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1Intraneuronal accumulation of Aβ42 induces age-dependent slowing of neuronal transmission in Drosophila显示文摘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.Jing-Ya Lin Wen-An Wang Xiao Zhang Hai-Yan Liu Xiao-Liang Zhao Fu-De Huang 2014Neuroscience Bulletin2014,30,2:5
2Illuminating Neural Circuits in Alzheimer’s Disease显示文摘Alzheimer’s disease(AD)is the most common neurodegenerative disorder and there is currently no cure.Neural circuit dysfunction is the fundamental mechanism underlying the learning and memory deficits in patients with AD.Therefore,it is important to understand the structural features and mechanisms underlying the deregulated circuits during AD progression,by which new tools for intervention can be developed.Here,we briefly summarize the most recently established cutting-edge experimental approaches and key techniques that enable neural circuit tracing and manipulation of their activity.We also discuss the advantages and limitations of these approaches.Finally,we review the applications of these techniques in the discovery of circuit mechanisms underlyingβ-amyloid and tau pathologies during AD progression,and as well as the strategies for targeted AD treatments.Yang Ying Jian-Zhi Wang 2021Neuroscience Bulletin2021,37,8:4
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