Inhibiting LINGO-1 Protein is a Potential Future Treatment for Cognitive Impairment in MS Patients

Patricia Inacio, PhD avatar

by Patricia Inacio, PhD |

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In a new study entitled “LINGO-1 antibody ameliorates myelin impairment and spatial memory deficits in experimental autoimmune encephalomyelitis mice”, a team of scientists report that the loss of myelin in multiple sclerosis (MS) patients’ brains contributes to their cognitive impairment. They showed that inhibiting protein LINGO-1 can ameliorate these cognitive deficits by promoting myelin growth, thereby establishing impairment of LINGO-1 as a potential new therapeutic avenue for cognitive deficits in MS patients. The study was published in the journal Science Reports.

MS is an autoimmune disease affecting the central nervous system, and is characterized by destruction of the myelin layer within nerve cells. Without any cure, MS affects more than 2,3 million people in the world. Patients exhibit, as a consequence of the demyelinating process, cognitive impairment, including attention and memory deficits, which severely impact patients’ daily life. However, the mechanisms underlying the characteristic cognitive impairment of MS patients are largely unknown.

The researchers used mouse models for human MS, specifically the experimental autoimmune encephalomyelitis (EAE) mouse model, to investigate the link between myelin impairment and cognitive decline. Moreover, despite the high incidence of cognitive impairment in MS patients, the treatments available have no benefits in improving patients’ cognitive features. Hence, there is an unmet need for an effective treatment.

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In the study, researchers observed that the deficits in both memory and learning skills occur at later stages of the disease. They followed previous studies suggesting that a protein called LINGO-1 (short for LRR and Ig domain containing NOGO receptor interacting protein 1) inhibits myelin production. Accordingly, the team used an antibody against LINGO-1 and discovered it significantly improved learning and memory in the EAE mouse model, while it activated the AKT/mTOR signaling pathway, a crucial regulator of myelin growth. This phenotype was accompanied by an increase and restoration of myelin basic protein (MBP) expression in the brain of these mice, a key protein in the myelination process of nerves.

These findings therefore suggest that demyelination may contribute to the learning and memory deficits of MS patients, and establish the potential action of LINGO-1 antibody as a strategy to promote myelin growth. Hence, inhibiting LINGO-1 protein is a potential future treatment for cognitive impairment in MS patients.

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