Lamotrigine attenuates deficits in synaptic plasticity and accumulation of amyloid plaques in APPPS1 transgenic mice》.pdfVIP

Neurobiology of Aging 35 (2014) 2713e2725 Contents lists available at ScienceDirect Neurobiology of Aging journal homepage: www.elsevi /locate/neuaging Lamotrigine attenuates deficits in synaptic plasticity and accumulation of amyloid plaques in APP/PS1 transgenic mice Mao-Ying Zhang a, Chuan-Yi Zheng a, Ming-Ming Zou a, Jian-Wei Zhu a, Yan Zhang a, Jing Wang a, Chun-Feng Liu b, Qi-Fa Li c, Zhi-Cheng Xiao d, Shao Li c, *, Quan-Hong Ma b, **, Ru-Xiang Xu a, *** a Affi liated Bayi Brain Hospital, Beijing Military Hospital, PLA and PhD Student Program of Southern Medical University, Beijing, China bJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Institute of Neuroscience, Soochow University, Suzhou, Jiangsu Province, China c Department of Physiology, Dalian Medical University, Dalian, China d Department of Anatomy and Developmental Biology, Monash University, Clayton, Australia a r t i c l e i n f o a b s t r a c t Article history: Hyperactivity and its compensatory mechanisms may causally contribute to synaptic and cognitive Received 2 February 2014 deficits in Alzheimer’s disease (AD). Blocking the overexcitation of the neural network, with levetir- Received in revised form 6 June 2014 acetam (LEV), a sodium channel blocker applied in the treatment of epilepsy, prevented synaptic and Accepted 10 June 2014 cognitive deficits in human amyloid precursor protein (APP) transgenic mice. This study has brought the Available online 16 June 2014