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. 2014 Apr 15;30(2):185–190. doi: 10.1007/s12264-013-1409-9

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

Jing-Ya Lin 1,2, Wen-An Wang 1,3,✉, Xiao Zhang 2, Hai-Yan Liu 1,2, Xiao-Liang Zhao 4, Fu-De Huang 2,✉
PMCID: PMC5562655  PMID: 24733651

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

Keywords: neuronal transmission, synaptic dysfunction, latency, Alzheimer’s disease, intraneuronal beta amyloid

Contributor Information

Wen-An Wang, Email: wangwenan312141030@163.com.

Fu-De Huang, Email: huangfude@yahoo.com.

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