Or are our stroke associations going to continue to sit on their asses?
http://www.ncbi.nlm.nih.gov/pubmed/23971733
Source
Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. chenj2@upmc.edu.Abstract
Strokes
are devastating as there are no current therapies to prevent the long
term neurological deficits that they cause. Soon after ischemic stroke,
there is proliferation and differentiation of neural stem/progenitor
cells as an important mechanism for neuronal restoration. However,
endogenous neurogenesis by itself is insufficient for effective brain
repair after stroke as most newborn neurons do not survive. One
fascinating strategy for stroke treatment would thus be maintaining the
survival and/or promoting the differentiation of endogenous neural
stem/progenitor cells. Using transgenic (Tg) mice over-expressing the C.
elegans fat-1 gene encoding an enzyme that converts endogenous omega-6
to omega-3 polyunsaturated fatty acids (n-3 PUFAs), we showed that fat-1
Tg mice with chronically elevated brain levels of n-3 PUFAs exhibited
less brain damage and significantly improved long-term neurological
performance compared to wild type littermates. Importantly, post-stroke
neurogenesis occurred more robustly in fat-1 Tg mice after focal
ischemia. This was manifested by enhanced neural stem cell
proliferation/differentiation and increased migration of neuroblasts to
the ischemic sites where neuroblasts matured into resident neurons.
Moreover, these neurogenic effects were accompanied by significantly
increased oligodendrogenesis. Our results suggest that n-3 PUFA
supplementation is a potential neurogenic and oligodendrogenic treatment
to naturally improve post-stroke brain repair and long-term functional
recovery.
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