Sulforaphane Inhibits the Generation of Amyloid-beta Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice
机构：[a]Department of Neurology, Inovation Center for Neurological Disorders, Xuan Wu Hospital, Capital Medical University, Beijing, P.R. China神经内科首都医科大学宣武医院[b]Beijing Key Laboratory of Geriatric Cognitive Disorders, Beijing, P.R. China[c]Clinical Center for Neurodegenerative Disease and Memory Impairment, Capital Medical University, Beijing, P.R. China[d]Center of Alzheimer’s Disease, Beijing Institute for Brain Disorders, Beijing, P.R. China[e]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing, P.R. China[f]National Clinical Research Center for Geriatric Disorders, Beijing, P.R. China
Abnormal amyloid-beta (A beta) aggregates are a striking feature of Alzheimer's disease (AD), and A beta oligomers have been proven to be crucial in the pathology of AD. Any intervention targeting the generation or aggregation of A beta can be expected to be useful in AD treatment. Oxidative stress and inflammation are common pathological changes in AD that are involved in the generation and aggregation of A beta. In the present study, 6-month-old PS1V97L transgenic (Tg) mice were treated with sulforaphane, an antioxidant, for 4 months, and this treatment significantly inhibited the generation and aggregation of A beta. Sulforaphane also alleviated several downstream pathological changes that including tau hyperphosphorylation, oxidative stress, and neuroinflammation. Most importantly, the cognition of the sulforaphane-treated PS1V97L Tg mice remained normal compared to that of wild-type mice at 10 months of age, when dementia typically emerges in PS1V97L Tg mice. Pretreating cultured cortical neurons with sulforaphane also protected against neuronal injury caused by A beta oligomers in vitro. These findings suggest that sulforaphane may be a potential compound that can inhibit A beta oligomer production in AD.
基金：
the Key Project of the National Natural Science Foundation of China (81530036);
the National Key Scientific Instrument and Equipment Development Project (31627803);
Mission Program of Beijing Municipal Administration of Hospitals (SML20150801);
Beijing Scholars Program, and Beijing Brain Initiative from Beijing Municipal Science & Technology Commission (Z161100000216137);
CHINACANADA Joint Initiative on Alzheimer’s Disease and Related Disorders (81261120571);
Beijing Municipal Commission of Health and Family Planning (PXM2017 026283 000002).
第一作者机构：[a]Department of Neurology, Inovation Center for Neurological Disorders, Xuan Wu Hospital, Capital Medical University, Beijing, P.R. China
共同第一作者：
通讯作者：
通讯机构：[*1]Inovation Center for Neurological Disorders, Department of Neurology, Xuan Wu Hospital, Capital Medical University, Beijing 100053, P.R. China.
推荐引用方式(GB/T 7714)：
Ting-Ting Hou,He-Yun Yang,Wei Wang,et al.Sulforaphane Inhibits the Generation of Amyloid-beta Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice[J].JOURNAL OF ALZHEIMERS DISEASE.2018,62(4):1803-1813.doi:10.3233/JAD-171110.
APA：
Ting-Ting Hou,He-Yun Yang,Wei Wang,Qiao-Qi Wu,Yuan-Ruhua Tian&Jian-Ping Jia.(2018).Sulforaphane Inhibits the Generation of Amyloid-beta Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice.JOURNAL OF ALZHEIMERS DISEASE,62,(4)
MLA：
Ting-Ting Hou,et al."Sulforaphane Inhibits the Generation of Amyloid-beta Oligomer and Promotes Spatial Learning and Memory in Alzheimer's Disease (PS1V97L) Transgenic Mice".JOURNAL OF ALZHEIMERS DISEASE 62..4(2018):1803-1813
