Understanding MS: A Q&A with Dr. Massimiliano Cristofanilli


Brain World interviewed Massimiliano Cristofanilli, Ph.D., a research scientist at the Tisch Multiple Sclerosis Research Center of New York (Tisch MSRCNY) about his work to find the cause and a cure for multiple sclerosis.

Brain World: Although symptoms of MS can occasionally get better, with progressive/secondary MS they rarely do. Is that correct?

Massimiliano Cristofanilli: I would say that if a patient gets diagnosed now, they have a nice chance of living a normal life … with progressive MS, it’s not so much a matter of whether the symptoms get better or worse; it’s that you have loss of neural tissue, which normally doesn’t happen.

Nonprogressive multiple sclerosis deals with demyelination. That is when the myelin, the neuron’s insulation, is lost around the axon, resulting in an interruption of neural connection; the information being carried through it is improperly transported from neural cell to neural cell. This can be repaired, which is what remission means. There are drugs that can keep the disease at bay, providing time for the brain to repair itself.

In secondary relapse/progressive MS, there’s a loss of myelin around the axons, and over time a loss of the axon itself. This is what’s called neural tissue loss. Currently, there are no drugs that can repair this; so we don’t really have a good way to manage progressive patients. This is where stem-cell trials come in, and that whole line of treatment for progressive MS.

BW: Because you have tissue that’s degenerating, does brain plasticity play a role in regeneration?

MC: Yes. The younger the person or brain, the more regenerative ability is in storage. We all have the ability to regenerate somehow. There are always new neurons being born in a normal adult brain. What happens in MS is that somehow the disease also attacks this very ability in the brain, and we don’t know how. We think it’s because we have endogenous stem cells in the brain, which is what probably gives the brain the plasticity to repair itself, and those cells could be attacked by the disease.

Usually, patients suffering from progressive MS are older. Because of age, the endogenous stem cells may not be working as efficiently and, along with a number of other factors, prevent a progressive patients’ ability to fully regenerate.

BW: Regarding the cause of MS, is it basically a combination of genetic factors and environmental factors, as well as our reaction to external influences like stress?

MC: We don’t really know. There’s a minimum genetic component to this. We have mothers with MS, children with MS, but you can have identical twins and one will get MS and the other won’t.

There’s been an extensive study of the genes related to MS. There are always a few genes related to the immune system that pop up during this research, but there are no straight correlations. So it’s not a genetic, per se, type of disease. The environment does play a big role.

What that role is we don’t really know. We also don’t know what triggers the disease; we know more about its progression. I might be genetically predisposed to MS but if I never encounter the trigger, I will never know it. So, it’s really hard to answer that question. I would say that 90 percent of the research is for finding the cause, and also to help patients showing progressive MS [to] live better.

BW: What is the difference between studying rats with MS and humans with MS?

MC: We usually work with mice, but rats as well. The type of disease that we can induce is called
EAE — experimental autoimmune encephalomyelitis. It is similar to a relapse type of MS, but they are not identical; there are many differences. The main difference is that the immune system of a mouse or a rat is different from that of a human. We introduce a protein into the rat and its body recognizes it as a foreigner, and it attacks. That protein is part of the myelin. We have many drugs that work well on EAE, but when you introduce them to humans with MS, they fail … It’s a good way to approach the disease, but we lack the information needed.

This article is updated from its initial publication in Brain World Magazine’s print edition.

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