Just when I thought I had "read it all"! Here's something I ran across that I found interesting. Don't ask me who this gentleman is exactly [EDIT: Oops, it's a woman!], but s/he's from the Brain Research Institute at the University of Zurich (that's Switzerland, right? )
Anyway, it's pretty easy reading. For some reason, I found "something" in it interesting, and maybe with some other comments from you all, we can pull it out and see where it leads. I think I'm sort of focusing on the specific "areas" of the brain he mentions. hmmmmmmmmm........... What ARE the correlations of MS to specific areas of the brain, etc. etc.?
Dr. Michaela Thallmair
I am interested in the cellular and molecular mechanisms underlying fate decisions of adult spinal cord progenitor cells and structural plasticity/nerve regeneration in the adult central nervous system (CNS).
During the last decade compelling evidence emerged that challenged the longstanding belief that regeneration in the CNS ceases with the end of development. Recent studies have shown that new neurons are continuously born throughout life in two areas of the brain: The subventricular zone of the forebrain and the dentate gyrus of the hippocampus.
Other adult CNS regions, such as the striatum, substantia nigra and the spinal cord, also contain proliferating cells. In vivo these cells give rise exclusively to glial cells. However, when proliferating cells from these so-called gliogenic/non-neurogenic regions are isolated and cultured, however, they are able to self-renew and to differentiate into the three major lineages of the CNS: astrocytes, oligodendrocytes and neurons. These findings suggest that adult progenitor cells are present not only in the neurogenic regions, the subventricular zone and the dentate gyrus, but along the entire neuroaxis.
A fundamental question in stem cell biology is how fate choices of stem cells are regulated.
Grafting experiments of cultured progenitor cells isolated from a gliogenic/non-neurogenic region into a neurogenic area demonstrated that heterotopically transplanted precursors migrate and differentiate according to their transplantation site. These observations suggest that the fate choice is due to extrinsic/environmental cues rather than to an intrinsic inability to respond to mitogenic and differentiation factors, and open the possibility to manipulate the fate choice of adult precursor cells.
The recruitment of endogenous progenitor cells for repair processes after a CNS injury or CNS disease might help to improve recovery. For example, modification of the local environment to manipulate the behavior of the endogenous precursors may be a possibility to control the differentiation of proliferating cells in neurogenic and gliogenic regions. The feasibility and limitations of remyelination and/or neuronal replacement through endogenous progenitor cells, however, remains to be investigated.
Spinal cord injury interrupts not only the communication between the brain and spinal cord, but triggers a cascade of events that eventually lead to neuronal degeneration, cell death, and scar formation. After an injury and in demyelinating diseases (e.g. multiple sclerosis, MS), axons that were not (initially) injured lose their myelin sheath. Although oligodendrocyte precursor cells proliferate after a CNS lesion and in MS, remaining intact fibers are only partially re-myelinated, one of the reasons for incomplete/missing recovery. The latter finding suggests that factors in the injured CNS inhibit or retard oligodendrocyte maturation and/or myelination or, alternatively, that factors that induce oligodendrocyte differentiation and myelination are absent.
Currently it is not known which factors instruct gliogenesis and/or suppress neurogenesis, the formation of new neurons, in the adult spinal cord. Understanding the regulation of gliogenesis in the intact spinal cord would help us finding means to influence the formation of astrocytes and oligodendrocytes. Manipulation of glial cells and ultimately regulating scar formation and myelination is especially important with respect to incomplete spinal cord injuries and diseases like multiple sclerosis, and may eventually improve recovery.
There remains a lot to be learned about the regulation of progenitor cells and gliogenesis in the intact and injured/diseased spinal cord. Which are the mechanisms that stimulate adult neural progenitor cells to proliferate in vivo in the intact or injured cord? Why do progenitor cells that proliferate after a CNS injury usually not replace the lost cell types? What are the factors that regulate the fate decision of adult spinal cord precursor in the intact and injured cord?
Understanding the basic mechanisms that regulate adult neural progenitor cell behavior are not only of great basic neurobiological interest, but are fundamental for developing strategies that aim to treat CNS injuries or diseases using neural stem cells.
P.S. Oh! Here is where I found this at: http://www.hifo.unizh.ch/research/neuro ... st.en.html I am now flipping through their whole website. It looks like they are looking into some pretty interesting stuff!!! Regeneration. Cool!