks. The Alzheimer's Disease Assessment Scale-cognitive subscale, Mini-Mental State Examination, Neuropsychiatric Inventory, and Cornell Scale for Depression in Dementia (CSDD) were also applied. RESULTS: We did not find any significant differences in the changes of hippocampal or whole brain volume between the groups. Escitalopram showed significant beneficial effects on the CSDD score at 28 weeks compared with placebo (t = -2.17, df = 50.42, p = 0.035), but this finding did not persist throughout the study. CONCLUSION: The findings of the present study do not support the role of escitalopram as a progression-delaying treatment for AD. However, the negative results of the present trial should be interpreted cautiously because of the relatively small sample size. Further large-scale escitalopram trials targeting the earlier stages of AD, even prodromal AD, are still needed.
Authors: Lisa Nobis; Sanjay G Manohar; Stephen M Smith; Fidel Alfaro-Almagro; Mark Jenkinson; Clare E Mackay; Masud Husain Journal: Neuroimage Clin Date: 2019-06-19 Impact factor: 4.881
Authors: Jennifer A Watt; Zahra Goodarzi; Areti Angeliki Veroniki; Vera Nincic; Paul A Khan; Marco Ghassemi; Yonda Lai; Victoria Treister; Yuan Thompson; Raphael Schneider; Andrea C Tricco; Sharon E Straus Journal: BMJ Date: 2021-03-24