Cognition, Behavior, and Memory
Author: Karen Agustina Nini | email: agustinanini@hotmail.com
Karen Agustina Nini 1°, Verónica Baez 1°, María Pilar Canal 1°, Mariana Munner 2°, Ornela Caruso 2°
1° Instituto de Biología Celular y Neurociencias “Prof. E. De Robertis” (IBCN, CONICET-UBA), Buenos Aires, Argentina
2° Hospital General de Agudos José María Penna, Buenos Aires, Argentina
Impaired Fasting Glucose (IFG) is the first step in DBT2 development, with fasting glucose levels between normal and DBT levels. However, it is not well understood if IFG per se, or the progression to DBT2, would cause cognitive decline. Several authors described that the increase in blood glucose levels would lead to central nervous system damage, mediated by stress signaling or the increase in pro-inflammatory cytokines. Since there are few in vitro models of IFG, we modeled a hyperglycemic condition in vitro, in primary mixed cultures and compared glucose, AGEs-RAGE and proinflammatory cytokines levels after 7 days. Our preliminary findings show lower levels of the proinflammatory cytokines TNF-α, IL-1β and RAGE in the mixed cultures that were subject to hyperglycemic conditions, in comparison to the control cultures. Further investigation is needed to establish the link between these conditions and cognitive impairments.