Abstract
Ceruloplasmin is the main protein involved in copper metabolism. Ceruloplasmin plays a significant role in iron metabolism; it facilitates oxidation ferrous ion to ferric ion and encourages binding ferric ion to transferrin and ferritin. Taking into account its iron oxidase activity, ceruloplasmin belongs to a ferroxidases subclass.
Ceruloplasmin activity is decreased in many neurodegenerative disorders: aceruloplasminemia, Alzheimer’s disease and Parkinson’s disease. This observation coexists with iron (ferric ion) deposits in many organs. In Alzheimer’s disease, Parkinson’s disease and aceruloplasminemia ferric ion accumulation results in apoptosis on free radicals damage pathway. In Wilson’s disease, impaired intracellular copper transport results in low serum ceruloplasmin and tissue copper accumulation. All periods of mechanisms of damages of cells have not been explained so far. Further research is essential concerning the damage to free radicals neurons in neurodegenerative diseases and possible ways of treatment.