THE ARTHUR AND ORIGINAL SOURCE WAS NOT SHOWN NOR THE AUTHENTICITY OF THE
ARTICLE, BUT IT SEEMS TO FOLLOW WHAT I HAVE BEEN POSTING.
Bob from Houston
> BRAIN AND SPINAL CORD INJURY
> The nervous system is highly vulnerable to injury from without. As
>communication from the brain to the body is disrupted, partial disability
or
>complete paralysis can result. In the 1990s, "acute" treatments-those
>administered within hours of the accident that caused the trauma-have
>improved prospects for recovery. Researchers are looking for ways to
improve
>these treatments and to restore the abilities of those whose window of
>opportunity for acute treatment has passed.
> Scientific opinion long held that, once injured, nerve cells in the
>central nervous system (the brain and spinal cord) cannot repair themselves
>or regenerate. Laboratory research in the 1990s, however, has chipped away
>at this belief. Certain proteins in the brain and spinal cord inhibit the
>growth of nerve cells-particularly the long fibers known as axons. A team
of
>Swiss researchers has designed antibodies that counteract these inhibitory
>proteins (Z'Graggen et al.). In a 1998 study, working with a rat model of
>brain injury, they found that a specially engineered antibody called IN-1
>could cause healthy axons to sprout in undamaged areas of the brain and
>spinal cord. These new axons took over for the damaged ones, appearing to
>connect with the damaged nerves' counterparts. The rats had been partially
>paralyzed with an experimental injury to the brain stem-a nexus of motor
>control where the spinal cord joins the brain. After treatment with IN-1,
>the rats were able to use their forepaws to climb ropes and grasp food
>pellets. This new insight into "compensatory" growth might provide new
>methods of treatment for brain injuries, including the devastation that
>follows stroke.
> Much of the destruction in the wake of spinal cord trauma is due not
>to the injury itself but to "secondary damage," in which the injured cells
>spill out toxic levels of chemicals, particularly the neurotransmitter
>glutamate. Acute treatments contain this damage, currently with high doses
>of a steroid called methylprednisolone. Since injury victims can function
>well with even a small number of axons intact, preventing secondary damage
>is a treatment priority.
> In 1998, scientists at the Washington University School of Medicine
>found a possible new approach. They found that key brain cells called
>oligodendrocytes are vulnerable to damage by glutamate. Oligodendrocytes do
>not actually transmit nerve impulses; their job is to produce myelin, the
>sheath that surrounds axons like the insulation on an electrical wire.
Since
>messages from the brain are disrupted when myelin is damaged, loss of
myelin
>is a chief reason for disability in both spinal cord injury and multiple
>sclerosis (MS). In the 1998 study, compounds called AMPA receptor
>antagonists, which blocked the effects of glutamate, were found to protect
>oligodendrocytes in animal models of stroke and spinal cord injury
(McDonald
>et al.). The safety of these compounds is being examined in clinical
trials,
>and it soon might be possible to test their effectiveness against central
>nervous system injury.
> Oligodendrocytes are the focus of another 1998 discovery. Compounds
>called growth factors or neurotrophins, which nourish and protect nerve
>cells, have been used in the laboratory to help axons grow across a spinal
>cord injury. But a group of researchers have now found that neurotrophins
>can also stimulate the growth of oligodendrocytes and increase myelin in
the
>growing nerve fibers. The team engineered cells to produce five different
>types of neurotrophins and then transplanted them into the spinal cords of
>rats given an experimental injury. All transplants resulted in newly
growing
>axons, but two compounds in particular, neurotrophin-3 and brain-derived
>neurotrophic factor, resulted in an increase in myelin and in the
>oligodendrocytes that produce it. These findings may have significant
>implications for injuries to the central nervous system or chronic
>demyelinating diseases such as multiple sclerosis (McTigue et al.).
> New insight into how axons normally grow comes from a 1998 study
>examining growth cones-the structures in the tip of axons that respond to
>chemical cues for guidance in their journey. A research team from the
>University of California at San Diego has determined that any given
chemical
>signal can either attract or repel (Song et al.). The deciding factor is
not
>the chemical signal itself, but the internal status of the growth cone-and
>that, in turn, is regulated by brain cell chemicals called cyclic AMP and
>GMP. Signals that are normally attractive become repulsive when levels of
>cyclic AMP and GMP are lowered in the growth cones. Signals that are
>normally repulsive become attractive when the levels are increased. Besides
>illuminating an elegant neurochemical mechanism that underlies a great deal
>of complex brain development, this work opens up new prospects for
>regenerating injured nerves by manipulating the chemical balance within
>axonal growth cones.