Abstract
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.
Highlights
Neurodegenerative diseases are a kind of progressive disease in which the structure or function of the neurons is gradually destroyed and leads to their death
As Aβ channels are permeable to all cations, in this study, we considered both sodium and potassium as two significant cations in the neuronal process in a single inhibitory neuron
Thisadelay or even fault in the turnover of ions disorders the loss membrane of functionality of aincritical created by channelopathies
Summary
Neurodegenerative diseases are a kind of progressive disease in which the structure or function of the neurons is gradually destroyed and leads to their death. According to the Office for National Statistics, dementia, including Alzheimer’s disease, has overtaken heart disease as the leading cause of mortality in the United Kingdom [3]. This deadly neurodegenerative disease causes problems with mental functioning such as cognitive, memory and behavioural impairments. The most important Alzheimer’s disease symptoms can be intracellular neurofibrillary tangles and extracellular deposition of amyloid beta (Aβ) plaques [4,5] It can be said the driving force for Alzheimer’s disease pathogenesis outside the cell is the accumulation of Aβ oligomers or plaques and as a result the formation of Aβ channels [6]. The exact mechanism is not fully understood [10]
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