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Activation of the peroxisome proliferator-activated receptor gamma (PPARγ), has been recently demonstrated to attenuate inflammatory response and improve cognitive dysfunction in neurodegenerative diseases. RBE is rich in polyunsaturated fatty acids, which were recently considered as new PPARγ modulators. Accordingly, the effect of RBE on memory and cognition in a neuroinflammatory mouse model was examined to investigate whether RBE improves cognition through modulating PPARγ. RBE administration significantly improved the spatial working, reference memory and non-spatial recognition memory where the effect was abolished in the presence of a PPARγ antagonist (GW9662). Moreover, nuclear brain extracts obtained from mice treated with RBE showed increase in the PPARγ binding to its response element, indicating activation of the receptor, which was attenuated in the presence of GW9662. These findings demonstrate that the involvement of RBE in the beneficial effects on cognitive performance is correlated with its action on PPARγ receptors.

Graphical abstract Highlights • RBE is able to enhance cognitive effects in the neuroinflammatory mouse model. • Beneficial effects of RBE on cognition were inhibited by PPARγ antagonist. • PPARγ binding to its response element is increased in brains from RBE treated mice. • RBE is more beneficial than Pioglitazone in improving memory without affecting weight. Abstract Activation of the peroxisome proliferator-activated receptor gamma (PPARγ), has been recently demonstrated to attenuate inflammatory response and improve cognitive dysfunction in neurodegenerative diseases. RBE is rich in polyunsaturated fatty acids, which were recently considered as new PPARγ modulators. Accordingly, the effect of RBE on memory and cognition in a neuroinflammatory mouse model was examined to investigate whether RBE improves cognition through modulating PPARγ. RBE administration significantly improved the spatial working, reference memory and non-spatial recognition memory where the effect was abolished in the presence of a PPARγ antagonist (GW9662). Moreover, nuclear brain extracts obtained from mice treated with RBE showed increase in the PPARγ binding to its response element, indicating activation of the receptor, which was attenuated in the presence of GW9662. These findings demonstrate that the involvement of RBE in the beneficial effects on cognitive performance is correlated with its action on PPARγ receptors. [ABSTRACT FROM AUTHOR]