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RanBP9 Overexpression Accelerates Loss of Dendritic Spines in a Mouse Model of Alzheimer's Disease.

Neurobiol Dis.. 2014-06;  69C:169-179
R Wang, JP Palavicini, H Wang, P Maiti, E Bianchi, Xu S, Lloyd BN, Dawson-Scully K, Kang DE, Lakshmana MK. Section of Neurobiology, Torrey Pines Institute for Molecular Studies, 11350 SW Village Parkway, Port Saint Lucie, FL 34987, USA.
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摘要

We previously demonstrated that RanBP9 overexpression increased Aβ generation and amyloid plaque burden, subsequently leading to robust reductions in the levels of several synaptic proteins as well as deficits in the learning and memory skills in a mouse model of Alzheimer's disease (AD). In the present study, we found striking reduction of spinophilin-immunoreactive puncta (52%, p<0.001) and spinophilin area (62.5%, p<0.001) in the primary cortical neurons derived from RanBP9 transgenic mice (RanBP9-Tg) compared to wild-type (WT) neurons. Similar results were confirmed in WT cortical neurons transfected with EGFP-RanBP9. At 6-months of age, the total spine density in the cortex of RanBP9 single... More

关键词

APΔE9 mice; Cortex; Dendritic spines; Hippocampus; RanBP9; Transgenic mice