Amyloid-β (Aβ) peptides aggregated into plaques deposited in the brain are the main hallmark of Alzheimer's disease (AD), a social and economic burden worldwide. In this context, insoluble Aβ fibrils are the main components of plaques. The recent trials that used approved AD drugs show that they can remove the fibrils from AD patients' brains, but they did not halt the course of the disease.
View Article and Find Full Text PDFCalcium ion regulation plays a crucial role in maintaining neuronal functions such as neurotransmitter release and synaptic plasticity. Copper (Cu ) coordination to amyloid-β (Aβ) has accelerated Aβ aggregation that can trigger calcium dysregulation by enhancing the influx of calcium ions by extensive perturbing integrity of the membranes. Aβ aggregation, calcium dysregulation, and membrane damage are Alzheimer disease (AD) implications.
View Article and Find Full Text PDFDiscrepin is a 38-residue α-toxin extracted from the venom of the Venezuelan scorpion , which inhibits ionic transit in the voltage-dependent potassium channels (Kv) of A-type current. The effect of specific residues on the IC between Discrepine and Kv4.3, the main component of A-type currents, is known; however, the molecular details of the toxin-channel interaction are not known.
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