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Manipulating a single gene dramatically improves regeneration in adult neurons: Finding may lead to new approaches for treating brain and spinal cord damage

Increasing the expression of a single gene that is important during development dramatically improves the ability of adult neurons to regenerate, a new study shows. The finding suggests that intrinsic properties of neurons play an important role in controlling neuronal regeneration and may lead to new approaches for treating damage from stroke, spinal cord injury, and other neurological conditions.

The study examined how genetically engineering adult neurons to produce larger amounts of a type of protein called integrin affects nerve fiber growth. This approach is one of the first to examine the critical missing half of the regeneration equation: the properties of adult neurons, rather than the environment of the adult brain, says study investigator Maureen L. Condic, Ph.D., of the University of Utah School of Medicine in Salt Lake City. The work was supported by the National Institute of Neurological Disorders and Stroke (NINDS) and will appear in the July 1, 2001, issue of the Journal of Neuroscience.(1)

Most neural regeneration studies in the past have manipulated factors in the environment of the adult nervous system to try to influence neuron growth. Studies have shown that nerve fibers can regenerate in the brain and spinal cord of newborn animals, but regeneration does not normally occur in the brain or spinal cord of older animals. Recent studies have linked neuronal regeneration to integrin proteins, which function as receptors that enable neurons to interact with specialized molecules in the surrounding environment during development. Neurons taken from developing animals typically have very high levels of integrin, but neurons from adult animals have very little of this protein.

In this study, Dr. Condic used a modified adenovirus to insert extra copies of a gene for one kind of integrin protein into sensory neurons taken from adult rats. A second group of neurons received extra copies of a different integrin gene. The a
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Contact: Natalie Frazin
301-496-5751
NIH/National Institute of Neurological Disorders and Stroke
30-Jun-2001


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