Aβ accumulation has been discovered to form large, relatively cation-permeable channels in the plasma membrane of a neuron. These channel formations in the membranes of a neuron could cause cell depolarisation, sodium and potassium dysregulation, depletion of neural energy stores and other types of cellular dysfunction. This study shows that the build-up of amyloid beta (Aβ) depositions during the onset of Alzheimer’s disease has profound effects on the activity of the local community of neurons in the central nervous system. These effects can include enhanced neural activity, spontaneous epileptiform activity and incidence of epileptic seizures. From the results in this area, it can be seen that the neurodegeneration observed in Alzheimer’s disease has been associated with the increase of toxicity of Aβ depositions. In this research paper, we examined this hypothesis in light of a computational model of a neuron.
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