P4–353: Methemoglobin catabolism and Alzheimer's disease

As a main aim we want to make a contribution to the establishment of sources of oxidants as key factors in understanding the role oxidants and oxidative stress play in the pathogenesis of neurodegeneration, namely as Alzheimer disease (AD) progression. Our original observation pointed out the main difference between the hemoglobin and methemoglobin degradation, do the heme oxygenation when a hemoglobin last products is Ferrous (Fe 2+) iron, but in the methemoglobin catabolism last products is Ferric (Fe 3+) iron. Abundant and permanent source of redox-active Ferric (Fe 3+) iron which without Ferrous-Ferric inversions, has “in situ” direct impact on the brain endothelial small vessels, accumulates and increases the r ate of capillary endothelial cell apoptosis and possibly crosses into brain parenchyma to the astrocytes, glia, neurons, and other neuronal cells (neurovascular unit). This postulated and made gain in understanding the transport and neuronal accumulation process of Ferric (Fe 3+) iron, and determines how iron is transported and accumulated intracellularly, identifiable as “Brain rust”. Previously obtained research found that the neonatal jaundice incidence (p=0.034), heart murmur at a later age (p=0.011) and children and adults mild disorders as dyslalia and learning/memory impairments (p=0.002) were significantly higher than in children and adult of control mothers without pregnancy methemoglobinemia. The consequence are performed as initial brain iron harmful effects from the mother-fetal pregnancy complication, and according to our hypothesis in humans could be followed with the neuronal death, and the disease aging process, and leading finally to the hard neurodegenerative disorders as AD, PD, MS and other neurodegenerative disease.