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	1. Update on Alzheimer's neurodegeneration induced by amyloid precursor protein
	ZHAO Dan,ZHAO Jie,LI Shao
	Basic Medicine 27 May 2016
	Show/Hide Abstract \| Cite this paper︱Full-text: PDF (4K B)

	Abstract:The loss of synapses between neurons as well as progressive neuronal degeneration and apoptosis is the basis of pathological Alzheimer's disease (AD), which directly induces progressive memorial and cognitive impairment of AD patients. Beta amyloid precursor protein (β-APP，APP) is commonly associated with senile plaques formation which is best known for the pathogenesis of AD. More and more studies have shown that the structure and the hydrolysic way of APP play very important roles in neuronal degeneration and apoptosis of AD by many ways. In this paper, we will overview the update progress for the pathophysiological mechanism of neuronal degeneration and apoptosis induced by APP, from the perspective of APP structure and its hydrolysis.
	TO cite this article:ZHAO Dan,ZHAO Jie,LI Shao. Update on Alzheimer's neurodegeneration induced by amyloid precursor protein[OL].[27 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693086


	2. Potassium Channels Depression is involved in the Apolipoprotein E4 enhanced Calcium Influx via N-Methyl-D-Aspartate receptor
	Qin Ying,Yang Lifan,Weng Yuteng,Luo Xiaoli
	Basic Medicine 29 January 2014
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	Abstract:Among many suggested mechanisms of the association between the ε4 allele of apoplipoprotein E gene (APOE) and Alzheimer's disease (AD), the present study focused on the link of apoE4 to Ca2+ homeostasis. On the acutely isolated hippocampal neurons, our observation showed that: 1) apoE4 increased the [Ca2+]i greatly and immediately. It was in a dose- and time- dependent manner, and irreversible; 2) removing Ca2+ from external solution abolished apoE4's effect on [Ca2+]i; 3) nicardipine showed little effect on apoE4-elicited [Ca2+]i increasing, while MK-801 almost blocked the apoE4-induced Ca2+ influx; and 4) pretreatment with K+ channel opener significantly reduced the apoE4-induced [Ca2+]i increasing. The results suggest that apoE4 increased [Ca2+]i by way of NMDA receptor channels but not L-type Ca2+ channels; and the depression of K+ channel activities was involved in this effects of apoE4.
	TO cite this article:Qin Ying,Yang Lifan,Weng Yuteng, et al. Potassium Channels Depression is involved in the Apolipoprotein E4 enhanced Calcium Influx via N-Methyl-D-Aspartate receptor[OL].[29 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4584364


	3. Apolipoprotein E4 Suppresses potassium currents in Hippocampal Neurons
	Qin Ying,Xie Dongping,Weng Yuteng,Luo Xiaoli,Yang Lifan
	Basic Medicine 13 January 2014
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	Abstract:apolipoprotein E epsilon 4 allele (APOE4) is one of the major risk factors for Alzheimer's disease，but the underlying mechanism remains unclear. Our data show that: 1) application of apoE4 in extracellular solution suppresses the delayed rectifier potassium current (synonym: IK) by 18.9± 2.8 % and 18.1 ± 3.6 % (n=10, P<0.01), at +30 mV and +60 mV of membrane potential. The effect is reversible and shows no voltage-dependency; 2) extracellular application of apoE4 does not show any obvious effect on A-type fast transient potassium current (synonym: IA); 3) application of apoE4 in the intracellular solution suppresses both IA and IK. In case of IK, the reduction rate is 56.2 ± 7.6 % and 58.7 ± 7.4 % (n=10, P<0.01) at +30 mV and +60 mV of membrane potential, respectively; in case of IA, the reductive rate is 58.6 ± 9.7 % and 65.3 ± 8.6 % (n=10, P<0.01) at +30 mV and +60 mV, respectively; 4) the effects of intracellular apoE4 on both IA and IK show obvious voltage-dependent; and 5) in the contrast, application of apoA and apoE3 exhibits no effects on IK or IA. The results indicate that apoE4 molecules could suppress the potassium currents from neurons on both the inner and outer side of neuronal membrane, which support the propulsions that apoE4 expressed by neurons might be responsible for neuronal damages related to the pathogenesis of Alzheimer's disease.
	TO cite this article:Qin Ying,Xie Dongping,Weng Yuteng, et al. Apolipoprotein E4 Suppresses potassium currents in Hippocampal Neurons[OL].[13 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581917


	4. Iron status and lipopolysaccharide regulate Ndfip1 by activation of nuclear factor-kappa B
	XU Huamin,CHANG Qing,JIA Wenting,JIANG Hong,SUN Peng,XIE Junxia
	Basic Medicine 30 August 2013
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	Abstract:Nedd4 family interacting protein 1 (Ndfip1) is an adaptor protein for the Nedd4 family of ubiquitin ligases that target proteins for degradation. Recent studies confirmed the role of Ndfip1 as a regulator of iron metabolism and pointed out that Ndfip1 was involved in iron homeostasis by regulating the degradation of iron importer divalent metal transporter 1 (DMT1). However, little is known about how Ndfip1 is regulated. The aim of this article was to investigate the regulation of Ndfip1 levels and the possible mechanisms. In this study, we investigated the effect of various stimuli, including iron status and lipopolysaccharide (LPS) on Ndfip1 expression in MES23.5 dopaminergic cell lines. Results showed that Ndfip1 expression in these cells was enhanced by ferrous iron overload, but not ferric iron overload, and decreased after iron deprivation by desferoxamine (DFO). In addition, LPS could significantly increase the expression of Ndfip1. Furthermore, we demonstrated that the regulation of Ndfip1 expression by these various stimuli was achieving by activation of nuclear factor-kappa B. We speculate that iron status and LPS may contribute to the changes of Ndfip1 expression by activation of nucle

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