Washington, Oct 23: Researchers at the University of Cambridge have found that a drug initially designed to treat a form of leukaemia may also be effective against combating the debilitating neurological disease multiple sclerosis (MS).

The findings are based on a study, in which researchers found that alemtuzumab not only stops MS from advancing in patients with early stage active relapsing-remitting multiple sclerosis 
(RRMS) but may also restore lost function caused by the disease.

In the new study, the researchers found that alemtuzumab reduces the number of attacks experienced by people with relapsing-remitting multiple sclerosis by 74 per cent over and above that achieved with interferon beta-1a, one of the most effective licensed therapies for similar cases of MS.

More importantly, they found that alemtuzumab also reduced the risk of sustained accumulation of disability by 71 per cent compared to interferon beta-1a.

In addition, the researchers showed that many individuals in the trial who received alemtuzumab recovered some of their lost functions and so were less disabled after three years than at the beginning of the study, in contrast to worsening disability in the interferon beta-1a treated patients.

These findings suggest that alemtuzumab may allow damaged brain tissue to repair, enabling the recovery of neurologic functions lost following poor recovery from previous MS attacks.

The new research shows that alemtuzumab is a much more effective treatment for early-stage RRMS than the currently approved drug interferon beta-1a.

However, as the study was a Phase 2 clinical trial, additional research will need to be conducted before the drug is considered for approval in the treatment of MS.

"Alemtuzumab is the most promising experimental drug for the treatment of multiple sclerosis, and we are hopeful that the Phase 3 trials will confirm that it can both stabilize and allow some recovery of what had previously been assumed to be irreversible disabilities," said the principal investigator Alastair Compston, Professor of Neurology and the Head of the Department of Clinical Neurosciences at the University of Cambridge.

Multiple sclerosis is an autoimmune disease, which is caused by the body''s immune system attacking nerve fibres and their protective insulation, the myelin sheath, in the central nervous system.

This damage prevents the nerves from ''firing'' properly, and then leads to their destruction, resulting in physical and intellectual disabilities.

Alemtuzumab works by destroying one population of white blood cell (lymphocytes) and, by shutting down the immune system, inhibits the damage to brain tissue that occurs in MS.

The study is published in the New England Journal of Medicine. (ANI)