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I.R.F. / Aging news / Cloning / 03012201

Perspectives to Treat Neuronal Degeneration Diseases Using Stem Cell Technology
Posted on: January 22, 2003

Snyder et al.* have made a very promising finding concerned with embryonic stem cell therapy in treating injured brain. They have found that injured brain, by hypoxic-ishemic injury, interacts with neural stem cells which reconstitute lost tissue. By seeding neural stem cells (NSCs) onto a polymer scaffold that was subsequently implanted into the infarction cavities of mouse brains injured by hypoxia-ischemia they have observed the multiple reciprocal interactions that spontaneously ensued between NSCs and the extensively damaged brain: parenchymal loss was dramatically reduced, an intricate meshwork of many highly arborized neurites of both host- and donor-derived neurons emerged, and some anatomical connections appeared to be reconstituted. The NSC-scaffold complex altered the trajectory and complexity of host cortical neurites. Reciprocally, donor-derived neurons were seemingly capable of directed, target-appropriate neurite outgrowth (extending axons to the opposite hemisphere) without specific external instruction, induction, or genetic manipulation of host brain or donor cells. These "biobridges" appeared to unveil or augment a constitutive reparative response by facilitating a series of reciprocal interactions between NSC and host, including promoting neuronal differentiation, enhancing the elaboration of neural processes, fostering the re-formation of cortical tissue, and promoting connectivity. Inflammation and scarring were also reduced, facilitating reconstitution. If such technology worked in hypoxic-ishemic injury, one can't reject that this should work in other neuronal injures or diseases concerned i.e. Parkinson's, Alzheimer's etc.

Figure: Embryonic fibroblasts migrating on the surface.
Source: Evan Y. Snyder et al. The injured brain interacts reciprocally with neural stem cells supported by scaffolds to reconstitute lost tissue; Nature; Nov 2002; Volume 20 Number 11 pp 1111 - 1117 (esnyder1@caregroup.harvard.edu)
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