Abstract
This review focuses on pathologic mechanisms of neurodegenerative diseases and Multiple Chemical Sensitivity (MCS) in order to find out common properties that give hints to their common origin and mechanisms. Many epidemiologic studies already have proven that both, MCS and neurodegenerative diseases, especially Alzheimer’s and Parkinson’s Disease, are initiated by exposure to environmental chemicals. The mechanisms following these exposures show similar properties. They are initiated by binding to and activation of receptors located at cells of the brain immune system and at neurons, mainly the so called “transient receptor potential receptors” (TRP-receptors). As a consequence, the activation of N-methyl-D-aspartat-receptors (NMDA-receptors) in the Central Nervous System (CNS) plays a central role in the expression of neurotoxic mechanisms such as excitotoxicity, apoptose (programmed cell death) and chronic inflammation in the brain. The inflammation in brain is mainly performed by activated astrocytes and gliacells that are part of the inborn immune system. Under normal conditions these cells support the functions of neurons in the brain. Under pathologic conditions caused by different environmental chemicals these cells are activated and turn into a pathogenic state that supports inflammation. They then secrete cytokines as signal molecules that activate different inflammation mechanisms, leading to production of oxygen radicals (“oxidative stress”) and peroxynitrite (“nitrosative stress”). These pathogenic mechanisms constitute self enhancing vicious cycles that cause a risk of proceeding neurodegeneration. There are hints that some of these mechanisms also have been proven for Multiple Chemical Sensitivity (MCS).