Metabolic syndrome and cognitive decline: impact of physical exercise

Abstract

Available evidences suggest a link between disrupted insulin signaling and cognitive impairment. Typical molecular alterations related to insulin resistance have been found in brains of patients with Alzheimer disease. Moreover, insulin resistance increases the load of amyloid plaque and phosphorylation of tau protein - the latter leading to the formation of neurofibrillary tangles. Furthermore, fructose-induced insulin-resistant rats are reported to show cognitive decline. Despite the evidences, it is not clear whether insulin signaling disruption is the cause or the consequence of cognitive impairment or if it is just an accompanying phenomenon. Physical exercise is one of the interventions currently under evaluation for treatment of dementia. It is well known that exercise can reduce amyloid deposition and prevent hippocampal atrophy. Since physical exercise can work through several mechanisms - including increases in insulin sensitivity - the objectives of this study are 1 - to evaluate if physical activity is capable of ameliorate cognitive decline associated with experimental fructose-induced insulin resistance and 2 -to determine if the cognitive improvement occurs by insulin resistance correction. To achieve these objectives, we will assess animals´ memory and learning on the Morris water maze. Intracellular insulin and inflammatatory signaling molecules of the hippocampal tissue will be assayed using Western blotting. (AU)