Man this seems simple, tell us what blocks nogo-A and we can send the researchers out to find out if it is useful in humans.
The role of Nogo-A in axonal plasticity, regrowth and repair
Abstract
Axonal
damage leads to permanent deficits in the adult central nervous system
(CNS) not only because of the weak intrinsic
ability of adult neurons to activate their growth program
but importantly also because of the presence of specific growth
inhibitors in the CNS tissue and the environment of the
damaged axons. The well-studied myelin-derived protein Nogo-A is
involved
in various cellular and molecular events contributing to the
failure of CNS axons to regrow and reconnect after transection.
Recent studies have shown that, by acting in a negative way
on the cytoskeleton and on the growth program of axotomized neurons,
Nogo-A exerts fast and chronic inhibitory effects on neurite
outgrowth. On the other hand, the blockade of Nogo-A results
in a marked enhancement of compensatory and regenerative
axonal extension in vivo; this enhancement is often paralleled by
significant functional recovery, for example, of locomotion
or skilled forelimb reaching after spinal cord or stroke lesions
in rats and monkeys. Surprisingly, the blockade of Nogo-A or
its receptor NgR in the hippocampus has recently been demonstrated
to enhance long-term potentiation. A role of Nogo-A in
synaptic plasticity/stability might therefore represent an additional,
new and important aspect of CNS circuit remodeling.
Function-blocking anti-Nogo-A antibodies are currently being tested in
a clinical trial for improved outcome after spinal cord
injury.
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