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Advances in the cellular and molecular biology of the beta-amyloid protein in Alzheimers disease

Kahn J, Gillespie A, Tsokos M, Ondos J, Dombi E, Camphausen K, et al

Bradley C, Lewis KS

Its therapeutic effects are primarily mediated through enhancement of -aminobutyric acid (GABA) activity, inhibition of GABA degradation, and blockade of voltage-gated sodium, calcium and potassium channels [1]

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This rapid GSH loss disrupts redox homeostasis, promotes ROS accumulation, and facilitates redox-dependent protein modifications that drive apoptotic commitment