Effects of Antibodies to Glutamate on Cerebral Expression of the Tnfrsf1A Gene under Conditions of Spatial Amnesia Induced by Proinflammatory Protein S100A9 Fibrils in Aging Mice.

Autor: Gruden MA; P. K. Anokhin Research Institute of Normal Physiology, Moscow, Russia. mgruden@mail.ru., Davydova TV; Research Institute of General Pathology and Pathophysiology, Moscow, Russia., Ratmirov AM; P. K. Anokhin Research Institute of Normal Physiology, Moscow, Russia., Sewell RDE; Cardiff School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff, UK.
Jazyk: angličtina
Zdroj: Bulletin of experimental biology and medicine [Bull Exp Biol Med] 2021 Nov; Vol. 172 (1), pp. 18-21. Date of Electronic Publication: 2021 Nov 19.
DOI: 10.1007/s10517-021-05322-0
Abstrakt: Proinflammatory S100A9 protein is a promoter of inflammation-linked neurodegeneration and the Tnfrsf1A gene encodes the TNF receptor 1A that binds TNFα to function as a regulator of inflammation. We studied the effects of chronic intranasal administration of in vitro prepared S100A9 fibrils alone or in combination with anti-glutamate antibodies on the expression of the Tnfrsf1A gene in the hippocampus, prefrontal cortex, and cerebellum of aging C57BL/6 mice under conditions of impaired spatial memory. A differential cerebral pattern of Tnfrsf1A gene activity and its modification by S100A9 fibrillar structures were observed: inhibition of Tnfrsf1A gene expression in the hippocampus and cerebellum and its activation in the prefrontal cortex. Anti-glutamate antibodies normalized the expression of the Tnfrsf1A gene in the prefrontal cortex by affecting the TNF signaling pathway and preventing the development of inflammation.
(© 2021. Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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