Multiple Sclerosis, MS, is a complex autoimmune disorder with unknown causes. It is widely accepted that genetic heritability only accounts for about 20-30% of MS susceptibility. Yet, the number of young adults suffering from Multiple Sclerosis has increased over the last few decades. Interestingly, Multiple Sclerosis affects mainly people in northern hemisphere and women are affected three times more than men. Numerous publications are emerging linking Multiple Sclerosis with environment. The lack of sun, cold temperature, smoking and social stress are among many argued triggers for Multiple Sclerosis. However, as the immune system attacks different areas of the nervous system from person to person, symptoms of Multiple Sclerosis vary widely making it difficult to diagnose prior to appearance of plaques and thus even more difficult to study potential environmental triggers. The animal models for Multiple Sclerosis are also not ideal for such studies. The best known EAE mouse model is induced by immunization protocols which makes it challenging to define long term triggers of Multiple Sclerosis. We, therefore, hypothesize that exposing a spontaneous EAE mouse model to a short-list of environmental triggers would allow us to identify the exact environmental factors causing Multiple Sclerosis. Moreover, as Multiple Sclerosis is often linked to mitochondria, we hypothesize that by manipulating mitochondria in spontaneous EAE mouse model we should be able to identify one of the potential genetic factors involved. To test our hypothesis we will test the environmental triggers for their effect on spontaneous EAE mice that differ in their mitochondrial genetics.
To identify exact environmental triggers for Multiple Sclerosis in spontaneous mouse model.
To characterize role of mitochondria in spontaneous multiple sclerosis mouse model.
To define pathways connecting environment, mitochondria and spontaneous multiple sclerosis.