Calcineurin: directing the damage in Alzheimer disease: An Editorial for ‘Neuronal calcineurin transcriptional targets parallel changes observed in Alzheimer disease brain’ on page 24

Research output: Contribution to journalEditorial

3 Scopus citations

Abstract

Ca2+ dysregulation is a hallmark of Alzheimer disease (AD) and affects numerous and diverse signaling cascades linked to neurodegeneration and cognitive decline. Increasing evidence suggests that the protein phosphatase calcineurin (CN) mediates or exacerbates AD pathophysiology through activation of the NFAT family of transcription factors. In this editorial, we discuss work by Hopp et al, which uncovered a novel role of CN/NFAT signaling in controlling global gene expression in hippocampal neurons of intact mice. Interestingly, the authors showed that elevated CN expression/activity in neurons plays a major role in transcriptional suppression. Many of the genes differentially affected by CN were related to synapse function and NFAT binding, and exhibited similar patterns of downregulation in previous studies on human AD biospecimens. Results are discussed in context with emerging roles for CN/NFATs in astrocyte signaling as they pertain to Ca2+ dysregulation and the progression of neurodegeneration and cognitive loss with AD. (Figure presented.).

Original languageEnglish
Pages (from-to)8-11
Number of pages4
JournalJournal of Neurochemistry
Volume147
Issue number1
DOIs
StatePublished - Oct 2018

Bibliographical note

Funding Information:
CMN is supported by NIH grants (AG027297, AG056998, AG051945) and a gift from the Hazel Embry Research Trust. Special thanks to Dr. Steven W. Barger at the University of Arkansas for Medical Sciences for helpful editorial suggestions. The author has no conflicts to report.

Publisher Copyright:
© 2018 International Society for Neurochemistry

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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