What is Anti-Nogo-A/NEP?

The therapy, known as Anti-Nogo-A/NEP, may be used to restore function even after ischemic brain damage has occurred, according to senior author Gwendolyn Kartje, MD, PhD, and colleagues. Nogo-A is a protein that inhibits the growth of nerve fibers. In anti-Nogo therapy, an antibody disables the Nogo protein, allowing for the growth of axons in the stroke-affected side of the body and the restoration of functions lost from stroke.
Rats that had received anti-Nogo therapy in the study regained 78 percent of their ability to grab pellets nine weeks after stroke, while rats that did not receive the treatment regained 47 percent of that same ability.
Anti-Nogo-A/NEP "can induce remarkable compensatory sprouting and fiber growth, indicating the responsiveness of the chronically injured brain to form new neural networks under the proper growth conditions," according to the study.
And the therapy's benefits aren't exclusive to stroke patients. The findings point to possible therapies for patients who suffer from spinal-cord injury and neurological disability due to brain damage.
Nogo-A is a myelin-associated neurite outgrowth inhibitory protein limiting recovery and plasticity after central nervous system injury.
Anti-Nogo is a treatment enhances corticospinal tract sprouting and functional recovery after unilateral cervical lesion in adult primates
NogoA is a member of a family of integral membrane proteins termed reticulons that are thought to be involved in numerous disorders including neurodegenerative diseases. Re ticulon proteins are known to regulate many cellular processes and interact with multiple proteins and receptors such as BACE (reviewed in 1). NogoA was initially identified as a myelin-associated neurite outgrowth inhibitor. It is highly expressed in oligodendrocytes in the white matter of the CNS; blocking its activity with antibodies or other factors results in improved axon regrowth and functional recovery in experimental CNS lesion models. NogoA has also been suggested to play a role in neurodegenerative diseases such as Amyotrophic lateral sclerosis, in which case NogoA is found at elevated levels in postmortem muscular samples, and multiple sclerosis (MS), in which case autoantibodies to NogoA have been found in serum andcerebrospinal fluid in MS patients. Despite its predicted molecular weight, NogoA typically migrates at 180kDa in an SDS-PAGE. At least five isoforms of Nogo are known to exist; this antibody is specific for NogoA.
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