PRKAG2 gene expression is elevated and its protein levels are associated with increased amyloid-β accumulation in the Alzheimer's disease brain

Prashant Bharadwaj*, Ralph N. Martins

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    3 Citations (Scopus)

    Abstract

    Increased amyloid-β (Aβ) accumulation associated with abnormal autophagy-lysosomal activity and nutrient kinase dysregulation are common features in Alzheimer's disease (AD) brain. Recent studies have identified PRKAG2 and TIPRL genes that control nutrient kinase regulated autophagy, and here we determined if their expression is altered in postmortem AD brains. Gene and protein expression of TIPRL were unchanged. However, gene expression of PRKAG2 was increased 3-fold and its protein levels positively correlated with Aβ accumulation in the AD brain. In summary, our findings suggest that increased PRKAG2 is an important contributing factor to Aβ accumulation in the AD brain.

    Original languageEnglish
    Pages (from-to)441-448
    Number of pages8
    JournalJournal of Alzheimer's Disease
    Volume74
    Issue number2
    DOIs
    Publication statusPublished - 2020

    Bibliographical note

    Copyright IOS Press and the Author(s) 2020. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

    Keywords

    • Alzheimer's disease
    • amyloid-β
    • autophagy
    • PRKAG2
    • TIPRL

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