Intraneuronal accumulation of Aβ42 induces age-dependent slowing of neuronal transmission in Drosophila.

Authors:
Jing-Ya Lin
Jing-Ya Lin
Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
China
Wen-An Wang
Wen-An Wang
University of Alberta
Canada
Xiao Zhang
Xiao Zhang
Peking University School and Hospital of Stomatology
China
Hai-Yan Liu
Hai-Yan Liu
Northeast Normal University
China
Xiao-Liang Zhao
Xiao-Liang Zhao
Shandong University
China
Fu-De Huang
Fu-De Huang
Vanderbilt University
United States

Neurosci Bull 2014 Apr 15;30(2):185-90. Epub 2014 Apr 15.

Department of Neurology, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.

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 age-dependent slowing of neuronal transmission along pathways involving multiple synapses.

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http://dx.doi.org/10.1007/s12264-013-1409-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562655PMC
April 2014
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3 Citations

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