Final answer:
Beta amyloid plaques in Alzheimer's disease activate the nervous system, leading to disruptions in glutamatergic transmission and excitotoxicity. This impairs synaptic connections, causing cognitive deficits and contributing to the neurodegenerative processes characteristic of AD.
Step-by-step explanation:
The formation of beta amyloid plaques is a hallmark of Alzheimer's disease (AD) and these plaques have been shown to impact the normal functioning of neuronal systems. Neurodegenerative processes are triggered by these plaques, including synaptic dysfunction in the nervous system. Beta amyloid plaques can lead to the disruption of glutamatergic transmission, increasing the population of NMDA receptors with the NR2B subunit, and affecting the number of metabotropic mGluR5 receptors. These changes may result in excitotoxicity, excessive calcium concentrations, and impaired synaptic connections crucial for memory formation and maintenance. Furthermore, Aß peptides are associated with a reduction of AMPA receptors and abnormal upregulation of NMDA receptors, contributing to further neurotoxicity and cognitive deficits associated with AD.