Objective To investigate whether intracellular amyloid β （iAβ） induces toxicity in wild type （WT） and APP/PS1 mice, a mouse model of Alzheimer＇s disease. Methods Different forms of Aβ aggregates were microinje...Objective To investigate whether intracellular amyloid β （iAβ） induces toxicity in wild type （WT） and APP/PS1 mice, a mouse model of Alzheimer＇s disease. Methods Different forms of Aβ aggregates were microinjected into cultured WT or APP/PS1 mouse hippocampal neurons. TUNEL staining was performed to examine neuronal cell death. Reactive oxidative species （ROS） were measured by MitoSOXTM Red mitochondrial superoxide indicator. Results Crude, monomer and protofibrilAβ induced more toxicity inAPP/PS1 neurons than in WT neurons. ROS are involved in mediating the vulnerability of APP/PS1 neurons to iAβ toxicity. Conclusion Oxidative stress may mediate cell death induced by iAβ in neurons.展开更多
基金supported by grants from the National Basic Research Development Program of the Ministry of Science and Technology of China (2009CB941301)Roche Research Grant, Peking University President Research Grant and the Recruiting Research Grant, Ministry of Education of China
文摘Objective To investigate whether intracellular amyloid β （iAβ） induces toxicity in wild type （WT） and APP/PS1 mice, a mouse model of Alzheimer＇s disease. Methods Different forms of Aβ aggregates were microinjected into cultured WT or APP/PS1 mouse hippocampal neurons. TUNEL staining was performed to examine neuronal cell death. Reactive oxidative species （ROS） were measured by MitoSOXTM Red mitochondrial superoxide indicator. Results Crude, monomer and protofibrilAβ induced more toxicity inAPP/PS1 neurons than in WT neurons. ROS are involved in mediating the vulnerability of APP/PS1 neurons to iAβ toxicity. Conclusion Oxidative stress may mediate cell death induced by iAβ in neurons.
