Peña-Ortega Fernando
Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, UNAM, Campus Juriquilla, Boulevard Juriquilla 3001, 76230 Querétaro, Qro, Mexico.
J Neurodegener Dis. 2013;2013:657470. doi: 10.1155/2013/657470. Epub 2013 Jan 30.
Understanding the neural mechanisms underlying brain dysfunction induced by amyloid beta-protein (Aβ) represents one of the major challenges for Alzheimer's disease (AD) research. The most evident symptom of AD is a severe decline in cognition. Cognitive processes, as any other brain function, arise from the activity of specific cell assemblies of interconnected neurons that generate neural network dynamics based on their intrinsic and synaptic properties. Thus, the origin of Aβ-induced cognitive dysfunction, and possibly AD-related cognitive decline, must be found in specific alterations in properties of these cells and their consequences in neural network dynamics. The well-known relationship between AD and alterations in the activity of several neural networks is reflected in the slowing of the electroencephalographic (EEG) activity. Some features of the EEG slowing observed in AD, such as the diminished generation of different network oscillations, can be induced in vivo and in vitro upon Aβ application or by Aβ overproduction in transgenic models. This experimental approach offers the possibility to study the mechanisms involved in cognitive dysfunction produced by Aβ. This type of research may yield not only basic knowledge of neural network dysfunction associated with AD, but also novel options to treat this modern epidemic.
了解由β-淀粉样蛋白（Aβ）引起的脑功能障碍背后的神经机制是阿尔茨海默病（AD）研究的主要挑战之一。AD最明显的症状是认知能力严重下降。认知过程与其他任何脑功能一样，源于相互连接的神经元的特定细胞集合的活动，这些神经元基于其内在和突触特性产生神经网络动力学。因此，Aβ诱导的认知功能障碍以及可能与AD相关的认知衰退的根源，必须从这些细胞特性的特定改变及其对神经网络动力学的影响中去寻找。AD与多个神经网络活动改变之间的众所周知的关系反映在脑电图（EEG）活动的减慢上。在AD中观察到的EEG减慢的一些特征，例如不同网络振荡的产生减少，在体内和体外应用Aβ或转基因模型中Aβ过量产生时均可诱发。这种实验方法为研究Aβ产生的认知功能障碍所涉及的机制提供了可能性。这类研究不仅可能产生与AD相关的神经网络功能障碍的基础知识，还可能带来治疗这种现代流行病的新选择。
