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- W2035331545 abstract "Alzheimer's disease is thought to be caused by β-amyloid peptide (Aβ)-dependent synaptic dysfunction. However, the signaling pathways connecting Aβ and synaptic dysfunction remain elusive. Here we report that Aβ transiently increases the expression level of centaurin-α1 (CentA1) in neurons, which induces a Ras-dependent association of Elk-1 with mitochondria, leading to mitochondrial and synaptic dysfunction in organotypic hippocampal slices of rats. Downregulation of the CentA1-Ras-Elk-1 pathway restored normal mitochondrial activity, spine structural plasticity, spine density, and the amplitude and frequency of miniature EPSCs in Aβ-treated neurons, whereas upregulation of the pathway was sufficient to decrease spine density. Elevations of CentA1 and association of Elk-1 with mitochondria were also observed in transgenic mice overexpressing a human mutant form of amyloid precursor protein. Therefore, the CentA1-Ras-Elk-1 signaling pathway acts on mitochondria to regulate dendritic spine density and synaptic plasticity in response to Aβ in hippocampal neurons, providing new pharmacological targets for Alzheimer's disease." @default.
- W2035331545 created "2016-06-24" @default.
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- W2035331545 date "2013-03-20" @default.
- W2035331545 modified "2023-10-12" @default.
- W2035331545 title "Centaurin- 1-Ras-Elk-1 Signaling at Mitochondria Mediates -Amyloid-Induced Synaptic Dysfunction" @default.
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- W2035331545 doi "https://doi.org/10.1523/jneurosci.2641-12.2013" @default.
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