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. 1. Introduction Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by severe cognitive impairments [1, 2]. Postmortem studies of brains from long-term AD patients have revealed the presence of senile plaques that contain the amyloid beta-peptide (Aβ) [3, 4]. Most studies of AD have focused on the biochemical mechanisms involved in the neurodegenerative processes triggered by the Aβ aggregates (for recent reviews, see [5, 6]). Such efforts have provided noteworthy evidence that has explained some aspects of the disease, mainly in its terminal stages; however, it has been difficult to link these findings to the known cognitive and behavioral symptoms that characterize the early stages of the disease. Moreover, new therapeutic approaches to treat AD based on this research have shown little or no benefit (for a recent review, see [7]). By looking at the cellular mechanisms involved in AD physiopathology from another perspective, it is becoming clear that cognitive decline associated with AD, or with any other neurological disease, should be examined in the context of the related neural network dysfunctions [1, 2, 8–10]. This approach, which might look novel for AD, has had proven success for the
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