2016
DOI: 10.1080/17513758.2016.1162856
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Study on dynamic characteristics’ change of hippocampal neuron reduced models caused by the Alzheimer’s disease

Abstract: In the paper, based on the electrophysiological experimental data, the Hippocampal neuron reduced model under the pathology condition of Alzheimer's disease (AD) has been built by modifying parameters' values. The reduced neuron model's dynamic characteristics under effect of AD are comparatively studied. Under direct current stimulation, compared with the normal neuron model, the AD neuron model's dynamic characteristics have obviously been changed. The neuron model under the AD condition undergoes supercriti… Show more

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Cited by 10 publications
(2 citation statements)
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“…With the world population grows, the incidence of AD and the cost of AD are growing at an ever-increasing rate, and it has become a social issue [ 1 ]. It is generally agreed that the neuropathologic hallmarks of AD can be summarized as extracellular deposits of amyloid-β protein (Aβ), intracellular neurofibrillary tangles (NFTs) and neuronal loss in the brain [ 2 , 3 ]. The early accumulation of Aβ may lead a series of downstream events including neuronal degeneration, then evolved into volume atrophy and cognitive functional damage of the corresponding brain area gradually.…”
Section: Introductionmentioning
confidence: 99%
“…With the world population grows, the incidence of AD and the cost of AD are growing at an ever-increasing rate, and it has become a social issue [ 1 ]. It is generally agreed that the neuropathologic hallmarks of AD can be summarized as extracellular deposits of amyloid-β protein (Aβ), intracellular neurofibrillary tangles (NFTs) and neuronal loss in the brain [ 2 , 3 ]. The early accumulation of Aβ may lead a series of downstream events including neuronal degeneration, then evolved into volume atrophy and cognitive functional damage of the corresponding brain area gradually.…”
Section: Introductionmentioning
confidence: 99%
“…The brains of AD patients are characterized by an accumulation of extracellular beta-amyloid (Aβ) plaques and the deposition of intracellular neurofibrillary tangles (NFTs) [ 2 ]. Although the pathology of AD has been characterized, the mechanisms of neuronal loss and cognitive impairment in AD remain elusive [ 3 , 4 ]. Most therapeutic agents used to clinically treat AD target Aβ and NFTs but do not stop or reverse disease progression.…”
Section: Introductionmentioning
confidence: 99%