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Alzheimer’s Disease (AD) is a common neurodegenerative disease that displays two hallmark protein accumulations in the brain – extracellular amyloid beta (Aβ) and intracellular hyperphosphorylated tau. Aβ has been shown to directly penetrate the neuronal cell membrane and damage the membrane. This compromises membrane integrity, increases membrane permeability that alters membrane conductance and elevates intracellular calcium concentrations which contribute to reactive oxygen species production and mitochondrial dysfunction. This damage to the plasma membrane requires a quick and efficient repair mechanism to restore the barrier function of the membrane and avoid neuronal cell death. However, a defect in membrane repair has not been examined as a contributor to AD. Here, we aimed to assess membrane repair capacity in AD in vitro models as a potential contributor to neuronal death …