Evolution And Epilepsy

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2009-01-21 12:46

Studies at the University of Pennsylvania School of Medicine on brain electrical signaling offer a fresh perspective on vertebrate evolution, provide additional evidence supporting Darwinian views of evolution, and may also lead to more effective treatment of epileptic seizures in infants. Researchers discovered how evolutionary changes produced a series of improvements in molecules generating electrical signals in nerves between 550 and 400 million years ago. By making nervous systems faster and smarter, these innovations appear to have contributed to the evolutionary success and diversity of vertebrate animals.

In an evolutionary comparison of nerve cell genes appearing in PLoS Genetics last month, Penn scientists show that improvements in the molecules that govern rapid nerve impulses occurred at major turning points in evolutionary history. By making nerve signals faster and more controllable, these innovations appear to have contributed to the building of smarter brains, and perhaps even to the success and diversity of vertebrates. In other experiments presented at the Society for Neuroscience meeting in November and soon to appear in the Annals of Neurology, the scientists found that the same electrical signaling molecules appear to be an effective target for anti-seizure drugs for human newborns.

The electrical signaling molecules at the center of both studies are two related types of nerve cell proteins called sodium and potassium channels. A decade ago, researchers found that mutations in genes for these molecules were a cause of some forms of epilepsy in newborn babies and infants. Sodium channels were already targets of anti-epileptic drugs. The team led by Assistant Professor of Neurology Edward C. Cooper, MD, PhD, focused on the potassium channels for therapeutic development.

Epilepsy is a common condition in which seizures, involuntary attacks of loss of awareness and bodily control, are experienced recurrently. Epilepsy can begin at any age, but incidence is highest in the vulnerable first few weeks of life and remains elevated in later infancy and early childhood.

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