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Dementia 2016
September 29-October 01, 2016
Volume 6 Issue 5(Suppl)
J Alzheimers Dis Parkinsonism 2016
ISSN:2161-0460 JADP, an open access journal
conferenceseries
.com
September 29-October 01, 2016 London, UK
5
th
International Conference on
Alzheimer’s Disease & Dementia
Wen-An Wang et al., J Alzheimers Dis Parkinsonism 2016, 6:5(Suppl)
http://dx.doi.org/10.4172/2161-0460.C1.022SH2B1 is involved in the accumulation of Aβ42 in Alzheimer’s disease model
Wen-An Wang
1,3
,Fu-De Huang
2
, Yijun Shen
1,2
, Yiling Xia
1,2
, Shiquan Meng
2
and
Nastasia K H Lim
2
1
Xin Hua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, China
2
Chinese Academy of Sciences, China
3
Shanghai Jiaotong University School of Medicine, China
I
nsulin has been identified as a modulator of the neuronal pathways involved in learning and memory, and is also implicated
as a modulator of Aβ and tau metabolism toxicity. Disrupted insulin signaling pathways are evident in Alzheimer’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 Aβ
42
.
Partial knockout of SH2B had a detrimental effect on mobility and neurotransmission, and increased levels and intraneuronal
accumulation of Aβ
42
in the Aβ
42
-expressing flies as assessed by ELISA and immunostaining, while, overexpression of SH2B
produced the opposite effect.Thus, SH2B1may be an upstreammodulator of Aβmetabolism, acting to inhibit Aβ 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.
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