Reactive oxidative species enhance amyloid toxicity in APP/PS1 mouse neurons

被引：8

作者：

Yang, Bin ^{[2
,3
]}

Sun, Xiaqin ^{[1
]}

Lashuel, Hilal ^{[4
]}

Zhang, Yan ^{[1
]}

机构：

[1] Peking Univ, Coll Life Sci, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China

[2] Minzu Univ China, Coll Life & Environm Sci, Lab Biotechnol, Beijing 100081, Peoples R China

[3] Minzu Univ China, Coll Life & Environm Sci, State Key Lab Chinese Ethn Minor Tradit Med, Beijing 100081, Peoples R China

[4] Ecole Polytech Fed Lausanne, Sch Life Sci, Lausanne, Switzerland

来源：

NEUROSCIENCE BULLETIN | 2012年 / 28卷 / 03期

关键词：

amyloid; reactive oxidative species; APP/; PS1; aggregation; toxicity; ALZHEIMERS-DISEASE; TRANSGENIC MICE; BETA-PEPTIDE; A-BETA-42; ACCUMULATION; PRECURSOR PROTEIN; PLAQUE-FORMATION; STRESS; APOPTOSIS; PATHOLOGY; OLIGOMERS;

D O I：

10.1007/s12264-012-1239-1

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

To investigate whether intracellular amyloid beta (iA beta) induces toxicity in wild type (WT) and APP/PS1 mice, a mouse model of Alzheimer's disease. Different forms of A beta aggregates were microinjected into cultured WT or APP/PS1 mouse hippocampal neurons. TUNEL staining was performed to examine neuronal cell death. Reactive oxidative species (ROS) were measured by MitoSOX (TM) Red mitochondrial superoxide indicator. Crude, monomer and protofibril A beta induced more toxicity in APP/PS1 neurons than in WT neurons. ROS are involved in mediating the vulnerability of APP/PS1 neurons to iA beta toxicity. Oxidative stress may mediate cell death induced by iA beta in neurons.

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收藏

页码：233 / 239

页数：7

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