http://www.garvan.org.au/news-events/news/harnessing-the-brains-own-ability-for-repair.html
New findings throw light on how the brain heals itself and may change the way we think about treating chronic neurodegenerative diseases like Parkinson's and Alzheimer's.
Neuroscientists at Sydney's Garvan Institute of Medical Research have shown that nerve cells in the brain produce an anti-inflammatory molecule that allows the brain to repair itself.
These findings, by Drs Bryce Vissel and Andrea Abdipranoto, are published online in the international journal Stem Cells (Abstract below).
Stem Cells. 2009 Jun;27(6):1330-46.
Activin A is essential for neurogenesis following neurodegeneration.
Abdipranoto-Cowley A, Park JS, Croucher D, Daniel J, Henshall S, Galbraith S, Mervin K, Vissel B. Neuroscience Program, The Garvan Institute of Medical Research, Sydney, Australia.
It has long been proposed that excitotoxicity contributes to nerve cell death in neurodegenerative diseases. Activin A, a member of the transforming growth factor-beta superfamily, is expressed by neurons following excitotoxicity. We show for the first time that this activin A expression is essential for neurogenesis to proceed following neurodegeneration. We found that intraventricular infusion of activin A increased the number of newborn neurons in the dentate gyrus, CA3, and CA1 layers of the normal adult hippocampus and also, following lipopolysaccharide administration, had a potent inhibitory effect on gliosis in vivo and on microglial proliferation in vivo and in vitro. Consistent with the role of activin A in regulating central nervous system inflammation and neurogenesis, intraventricular infusion of follistatin, an activin A antagonist, profoundly impaired neurogenesis and increased the number of microglia and reactive astrocytes following onset of kainic acid-induced neurodegeneration. These results show that inhibiting endogenous activin A is permissive for a potent underlying inflammatory response to neurodegeneration. We demonstrate that the anti-inflammatory actions of activin A account for its neurogenic effects following neurodegeneration because co-administration of nonsteroidal anti-inflammatory drugs reversed follistatin's inhibitory effects on neurogenesis in vivo. Our work indicates that activin A, perhaps working in conjunction with other transforming growth factor-beta superfamily molecules, is essential for neurogenesis in the adult central nervous system following excitotoxic neurodegeneration and suggests that neurons can regulate regeneration by suppressing the inflammatory response, a finding with implications for understanding and treating acute and chronic neurodegenerative diseases.
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