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A Novel Mechanism Underlies Pathological, β-amyloid-induced Neuronal Hyperexcitation

Abstract Patients with Alzheimer's disease (AD) exhibit a significantly higher incidence of unprovoked seizures compared to age-matched non-AD controls, and animal models of AD (i.e., transgenic human amyloid precursor protein, hAPP mice) display neural hyper-excitation and epileptic seizures. Hyperexcitation is particularly important because it contributes to the high incidence of epilepsy in AD patients as well as AD-related synaptic deficits and neurodegeneration. Given that there is significant amyloid-β (Aβ) accumulation and deposition in AD brain, Aβ exposure ultimately may be responsible for neural hyper-excitation in both AD patients and animal models. Emerging evidence indicates that α7 nicotinic ace... (more)
Created Date 2011
Contributor Liu, Qiang (Author) / Wu, Jie (Advisor) / Lukas, Ronald J (Committee member) / Chang, Yongchang (Committee member) / Sierks, Michael (Committee member) / Smith, Brian (Committee member) / Vu, Eric (Committee member) / Arizona State University (Publisher)
Subject Neurosciences / amyloid / excitotoxicity / hyperexcitation / nicotinic receptor / patch clamp
Type Doctoral Dissertation
Extent 129 pages
Language English
Reuse Permissions All Rights Reserved
Note Ph.D. Neuroscience 2011
Collaborating Institutions Graduate College / ASU Library
Additional Formats MODS / OAI Dublin Core / RIS

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Description Dissertation/Thesis