Involvement of p38 mapk in synaptic function and dysfunction

Chiara Falcicchia, Francesca Tozzi, Ottavio Arancio, Daniel Martin Watterson, Nicola Origlia*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations

Abstract

Many studies have revealed a central role of p38 MAPK in neuronal plasticity and the regulation of long-term changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). However, p38 MAPK is classically known as a responsive element to stress stimuli, including neuroinflammation. Specific to the pathophysiology of Alzheimer’s disease (AD), several studies have shown that the p38 MAPK cascade is activated either in response to the Aβ peptide or in the presence of tauopathies. Here, we describe the role of p38 MAPK in the regulation of synaptic plasticity and its implication in an animal model of neurodegeneration. In particular, recent evidence suggests the p38 MAPK α isoform as a potential neurotherapeutic target, and specific inhibitors have been developed and have proven to be effective in ameliorating synaptic and memory deficits in AD mouse models.

Original languageEnglish (US)
Article number5624
Pages (from-to)1-14
Number of pages14
JournalInternational journal of molecular sciences
Volume21
Issue number16
DOIs
StatePublished - Aug 2 2020

Keywords

  • Alzheimer’s disease
  • Neuroinflammation
  • P38-MAPK α inhibitor
  • Synaptic plasticity
  • Tau
  • β-amyloid

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

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