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  • A link in the pathogenesis of B-amyloid peptide

    images42Alzheimer’s disease (AD) and other neurodegenerative processes are characterized by a deregulation of intracellular levels of neuronal Ca 2 +. This alteration seems to carry an implicit cause-effect relationship to toxicity by the β-amyloid peptide and neuronal death, although the mechanisms involved are discussed. One of the systems with higher affinity for Ca 2 + is formed by the Ca 2 +-ATPase. In a study conducted by Ana M. Mata, Department of Biochemistry and Molecular Biology and Genetics, University of Extremadura, have investigated the functional dependence of Ca 2 + ATPase of plasma membranes and intracellular in human brains affected by AD.

    The results show clear differences in response to Ca 2 + between the brain affected and controls specific to the activity of the plasma membrane ATPase (PMCA) and observed in AD brain stimulation at low concentrations of Ca 2 + and less inhibition at high concentrations.Control membranes show a similar dependence on Ca 2 + only after the addition of β-amyloid peptide.

    The results indicate that altered sensitivity to Ca 2 + ATPase activity in AD is due to the presence of B-amyloid in the affected tissue. The effects are specific and not present in all isoforms. Moreover, the action of β-amyloid is zero to high concentrations of cholesterol, which could modify the conformation of the PMCA or facilitate peptide binding to the membrane, affecting the interaction péptidoproteína.

    In short, this study reveals that the neurotoxic process in AD is partly mediated by an interaction between β-amyloid and the PMCA, which affects their ability to regulate Ca 2 +, and opens prospects for addressing new therapeutic strategies.

    Published on November 13, 2012 · Filed under: Bioscience; Tagged as: , , , ,
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