To this day, our studies designed to formulate therapies for Multiple Sclerosis (MS) are dependent on animal models. However, it is vital that the processes targeted by the therapies are identical in the human patient and in the animal model.
MS is caused by damage to the insulating covers of the nerve fibres. This releases iron molecules that cause further damage to the brain because they increase the damage caused by toxic forms of oxygen (radicals). These processes have been found to be less common in rodent models for MS, meaning that new therapies that counter these processes cannot be tested in rats or mice.
Marmosets are more closely genetically related to human beings, and are already being used as animal models for MS. BPRC-affiliated researchers have now investigated whether the same iron redistribution processes that occur in humans also occur in these monkeys.
They found that, just like humans, animals in whom MS-like symptoms had been induced suffered blocked localisation of iron in the brain tissue. This blocked localisation was closely related to the symptoms observed in these animals. The same was true for other proteins involved in the oxygen compound imbalance.
These results, published in the Journal of Neuropathology & Experimental Neurology, enable us to better evaluate MS therapies designed to combat the processes described above.