There is ample evidence for disruption of calcium regulation in aging and age-associated neuropathologies such as Alzheimer's disease. Our work indicates that changes in the calcium-dependent processes for neuronal signaling are altered during aging and are associated with memory impairments similar to those observed early in the clinical course of the disease. Using aging rats as a model, our research indicates that changes in the electrical transmission properties of the brain and age-related impairments in memory can be reversed by treatments that block calcium entry into brain cells. This raises the possibility that future pharmacological interventions might be devised to act on calcium dependent processes for the prevention or treatment of age-associated neurological disorders. The cause of high IL-6 levels in the brain, in turn, is unknown, but chemical substances called free radicals may contribute to this.
Free radicals are chemicals that damage fats, proteins and genes.
They increase with age and increase IL-6 levels in many different tissues. We believe that free radicals contribute to the development of AD by increasing IL-6 levels in the brain. To examine this possibility, we treated rats with high levels of oxygen to increase free radical activity in their brains. We then measured IL-6 protein levels in the hippocampal region of the brain. We found that IL-6 levels were increased by free radicals in the hippocampus.