Blocking Newly Identified Molecule May Improve And Speed
Recovery From Stroke
Researchers at UCLA have identified a novel molecule in the
brain that, after stroke, blocks the formation of new connections between neurons.
As a result, it limits the brain's recovery. In a mouse model, the researchers
showed that blocking this molecule - called ephrin-A5 - induces axonal
sprouting, that is, the growth of new connections between the brain's neurons,
or cells, and as a result promotes functional recovery.
If duplicated in humans, the identification of this molecule
could pave the way for a more rapid recovery from stroke and may allow a
synergy with existing treatments, such as physical therapy.
Stroke is the leading cause of adult disability because of the
brain's limited capacity for repair. An important process in recovery after
stroke may be in the formation of new connections, termed axonal sprouting. The
adult brain inhibits axonal sprouting and the formation of these connections.
In previous work the researchers found, paradoxically, that the brain sends
mixed signals after a stroke - activating molecules that both stimulate and
inhibit axonal sprouting. In this present work, the researchers have identified
the effect of one molecule that inhibits axonal sprouting and determined the
new connections in the brain that are necessary to form for recovery.
The researchers also developed a new tissue bioengineering
approach for delivering drugs to the brain after stroke. This approach uses a
biopolymer hydrogel, or a gel of naturally occurring brain proteins, to release
neural repair molecules directly to the target region for recovery in stroke -
the tissue adjacent to the center of the stroke.
Last, the paper also shows that the more behavioral activity
after stroke, such as the amount an impaired limb is used, the more new
connections are directly stimulated to form in the injured brain. This direct
link between movement patterns, like those that occur in neurorehabilitation,
and the formation of new brain connections, provides a biological mechanism for
the effects of some forms of physical therapy after stroke.
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