The findings of the study, conducted by Konstantinos
Meletis, a postdoctoral fellow at MIT''s Picower Institute for Learning and
Memory, and colleagues at the Karolinska Institute in Sweden, could lead to
drugs that might restore some degree of mobility to the 30,000 people worldwide
afflicted each year with spinal-cord injuries.
In a developing embryo, stem cells differentiate into all
the specialized tissues of the body.
In adults, stem cells act as a repair system, replenishing
specialized cells, but also maintaining the normal turnover of regenerative
organs such as blood, skin or intestinal tissues.
The tiny number of stem cells in the adult spinal cord
proliferate slowly or rarely, and fail to promote regeneration on their own.
However, recent experiments showed that these same cells,
grown in the lab and returned to the injury site, could restore some function
in paralysed rodents and primates.
Researchers found that neural stem cells in the adult spinal
cord are limited to a layer of cube- or column-shaped, cilia-covered cells
called ependymal cells.
These cells make up the thin membrane lining the inner-brain
ventricles and the connecting central column of the spinal cord.
"We have been able to genetically mark this neural stem
cell population and then follow their behaviour. We find that these cells
proliferate upon spinal cord injury, migrate toward the injury site and
differentiate over several months," Meletis said.
The study uncovers the molecular mechanism underlying the
tantalizing results of the rodent and primate and goes one step further: By
identifying for the first time where this subpopulation of cells is found, they
pave a path toward manipulating them with drugs to boost their inborn ability
to repair damaged nerve cells.
"The ependymal cells'' ability to turn into several
different cell types upon injury makes them very interesting from an
intervention aspect: Imagine if we could regulate the behaviour of this stem
cell population to repair damaged nerve cells," Meletis said.
When an injury occurs, ependymal cells proliferate and
migrate to the injured area, producing a mass of scar-forming cells, plus fewer
cells called oligodendrocytes.
The oligodendrocytes restore the myelin, or coating, on
nerve cells'' long, slender, electrical impulse-carrying projections called
Myelin is like the layer of plastic insulation on an
electrical wire; without it, nerve cells don''t function properly.
"The limited functional recovery typically associated
with central nervous system injuries is in part due to the failure of severed
axons to regrow and reconnect with their target cells in the peripheral nervous
system that extends to our arms, hands, legs and feet. The function of axons
that remain intact after injury in humans is often compromised without
insulating sheaths of myelin," Meletis said.
Researchers said that if scientists could genetically
manipulate ependymal cells to produce more myelin and less scar tissue after a
spinal cord injury, they could potentially avoid or reverse many of the
debilitating effects of this type of injury.
The study is published in the July issue of the journal PloS