Commentary on Giralt et al. PTK2B/Pyk2 overexpression improves a mouse model of Alzheimer's disease

Baruh Polis, Hava Gil-Henn

Research output: Contribution to journalComment/Debate

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common cause of dementia and the 6th leading cause of death. Although research has revealed significant information about AD, much is yet to be discovered about the precise biological changes that cause AD and how the disease could be prevented, slowed, or stopped. Accumulating evidence suggests the involvement of the non-receptor proline-rich tyrosine kinase 2 (Pyk2) in AD, but the downstream signaling events triggered by this protein and their implications on the pathology of the disease were unclear until recently. A recent paper by Giralt et al. used genetically depleted and overexpression mouse models to elucidate the role of Pyk2 in AD. Here, we discuss the findings presented in this paper in light of previous information and hypotheses, and suggest interpretations and explanations for this surprising and unexpected phenotype.

Original languageEnglish
Pages (from-to)313-317
Number of pages5
JournalExperimental Neurology
Volume311
DOIs
StatePublished - Jan 2019
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2018 Elsevier Inc.

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

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