Biogen Idec is pushing forward with a therapeutic antibody that can turn myelin producing cells back on and so could reverse the damaging effects of multiple sclerosis (MS).
Biogen has published the latest preclinical data on its anti-Lingo-1 antibody in this month's issue of Nature Medicine, which suggest the drug can promote myelin production and placement around damaged nerves, at least in animals.
Normally myelin acts a protective cellular sheath around nerve fibres but if it is destroyed, as is the case in MS patients, the cells lose their ability to send signals to the body and can eventually die. This contributes to the disability seen in MS sufferers.
Current MS treatments focus on slowing down this destruction. However, there is no drugs currently available that can repair the damage already done. There are several plausible drug targets being pursued within the pharma industry that could lead to regenerative therapies. On top of Lingo-1, these include Nogo, Notch and Jagged. Stem cell treatment represents a further option that needs investigating further.
Lingo-1 itself appears to be a molecular switch which blocks the ability of cells in the central nervous system to produce myelin. A Lingo-1 antibody effectively 'blocks the blocker' and the end result is that myelin production is restarted.
"While preliminary, these findings are encouraging and suggest that the anti-Lingo-1 antibody has the potential to repair some of the damage caused to the CNS. This may be an entirely new approach to treating MS," said Dr Alfred Sandrock, Senior Vice President of Neurology Research and Development at Biogen.
A disease called experimental autoimmune encephalomyelitis (EAE) is used instead of MS in animal studies to track myelin destruction. If the antibody is introduced before disease onset it can decrease the severity of EAE and can also reduce symptoms if it is given after disease onset, according to Biogen.
Physical improvements in axonal integrity were seen using magnetic resonance DTI imaging, and new myelin sheaths were seen at the cellular level, using histological staining and electron microscopy.
"This....opens the door for the identification of additional regulators of myelin repair that might be used to enhance functional recovery in patients with MS," said Dr Robert Miller, who is the Director of the Center for Translational Neuroscience at Case Western Reserve University and also the principal investigator on the study.
Each of this new set of targets represents an exciting possibility for new MS therapies - and other demyelinating diseases, such as leukodystrophies - although it will be several years before one might make it to the market.