Multiple Sclerosis (MS) is a chronic-inflammatory autoimmune disease of the central nervous system (CNS). It is characterized by demyelinisation and astrogliosis as well as a loss of oligodendrocytes and neurons. Regardless of the yet not fully clear cause for the activation of autoreactive lymphocytes, various predisposing genetic riskfactors and environmental influences, which play a major role in the disease development, could be identified. The “Western Diet”, consisting of “too much”, “too fatty”, “too salty” regular intake of industrial processed food and “fastfood”, as well as a high bodymassindex (BMI), represent riskfactors with an enormous potential for intervention. The increasing prevalence of MS illustrates that basic pathomechanisms of autoimmune diseases need further investigations and understanding in order to develop potent preventative actions and treatments, thus standing up against the rising number of autoimmune diseases. In various animal models, the intake of galactose leads to early aging and reduced life expectancy by oxidative stress and chronic inflammation. Therefore galactose-diet is used as a model to study the processes of aging. Along with impacts on neurodegenerative diseases like Alzheimers-Disease, it is becoming more and more obvious, that galactoserich diet also influences the genesis of autoimmune disease like MS. Which leads to the first hypothesis of this dissertation, that galactose has an impact on neuroinflammatory processes and shows effects on the course of experimental autoimmune encephalomyelitis (EAE), an animal model for autoimmune-inflammatory diseases of the CNS. Designs and methods To test this, the myelin oligodendrocyte glycoprotein (MOG)-EAE-Model in C57BL/6-mice was used and the influence of nutrition was simulated by drinking water enriched with 10% galactose. Observations and results Under galactoserich diet a more severe course of EAE was observed, which is presented histological through increased demyelinisation and a larger number of lesions in the chronic course. Also, the number of neurons and the axonaldensity were reduced. On top a decreased number of oligodendroglial cells could be proved in the chronic course. Without a previously induced EAE, galactoserich diet did not show any clinical or histological alteration compared to naïve control mice, which confirms the second hypotheses of this dissertation, that the effect of galactose in young C57BL/6-mice is EAE-dependent. Conclusion To put it in a nutshell the gathered data point out a galactose-intake related modulation of the CNS-autoimmunity and grant deeper insight into the effects of the nutritional factor galactose on neuroinflammatory processes, thus reinforcing the concept of a major role of nutritional factors in the development of autoimmunreactions. This could result in another starting point for future therapeutic approaches and preventative measures.