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Curr Opin Cell Biol. 2011 Apr;23(2):223-30. doi: 10.1016/j.ceb.2010.12.006. Epub 2011 Feb 2.

Role of calcineurin in neurodegeneration produced by misfolded proteins and endoplasmic reticulum stress.

Author information

1
Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, The University of Texas Medical School at Houston, 6431 Fannin St., Houston, TX, United States.

Abstract

A hallmark event in neurodegenerative diseases is the accumulation of misfolded aggregated proteins in the brain leading to neuronal dysfunction and disease. Compelling evidence suggests that misfolded proteins damage cells by inducing endoplasmic reticulum (ER) stress and alterations in calcium homeostasis. Changes in cytoplasmic calcium concentration lead to unbalances on several signaling pathways. Recent data suggest that calcium-mediated hyperactivation of calcineurin (CaN), a key phosphatase in the brain, triggers synaptic dysfunction and neuronal death, the two central events responsible for brain degeneration in neurodegenerative diseases. Therefore, blocking CaN hyper-activation might be a promising therapeutic strategy to prevent brain damage in neurodegenerative diseases.

PMID:
21295458
PMCID:
PMC3078182
DOI:
10.1016/j.ceb.2010.12.006
[Indexed for MEDLINE]
Free PMC Article

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