Department of Pharmacology, Biocenter, Campus Riedberg, Goethe-University, Frankfurt, Germany.
Int J Biochem Cell Biol. 2013 Jan;45(1):76-80. doi: 10.1016/j.biocel.2012.06.009. Epub 2012 Jun 26.
Mitochondria are membrane bound organelles that provide cellular energy in form of ATP. In addition to ATP synthesis mitochondria are key regulators of calcium homeostasis, free radical production, steroid synthesis and apoptosis, each of these factors could also be associated with essential mechanisms involved in neurodegenerative diseases. Recent studies revealed that changes in mitochondria membrane fluidity might have a direct impact on membrane-based processes such as fission-associated morphogenic changes, opening of the mitochondrial permeability transition pore or oxidative phosphorylation at the complexes of the electron transport chain. We investigated synaptosomal plasma and mitochondrial membranes isolated from brains of mouse models for ageing, Alzheimer's disease, Huntington's disease and Amyotrophic lateral sclerosis. Membrane properties are disease specifically altered, identifying mitochondrial membranes as targets for possible therapeutic strategies in neurodegenerative diseases. This article is part of a Directed Issue entitled: Bioenergetic dysfunction, adaptation and therapy.
线粒体是具有膜结构的细胞器,以三磷酸腺苷(ATP)的形式为细胞提供能量。除了合成 ATP,线粒体还是钙稳态、自由基生成、甾体合成和细胞凋亡的关键调节因子,这些因素中的每一个都可能与神经退行性疾病相关的基本机制有关。最近的研究表明,线粒体膜流动性的变化可能会对基于膜的过程产生直接影响,如与分裂相关的形态发生变化、线粒体通透性转换孔的开放或电子传递链复合物的氧化磷酸化。我们研究了从衰老、阿尔茨海默病、亨廷顿病和肌萎缩性侧索硬化症的小鼠模型中分离的突触体血浆和线粒体膜。膜特性发生了特定于疾病的改变,确定线粒体膜是神经退行性疾病中可能的治疗策略的靶点。本文是题为“生物能量功能障碍、适应和治疗”的专论的一部分。