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*Corresponding Author E-mail: khoshimovn@gmail.com
*****mamadaminovraxmatjon@gmail.com
Increasing amount of evidence suggests that age-related dysregulation of neuronal Ca2+ homeostasis may play a proximal role in the pathogenesis of Alzheimer's disease, as impaired Ca2+ can cause synaptic deficits and contribute to the accumulation of Aβ plaques and neurofibrillary tangles.Ca2+ disruption is known to be mostly involved in all pathologies of Alzheimer's disease, the use of chemical agents or small molecules specific for Ca2+ channels, or the treatment of proteins on the plasma membrane and intracellular organelle membranes for correction is quite possible. Neuronal dysregulation of Ca2+ may open up a new approach to the prevention and treatment of Alzheimer's disease. The article shows the possible competition between the polyphenols PC-6, PC-7 and glutamate for the area of regulation of the opening of ion channels of ionotropic NMDA-receptors in the brain of rats.
Synaptosome, NMDA-receptors, Glutamate, Calcium