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Alzheimer's disease (AD) is now the sixth leading cause of death among Americans,affecting nearly 1 in 8 people over the age of 65. There iscurrently no treatment that alters the course of this disease.However, an increasing amount of evidence suggests that changes inthe way the body handles iron and other metals like copper and zincmay start years before the onset of AD symptoms. A new study showsthat reducing iron levels in blood plasma may protect the brainfrom changes related to AD. In the current study a group of investigators from led by Dr.Othman Ghribi, PhD, Associate Professor, Department ofPharmacology, Physiology, and Therapeutics, University of NorthDakota School of Medicine and Health Sciences, rabbits were fed ahigh-cholesterol diet which caused them to accumulate plaques of asmall protein called beta-amyloid (A ). These plaques are toxic toneurons and central to the development of Alzheimer's disease. Therabbits also developed changes in tau protein, which is part of theskeleton of neurons. When this protein becomes heavilyphosphorylated, the ability of neurons to conduct electricalsignals is disrupted. Following treatment with a drug calleddeferiprone (an iron chelator), the iron level in the rabbits'blood plasma was reduced and the levels of both beta-amyloid andphosphorylated tau in the brain were returned to normal levels. Another degenerative process in AD involves the production ofreactive oxygen species (ROS) that can damage neurons in the brain.Deferiprone is also thought to suppress this reactive oxygen damagecaused by free iron in the bloodstream, however in this study therewas no difference in reactive oxygen species in the treated group.It appears that iron in the AD brain is located in the wrong places- in particular it accumulates to very high levels in the cores ofbeta-amyloid plaques and is very reactive in this setting. According to Dr. Ghribi, "Our data show that treatment with theiron chelator deferiprone opposes several pathological eventsinduced by a cholesterol-enriched diet...Deferiprone reduced thegeneration of A and lowered levels of tau phosphorylation." Whilethere was no effect on ROS levels, he comments that "It is possiblethat a higher dose of deferiprone, or combination therapy ofdeferiprone together with an antioxidant to prevent ROS generationwould more-fully protect against the deleterious effects ofcholesterol-enriched diet that are relevant to AD pathology." Noted expert on metals metabolism research on AD Ashley Bush, MD,PhD, Mental Health Research Institute, Melbourne, Australia, addsthat "this research highlights the role of metal ions as keymodulators for the toxic interactions of risk factors forAlzheimer's disease, in this case cholesterol . Drugs targeting these metal interactions hold promise asdisease-modifying agents." Additional References Citations. The e-commerce company in China offers quality products such as Control cable , Xlpe power cable Manufacturer, and more. For more , please visit ACSR today!
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