Brain cells become increasingly unable to regulate calcium loads as they age, becoming more vulnerable to injury and premature death, according to new findings that Virginia Commonwealth University researchers will present at an international conference this month.
The findings could help scientists better understand premature aging and how it is linked to aging-related disorders like Alzheimer’s disease and dementia, according to research that VCU neurologists and pharmacologists will present at Neuroscience 2004, the Society of Neuroscience’s 34th Annual Meeting in San Diego, Calif., Oct. 23-27.
Approximately 30,000 experts, researchers, and academic leaders from around the world are expected to network and explore the latest developments in neuroscience research.
Robert DeLorenzo, M.D., Ph.D., MPH, a professor in neurology at VCU, and his research team will present the key findings from a preliminary study suggesting that as neurons age the ability to regulate the normal physiological calcium loads becomes greatly diminished.
Researchers compared acutely isolated hippocampal neurons, which are involved with memory, from young and old animals. They observed that the younger hippocampal neurons were better able to regulate the calcium loads than the older neurons.
“This research is significant because it provides a possible mechanism underlying neuronal injury and cell death,” said DeLorenzo, who is the lead investigator of the study.
“As neurons get older, they experience a build-up of intracellular calcium which causes the aging cell to become damaged and prematurely die,” he said. “When this happens in the brain, the result could be Alzheimer’s disease or dementia.”