Possible link between elevated calcium levels in older neurons and aging-related disorders of the brain

Oct 20 2004

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.”

According to DeLorenzo, the increase in intracellular calcium levels in brain cells may be due to an alteration in the calcium regulatory mechanism. Intracellular calcium is critical to brain cell function because it is a major second messenger in the brain that regulates gene expression and enzyme control.

“If we are able to understand the normal aging process, we can better understand what causes the premature aging that can lead to such devastating illness as Alzheimer’s disease,” he said.

In addition to these preliminary findings, DeLorenzo’s group also will be presenting on the topics of epilepsy and calcium dynamics, as well as marijuana and its receptor protein in the brain, which may play a role in controlling epileptic seizures.

“The Department of Neurology is one of the primary centers studying the important role of alterations in calcium homeostatic mechanisms in neurological diseases such as Alzheimer's disease, epilepsy and stroke,” DeLorenzo said.