Multiple sclerosis (MS) is a debilitating neurological disease with major unmet medical needs. It is the primary neurological disorder diagnosed in young adults, with more than two million people affected worldwide. In an effort to develop next-generation therapies that target the underlying cause of multiple sclerosis and not just its symptoms, new theories are being explored on what causes the disease, including the concept that mitochrondia, the powerhouse of cells, might be disturbed in those with MS.
Conventional views on MS within the research community include the observation that inflammation and the degeneration of myelin cause loss of bodily functions. Myelin wraps around nerve cells and facilitates communication in the nervous system. When an immune attack is launched on myelin by cells known as leukocytes, the fatty wrapping degenerates, causing nerve and neurological damage. This damage leads to loss of movement, vision, pain and loss of balance. Certainly, myelin loss and even the loss of nerve cells (neurons) is important for understanding the disease, however, a recent report suggests that targeting the mitochondria within cells might provide new insights into treating MS.
According to a paper published by Peizhong Mao and P. Hemachandra Reddy of Oregon Health & Science University in Portland, MS could be a mitochondrial related disease. Factors causing MS are not known, but in their report the scientists speculated ” . . . it is possible that multiple factors are involved in causing multiple sclerosis, including DNA defects in nuclear and mitochondrial genomes, viral infection, hypoxia and oxidative stress, lack of sunlight or sufficient levels of vitamin D, and increased macrophages and lymphocytes in the brain.”
Defects in the mitochondria could reduce cellular energy, contributing to loss of myelin directly and even causing a cascade of immune responses that are damaging to the body. The authors noted in their report that “mitochondrial abnormalities and mitochondrial energy failure may impact other cellular pathways, including increased demyelination and inflammation in neurons and tissues that are affected by multiple sclerosis.”
To support this idea, in people with multiple sclerosis and MS animal models (called experimental autoimmune encephalitis), several researchers have identified abnormalities in mitochondria function and in the enzymes used by mitochondria. Scientists have also identified DNA mutations in genes involved in mitochrondrial function in people with MS.
What could this association with mitochondrial problems mean for treatments for MS? Current treatments focus on blocking immune responses, which reduce clinical symptoms in some people with MS but unfortunately do not cure the disease and do not help everyone. It is possible that blocking an overactive immune system is a strategy that occurs too late in the development of MS. Targeting mitochondria disturbances, either through medications or by gene therapy, might prevent the progression of MS from happening in the first place.
Treatment of mitochondrial diseases are still in an early stage, and according to an article by Sumit Parikah and colleagues, nutritional supplements could also protect mitchondria. They state that for the treating of mitochondrial conditions “Most experts use a combination of vitamins, optimize patients’ nutrition and general health, and prevent worsening of symptoms during times of illness and physiologic stress.”