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SH2B1 is involved in the accumulation of A�?²42 in Alzheimer′s disease model
5th International Conference on Alzheimer’s Disease & Dementia
Wen-An Wang , Fu-De Huang, Yijun Shen, Yiling Xia, Shiquan Meng and Nastasia K H Lim
Xin Hua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, China Chinese Academy of Sciences, China Shanghai Jiaotong University School of Medicine, China
Posters & Accepted Abstracts: J Alzheimers Dis Parkinsonism
Abstract
Insulin has been identified as a modulator of the neuronal pathways involved in learning and memory, and is also implicated as a modulator of A�?² and tau metabolism toxicity. Disrupted insulin signaling pathways are evident in Alzheimerâ�?�?s disease (AD) patients and it is understood that type II diabetes can increase the risk of developing AD, suggesting a possible link between metabolic disorders and neurodegeneration. SH2B1 is a key protein in the insulin signaling involved in regulating the activity of the insulin receptor. To further identify the role of the insulin signaling in the pathology of AD, SH2B (Drosophila SH2B1 homologue) in neurons was partially knocked out or overexpressed in an AD Drosophila model expressing A�?²42. Partial knockout of SH2B had a detrimental effect on mobility and neurotransmission, and increased levels and intraneuronal accumulation of A�?²42 in the A�?²42-expressing flies as assessed by ELISA and immunostaining, while, overexpression of SH2B produced the opposite effect. Thus, SH2B1 may be an upstream modulator of A�?² metabolism, acting to inhibit A�?² accumulation, and has a role in the pathogenesis of AD. SH2B1 may therefore have potential as a therapeutic target for this common form of dementia.Biography
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