Table of Contents
Journal of Neurodegenerative Diseases
Volume 2013, Article ID 657470, 8 pages
Review Article

Amyloid Beta-Protein and Neural Network Dysfunction

Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, UNAM, Campus Juriquilla, Boulevard Juriquilla 3001, 76230 Querétaro, Qro, Mexico

Received 27 October 2012; Accepted 6 December 2012

Academic Editor: Gal Bitan

Copyright © 2013 Fernando Peña-Ortega. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.