With spontaneous recurrent seizure activity — a condition called epilepsy — people can develop brain damage due to the over-stimulation of brain cells. Essentially, your brain cells get fried. We know some of the brain regions vulnerable to epilepsy-induced brain damage, a process called epileptogenesis, but we still have a poor grasp on what exactly is going on in the affected brain cells.
In an article published in Brain Research, Khodaverdiana and colleagues show that during seizures and epileptogenesis in mice there is a dramatic decline in the levels of nicotinamide adenine dinucleotide (NAD+). Corresponding with this decrease in NAD+ levels, the research team based out of Tarbiat Modares University in Tehran, Iran, saw an increase in the levels and activity of an enzyme that degrades NAD+ called CD38 in a brain region vulnerable to epileptogenesis — the hippocampus, which is linked to learning and memory. The study goes on to show that these changes in NAD+ and CD38 levels are linked to dysregulated calcium signaling, which is fundamental to the excitability of brain cells and may explain epileptogenesis.
Taken together, these results revealed that CD38-induced elevation of cell calcium levels could be a key damage-causing event in epilepsy and present targets for developing an effective treatment strategy to combat epileptogenesis.