n-oleoylethanolamine and Memory-Disorders

Brain is a site of diabetic end-organ damage. Diabetes-associated cognitive dysfunction, referred as "diabetic encephalopathy" (DE) has been coined for the patients with type 2 diabetes mellitus showing decline in their cognitive function, especially weak episodic memory, cognitive inflexibility and poor psychomotor performance leading towards Alzheimer's disease. Current evidence supported that aberrant synapses, energy metabolism imbalance, advanced glycation end products (AGEs) accumulation and Tau hyperphosphorylation are associated with cognition deficits induced by diabetes. Oleoylethanolamide (OEA), an endogenous peroxisome proliferator-activated receptor alpha (PPARα) agonist, has anti-hyperlipidemia, anti-inflammatory and neuroprotective activities. However, the effect of OEA on DE is unknown. Therefore, we tested its influence against cognitive dysfunction in high fat diet and streptozotocin (HFD + STZ)-induced diabetic C57BL/6J and PPARα

Topics: Animals; Blood Glucose; Brain Diseases; Cognition Disorders; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Diet, High-Fat; Endocannabinoids; Glycation End Products, Advanced; Hippocampus; Insulin Resistance; Lipids; Male; Maze Learning; Memory Disorders; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurogenesis; Neuronal Plasticity; Oleic Acids; PPAR alpha; Specific Pathogen-Free Organisms; Streptozocin; tau Proteins