In a previous paper, the authors have described the effect of Ca2+-antagonist. verapamil on Na,K-ATPase in experimental model of Alzheimer's disease (AD-[38,39]. The present paper is concerned with the effect of magnetic, stimulation of. pineal complex on Na,K-ATPase activity in the same experimental model of AD. Because accumulating data indicate that free radicals mediate injury and death of neurons in AD, and because magnetic fields (MFs) can alter- free radicals. reactions; we tested the hypothesis that stationary MFs mediates ion homeostasis through membrane Na;K-ATPase activity. Results are presented as Vmax/Km - parameters on erythrocyte membranes in peripheral blood of rats with lesioned nucleus basalis magnocellularis. Bilateral electrolytic or by kainic acid induced lesions of NBM induce significant decrease of Vmax/Km activity on erythrocyte membranes obtained by cardiac punction. Stimulation of - pineal complex of the brain more than ten days, by magnetic beards (600-Gauss ...flux density), fixed on the skull upon pineal gland, significantly increase impaired by lesions of NBM, Na, K-ATPase activity. Results are presented as Vmax/Km parameters. on erythrocyte membranes in peripheral blood of rats with lesioned NBM of the basal forebrain bundle. Chronically magnetic stimulation of the pineal complex significantly increase maximum velocity (Vmax; nmol Pi/mg protein/min) of proteins in both lesioned group, even more than 2-fold in by kainic acid (ka)lesioned animals in comparison of lesioned sham-stimulated and increase Vmax in comparison to both controls (sham-lesioned m-sham-stimulated, and intact controls, and return desturbed by lesions affinity of enzyme to substrate (Km; nM) near to the control values. These results confirm the hypothesis that altered ion homeostasis disturbed by neurodegenerations play an essential role in pathogenesis of experimental Alzheimer's disease (AD) and that magnetic stimulation of the pineal complex might successfully restore disturbed by neuronal death Na, K-ATPase activity.
TY - CONF
AU - Jovanova-Nešić, Katica
AU - Erić-Jovičić, Milena
AU - Popović, M.
AU - Popović, N.
AU - Rakić, L.
AU - Spector, Novera Herbert
PY - 2002
UR - http://intor.torlakinstitut.com/handle/123456789/149
AB - In a previous paper, the authors have described the effect of Ca2+-antagonist. verapamil on Na,K-ATPase in experimental model of Alzheimer's disease (AD-[38,39]. The present paper is concerned with the effect of magnetic, stimulation of. pineal complex on Na,K-ATPase activity in the same experimental model of AD. Because accumulating data indicate that free radicals mediate injury and death of neurons in AD, and because magnetic fields (MFs) can alter- free radicals. reactions; we tested the hypothesis that stationary MFs mediates ion homeostasis through membrane Na;K-ATPase activity. Results are presented as Vmax/Km - parameters on erythrocyte membranes in peripheral blood of rats with lesioned nucleus basalis magnocellularis. Bilateral electrolytic or by kainic acid induced lesions of NBM induce significant decrease of Vmax/Km activity on erythrocyte membranes obtained by cardiac punction. Stimulation of - pineal complex of the brain more than ten days, by magnetic beards (600-Gauss flux density), fixed on the skull upon pineal gland, significantly increase impaired by lesions of NBM, Na, K-ATPase activity. Results are presented as Vmax/Km parameters. on erythrocyte membranes in peripheral blood of rats with lesioned NBM of the basal forebrain bundle. Chronically magnetic stimulation of the pineal complex significantly increase maximum velocity (Vmax; nmol Pi/mg protein/min) of proteins in both lesioned group, even more than 2-fold in by kainic acid (ka)lesioned animals in comparison of lesioned sham-stimulated and increase Vmax in comparison to both controls (sham-lesioned m-sham-stimulated, and intact controls, and return desturbed by lesions affinity of enzyme to substrate (Km; nM) near to the control values. These results confirm the hypothesis that altered ion homeostasis disturbed by neurodegenerations play an essential role in pathogenesis of experimental Alzheimer's disease (AD) and that magnetic stimulation of the pineal complex might successfully restore disturbed by neuronal death Na, K-ATPase activity.
PB - IEEE, New York
C3 - 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings
T1 - Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease
EP - 170
SP - 165
ER -
@conference{
author = "Jovanova-Nešić, Katica and Erić-Jovičić, Milena and Popović, M. and Popović, N. and Rakić, L. and Spector, Novera Herbert",
year = "2002",
url = "http://intor.torlakinstitut.com/handle/123456789/149",
abstract = "In a previous paper, the authors have described the effect of Ca2+-antagonist. verapamil on Na,K-ATPase in experimental model of Alzheimer's disease (AD-[38,39]. The present paper is concerned with the effect of magnetic, stimulation of. pineal complex on Na,K-ATPase activity in the same experimental model of AD. Because accumulating data indicate that free radicals mediate injury and death of neurons in AD, and because magnetic fields (MFs) can alter- free radicals. reactions; we tested the hypothesis that stationary MFs mediates ion homeostasis through membrane Na;K-ATPase activity. Results are presented as Vmax/Km - parameters on erythrocyte membranes in peripheral blood of rats with lesioned nucleus basalis magnocellularis. Bilateral electrolytic or by kainic acid induced lesions of NBM induce significant decrease of Vmax/Km activity on erythrocyte membranes obtained by cardiac punction. Stimulation of - pineal complex of the brain more than ten days, by magnetic beards (600-Gauss flux density), fixed on the skull upon pineal gland, significantly increase impaired by lesions of NBM, Na, K-ATPase activity. Results are presented as Vmax/Km parameters. on erythrocyte membranes in peripheral blood of rats with lesioned NBM of the basal forebrain bundle. Chronically magnetic stimulation of the pineal complex significantly increase maximum velocity (Vmax; nmol Pi/mg protein/min) of proteins in both lesioned group, even more than 2-fold in by kainic acid (ka)lesioned animals in comparison of lesioned sham-stimulated and increase Vmax in comparison to both controls (sham-lesioned m-sham-stimulated, and intact controls, and return desturbed by lesions affinity of enzyme to substrate (Km; nM) near to the control values. These results confirm the hypothesis that altered ion homeostasis disturbed by neurodegenerations play an essential role in pathogenesis of experimental Alzheimer's disease (AD) and that magnetic stimulation of the pineal complex might successfully restore disturbed by neuronal death Na, K-ATPase activity.",
publisher = "IEEE, New York",
journal = "2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings",
title = "Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease",
pages = "170-165"
}
Jovanova-Nešić, K., Erić-Jovičić, M., Popović, M., Popović, N., Rakić, L.,& Spector, N. H. (2002). Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease.
2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings
IEEE, New York., 165-170.
Jovanova-Nešić K, Erić-Jovičić M, Popović M, Popović N, Rakić L, Spector NH. Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease. 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings. 2002;:165-170
Jovanova-Nešić Katica, Erić-Jovičić Milena, Popović M., Popović N., Rakić L., Spector Novera Herbert, "Effect of magnetic stimulation of pineal complex of the brain on Na,K-ATPase in experimental Alzheimer's Disease" 2002 6th Seminar on Neural Network Applications in Electrical Engineering, NEUREL 2002 - Proceedings (2002):165-170
