Pathological Progression of Multiple Sclerosis Documented For The First Time
An international group of researchers from the Center for Brain Research at the MedUni Vienna have published a paper in the Lancet Neurology journal titled “Pathological mechanisms in progressive multiple sclerosis,” documenting the pathological progress of MS since its early stages to what is known about the disease today. The study reveals how neurodegenerative and inflammatory processes play a crucial role in MS and how unveiling these particularities can result in new treatment options.
So far, there have been two approaches to categorizing MS: the first perceives the disease as a condition of the nervous system that is caused by an inflammatory complication with related neurodegenerative damages; the second hypothesizes that the disease evolves from an inflammatory condition into a neurodegenerative one.
The research team, led by Hans Lassmann, showed that the disease progresses from an inflammatory into a neurodegenerative condition since the inflammatory process acts as a driving force and, ultimately, the neurodegenerative processes occur in the late phases of the disease, inflicting damage in the brain.
“The inflammatory process, which can be treated effectively in the early stages, becomes less pronounced with age. However the neurodegenerative damage increases. This also explains why drugs that initially work well later lose their effectiveness,” said Dr. Lassmann in a press release.
The so called “amplification mechanisms” are triggered in the later stages of the disease. Neurodegenerative injuries in the brain cause the activation of microglial cells, which reinforce and push the disease forward, allowing more oxygen radicals that destroy lipids and proteins to be formed. Furthermore, mitochondrial damage also begins to occur.
Dr. Lassmann noted: “There are two routes. First, drugs could be developed that have an anti-inflammatory effect in the brain too, not just suppressing the defence response in the blood and lymphatic organs. Secondly, neuroprotective treatments could be developed that preventively block the amplification mechanisms and damage to the mitochondria, thereby preventing consequential damage.”
The results from these new approaches and information will be available in the next 5 to 10 years: “I firmly believe that in the foreseeable future, so within the next five to ten years, we will be successful in fighting the amplification mechanisms and slowing down the progressive phase further,” the researcher said.