1Department of Neurology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
2Center for Stem Cell and Nanomedicine, Laboratory for System Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai 201210, China
3Department of Neurology, Xin Hua Hospital Affiliated to Shanghai Jiaotong University School of Medicine Chongming Branch, Shanghai 202150, China
4Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China

Abstract 

Beta amyloid (Aβ42)-induced dysfunction and loss of synapses are believed to be major underlying mechanisms for the progressive loss of learning and memory abilities in Alzheimer’s disease (AD). The vast majority of investigations on AD-related synaptic impairment focus on synaptic plasticity, especially the decline of long-term potentiation of synaptic transmission caused by extracellular Aβ42. Changes in other aspects of synaptic and neuronal functions are less studied or undiscovered. Here, we report that intraneuronal accumulation of Aβ42 induced an agedependent slowing of neuronal transmission along pathways involving multiple synapses.

Keywords

neuronal transmission; synaptic dysfunction; latency; Alzheimer’s disease; intraneuronal beta amyloid

[SpringerLink]