26 Copper Failure in Wilson and Alzheimer Disease
نویسندگان
چکیده
منابع مشابه
Mitoenergetic failure in Alzheimer disease.
Brain cells are highly energy dependent for maintaining ion homeostasis during high metabolic activity. During active periods, full mitochondrial function is essential to generate ATP from electrons that originate with the oxidation of NADH. Decreasing brain metabolism is a significant cause of cognitive abnormalities of Alzheimer disease (AD), but it remains uncertain whether this is the cause...
متن کاملFailure of prophylactic zinc in Wilson disease.
Early institution of prophylactic therapy of asymptomatic Wilson disease patients can prevent the expression of the disease. Zinc is currently preferred therapy for presymptomatic patients. We report onset of symptomatic disease in a presymptomatic patient and deterioration of biochemical parameters in another, despite appropriate zinc therapy.
متن کاملHeart failure and Alzheimer′s disease
It has recently been proposed that heart failure is a risk factor for Alzheimer's disease. Decreased cerebral blood flow and neurohormonal activation due to heart failure may contribute to the dysfunction of the neurovascular unit and cause an energy crisis in neurons. This leads to the impaired clearance of amyloid beta and hyperphosphorylation of tau protein, resulting in the formation of amy...
متن کاملMolecular mechanism of copper transport in Wilson disease.
Wilson disease is an autosomal recessive disorder of copper metabolism. The Wilson disease protein is a putative copper-transporting P-type ATPase, ATP7B, whose malfunction results in the toxic accumulation of copper in the liver and brain, causing the hepatic and/or neurological symptoms accompanying this disease. The cytosolic N-terminal domain (approximately 70 kDa) of this ATPase comprises ...
متن کاملPossible involvement of copper(II) in Alzheimer disease.
The beta-amyloid (Abeta) peptide is a principal component of insoluble amyloid plaques that are characteristic neuropathological features of Alzheimer disease (AD). The amyloid peptide also exists as a normal soluble protein that undergoes a pathogenic transition to an aggregated, fibrous form. This transition can be affected by extraneous proteinaceous elements and nonproteinaceous elements su...
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ژورنال
عنوان ژورنال: American Journal of Clinical Pathology
سال: 2018
ISSN: 0002-9173,1943-7722
DOI: 10.1093/ajcp/aqx115.025