tailieunhanh - Báo cáo khoa học: Interactions between the amyloid precursor protein C-terminal domain and G proteins mediate calcium dysregulation and amyloid b toxicity in Alzheimer’s disease

Alzheimer’s disease is characterized by neuropathological accumulations of amyloidb(1–42) [Ab(1–42)], a cleavage product of the amyloid precursor protein (APP). Recent studies have highlighted the role of APP in Ab-med-iated toxicity and have implicated the G-protein system; however, the exact mechanisms underlying this pathway are as yet undetermined. | Interactions between the amyloid precursor protein C-terminal domain and G proteins mediate calcium dysregulation and amyloid b toxicity in Alzheimer s disease Gideon M. Shaked1 Stephanie Chauv1 Kiren Ubhi1 Lawrence A. Hansen1 2 and Eliezer Masliah1 2 1 Department of Neurosciences University of California San Diego CA USA 2 Department of Pathology University of California San Diego CA USA Keywords caspase endoplasmic reticulum neurodegeneration voltage gated calcium channels Correspondence E. Masliah Department of Neurosciences University of California San Diego La Jolla CA 92093-0624 USA Fax 1 858 534 6232 Tel 1 858 534 8992 E-mail emasliah@ Received 11 December 2008 revised 22 February 2009 accepted 9 March 2009 doi Alzheimer s disease is characterized by neuropathological accumulations of amyloid b 1-42 Ab 1-42 a cleavage product of the amyloid precursor protein APP . Recent studies have highlighted the role of APP in Ab-med-iated toxicity and have implicated the G-protein system however the exact mechanisms underlying this pathway are as yet undetermined. In this context we sought to investigate the role of calcium upregulation following APP-dependent Ab-mediated G-protein activation. Initial studies on the interaction between APP Ab and Go proteins demonstrated that the interaction between APP specifically its C-terminal -YENPTY- region and Go was reduced in the presence of Ab. Cell death and calcium influx in Ab-treated cells were shown to be APP dependent and to involve G-protein activation because these effects were blocked by use of the G-protein inhibitor pertussis toxin. Collectively these results highlight a role for the G-protein system in APP-dependent Ab-induced toxicity and calcium dys-regulation. Analysis of the APP Go interaction in human brain samples from Alzheimer s disease patients at different stages of the disease revealed a decrease in the interaction correlating with disease progression. Moreover .

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