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RanBP9 Overexpression Down-Regulates Phospho-Cofilin, Causes Early Synaptic Deficits and Impaired Learning, and Accelerates Accumulation of Amyloid Plaques in the Mouse Brain.

J Alzheimers Dis.. 2013-11; 
Palavicini JP, Wang H, Minond D, Bianchi E, Xu S, Lakshmana MK. Section of Neurobiology, Torrey Pines Institute for Molecular Studies, Port Saint Lucie, FL, USA.
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摘要

Loss of synaptic proteins and functional synapses in the brains of patients with Alzheimer's disease (AD) as well as transgenic mouse models expressing amyloid-β protein precursor is now well established. However, the earliest age at which such loss of synapses occurs, and whether known markers of AD progression accelerate functional deficits is completely unknown. We previously showed that RanBP9 overexpression leads to enhanced amyloid plaque burden in a mouse model of AD. In this study, we found significant reductions in the levels of synaptophysin and spinophilin, compared with wild-type controls, in both the cortex and the hippocampus of 5- and 6-month old but not 3- or 4-month old APΔE9/Ra... More

关键词

Amyloid plaques; RanBP9; cofilin; learning and memory; spinophilin; synaptophysin