A novel mechanism of memory loss in Alzheimer’s disease mice via the degeneration of entorhinal–CA1 synapses

Abstract

The entorhinal cortex (EC) is one of the most vulnerable brain regions that is attacked during the early stage of Alzheimer’s disease (AD). Here, we report that the synaptic terminals of pyramidal neurons in the EC layer II (ECIIPN) directly innervate CA1 parvalbumin (PV) neurons (CA1PV) and are selectively degenerated in AD mice, which exhibit amyloid-β plaques similar to those observed in AD patients. A loss of ECIIPN–CA1PV synapses disables the excitatory and inhibitory balance in the CA1 circuit and impairs spatial learning and memory. Optogenetic activation of ECIIPN using a theta burst paradigm rescues ECIIPN–CA1PV synaptic defects and intercepts the decline in spatial learning and memory. These data reveal a novel mechanism of memory loss in AD mice via the selective degeneration of the ECIIPN–CA1PV pathway.

Extracted Key Phrases

2 Figures and Tables

Statistics

05002017
Citations per Year

86 Citations

Semantic Scholar estimates that this publication has 86 citations based on the available data.

See our FAQ for additional information.

Cite this paper

@inproceedings{Yang2016ANM, title={A novel mechanism of memory loss in Alzheimer’s disease mice via the degeneration of entorhinal–CA1 synapses}, author={X Yang and C . Huang P . Yao and Tiantian Tian and Xuemin Li and H Yan and J Wu and H Li and Ling Ling Pei and Dan Liu}, year={2016} }