Amyloid Beta-Protein and Neural Network Dysfunction. (30th January 2013)

• Record Type: Journal Article
• Authors: Peña-Ortega, Fernando
• Other Names: Bitan Gal Academic Editor.
• Is Part Of: Journal of neurodegenerative diseases. Volume 2013(2013)
• Publication Date: 2013-01-30
• Subjects: Nervous system -- Degeneration -- Periodicals; Neurodegenerative Diseases; Nervous system -- Degeneration; Periodicals; 616.8
• DOI: 10.1155/2013/657470
• Languages: English
• ISSNs: 2090-858X

Abstract

Abstract : Understanding the neural mechanisms underlying brain dysfunction induced by amyloid beta-protein (A β ) 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 A β -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 A β application or by A β overproduction in transgenic models. This experimental approach offers the possibility to study the mechanisms involved in cognitive dysfunction produced by A β . 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.