Reduction of advanced tau-mediated memory deficits by the MAP kinase p38γ

Research output: Contribution to journalMeeting Abstractpeer-review

Abstract

BACKGROUND: Hyperphosphorylation of the neuronal tau protein contributes to Alzheimer's disease (AD) by promoting tau pathology and neuronal and cognitive deficits. In contrast, we have previously shown that site-specific tau phosphorylation can inhibit toxic signals induced by amyloid-β (Aβ) in mouse models. The post-synaptic mitogen-activated protein (MAP) kinase p38γ mediates this site-specific phosphorylation on tau at Threonine-205 (T205). 

Original languageEnglish
Pages (from-to)e054596
Number of pages1
JournalAlzheimer's & dementia : the journal of the Alzheimer's Association
Volume17
Issue numberS3
DOIs
Publication statusPublished - Dec 2021
Externally publishedYes
EventAlzheimer's Association International Conference 2021 - Denver, United States
Duration: 26 Jul 202130 Jul 2021

Keywords

  • Hyperphosphorylation
  • Tau protein
  • MAP kinase
  • p38 MAP kinase
  • memory deficits

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