The therapeutic plasticity of neural stem/precursor

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The therapeutic plasticity of neural stem/precursor

Postby Lyon » Mon Aug 20, 2007 1:47 pm

This excerpt is off track from the general gist of the article but I thought it was interesting that they specifically enter into the inflammation healing/hurting effect Cure and I had discussed/debated earlier. Additionally, the talk a little about plasticity, which if my flavor of the month right now.

Journal of the Neurological Sciences xx (2007) xxx–xxx

The therapeutic plasticity of neural stem/precursor
cells in multiple sclerosis
Stefano Pluchino ⁎, Gianvito Martino
Neuroimmunology Unit-DIBIT and Institute of Experimental Neurology, San Raffaele Scientific Institute, Via Olgettina 58, I-20132 Milan, Italy

2. The brain repairs itself
In the early 20th century, the seminal work of Francisco
Tello showed that the CNS has the ability to regenerate itself
after an injury. This observation has been rejuvenated by
detailed in vitro and in vivo mechanistic evidence supporting
the existence of an innate self-maintenance program, ‘the
brain repair system’, which sustains tissue homeostasis and
repair [14]. This work led to the idea that further dissection
of the molecular and cellular events that control the intrinsic
brain repair mechanisms might provide an attractive
framework for developing more efficacious therapies for
neurological diseases.Several molecular and cellular mechanisms involved in
intrinsic brain repair have been described so far. They can be
divided into three distinct, although strictly interrelated,
categories. (i) Inflammation-driven processes – these
contribute to brain repair if the humoral and cellular
inflammatory components shift balance (function) over
time from a tissue-damaging mode to a mode promoting
tissue repair (e.g., neurotrophic support from inflammatory
cells) ; (ii) Brain plasticity – the recruitment of alternative
“non-damaged” functioning neuronal pathways (cortical
maps) mainly via axonal branching and synaptogenesis,
occurs as a consequence of brain damage. Whether or not
and to what extent recapitulation of developmental pathways
is the underlying phenomenon sustaining brain plasticity is
still matter of investigation; (iii) Endogenous adult neural
stem/precursor cells – if these cells survive the inflammatory
and/or degenerative insult, they may be capable of migrating
within damaged areas and promoting repair via several
mechanisms of action, such as cell replacement, remyelination,
and/or neuroprotection [15]. In addition to the
contribution of brain stem cells, there remains much debate
as to whether there may also be a contribution to brain repair
by stem cells of a different embryonic origin. A number of
possible roles have been attributed to these cells, including
cell replacement by trans-differentiation, fusion, and immunosuppression.
However, continued study will be required to
determine the relative contribution, if any, of these cells.
Brain repair spontaneously occurs in MS. This is
supported by data from autopsy or biopsy studies indicating
that almost 40% of MS lesions show evidence of
remyelination [16]. Oligodendrocyte precursors (OPCs)
play an unquestionable role in promoting remyelination
[17,18] but there are data indicating that this is not the sole
and exclusive cell-mediated mechanism underlying remyelination
in MS.
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