CONICET | Buscador de Institutos y Recursos Humanos

Nowadays obesity has become a worldwide disease affectingmillions of people. Clinical studies have shown an association betweencognitive impairment and obesity, marking it as a risk factorfor dementia development, such as Alzheimer?s disease. In aprevious study we?ve gathered evidence showing that in C57BL/6Jmice, a high fat diet (HFD) decreases learning and memory capacity,and desregulates sugar metabolism. Chronic Mild Stress (CMS)enhanced the metabolic desregulation while causing anxious-likebehaviour.The objective of this study is to analize the role of neurotrophinand cytokines expression in behavioural alterations and theirpotential use as conductual disfunction markers. For this purposeone month old male C57BL/6J mice were randomly divided in twogroups receiving either HFD (35% fat w/w) or standard diet (SD, 5%fat w/w) during 6 months. Two months after starting the diet, mice underHFD were randomly subdivided: One group received CMS andthe other served as control. Cytokines and neurotrophins mRNAlevels were determined in hippocampus and spleen by real-timeRT-PCR, using GAPDH as housekeeper. In spleen, HFD+CMS increasedboth IL4 and IL10 mRNA levels (p<0.05 vs SD) while HFDand HFD+CMS lowered BDNF expression (p<0.05 vs SD). In hippocampusBDNF levels diminished non-significantly with HFD andHFD+CMS (p=0.18). Furthermore, we found a positive correlationbetween discrimination index and BDNF mRNA levels in both hippocampus(coefficient=0.52) and spleen (coefficient=0.62). No relevantcorrelations were found between neurotrophins or cytokineslevels and anxious-like behaviour. In conclusion, neurotrophin andcytokine participate in behavioural alterations induced by HFD and/or HFD+CMS. In particular BDNF mRNA levels, both periphericaland central, correlated with cognitive performance. These findingssuggest that BDNF expression in spleen could be a potential markerof cognitive deficit in obesity-

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