Goldberg’s laboratory studies how neurons stay connected to each other when they are damaged. He is particularly interested in keeping neurons alive after stroke and seeing if the regeneration of neurons can be promoted.

“Maintaining neuronal connections is very important in stroke, and in other brain diseases as well,” Goldberg says. “One of the closest interactions is MS.”

Anne Cross, professor of neurology and the Manny and Rosalyn Rosenthal and Dr. John L. Trotter MS Center Chair in Neuroimmunology at Barnes-Jewish Hospital, focuses on multiple sclerosis in her lab, studying axon degeneration and regeneration.

Most experts now believe that MS is an autoimmune disease that affects the central nervous system. The body’s natural defense mechanisms somehow go awry and destroy myelin, a fat and protein compound that is wrapped around the long fibers that sprout out of nerve cells. It is these fibers, or axons, that carry nerve signals. In people with MS, myelin is lost in multiple areas, and the nerve fiber itself is damaged or broken, disrupting the ability of the nerve to send and receive electrical impulses to and from the brain.

Anne Cross, professor of neurology, focuses on multiple sclerosis in her laboratory and studies axon degeneration and regeneration. In the past 10 years, Cross, also the Manny and Rosalyn Rosenthal and Dr. John L. Trotter MS Center Chair in Neuroimmunology at Barnes-Jewish Hospital, says researchers have demonstrated that the body sometimes naturally regenerates myelin that is damaged. She is trying to determine if the body also can regenerate axons.

“Many of us think that it is the failure of axons to regenerate that causes many people to get disabled and unable to recover,” Cross says. “We’re stepping back a bit, thinking about those who have longstanding disability and why they’re not improving.”

Using an imaging methodology developed by Sheng-Kwei Song, M.A. ’89, Ph.D. ’90, assistant professor of radiology, who is also a member of the Hope Center, Cross is studying living mice and trying to differentiate myelin and axon degeneration in a noninvasive way that could be used in people. “Identifying ways to preserve axons and neurons would have a wide-ranging potential for helping people,” Cross says.

Jeffrey Milbrandt was named the David Clayson Professor of Neurology in 2005 to support his ALS research, particularly nerve growth factors and receptors that are important to the development of nerve cells and axons.

In patients with ALS, paralysis is caused by the gradual death of motor nerve cells, the nerve cells that control muscles. Researchers such as Jeffrey Milbrandt, the David Clayson Professor of Neurology, suspected in recent years that nerve cell die-off begins with the loss of axons and synapses, the areas where nerve cells meet.

Last year, Milbrandt’s group showed that axons could be protected from degeneration by increasing the function of a pathway involving NAD, a molecule vital to cell metabolism, and Sirt1, a protein associated with longevity. This discovery provided a new set of targets for the development of ALS treatments.

“If this mechanism for delaying or preventing neuronal axonal degeneration after an injury proves to be something we can activate via genetic or pharmaceutical treatments, then we may be able to use it to delay or inhibit nerve cell death in neurodegenerative diseases,” Milbrandt says.

In collaboration with neurology Professor Eugene Johnson’s laboratory, the Milbrandt lab discovered a family of nerve growth factors and receptors that are important to the development of nerve cells and axons. These molecules may be useful for the treatment of many kinds of neurological disorders. One of them, a protein called Neurturin, is now being tested as a treatment for Parkinson’s disease in a clinical trial partially sponsored by the Michael J. Fox Foundation for Parkinson’s Research.

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