Amyotrophic lateral sclerosis-associated mutant profilin 1 increases dendritic arborisation and spine formation in primary hippocampal neurons

Merryn Brettle, Alexandra K. Suchowerska, Sook W. Chua, Lars M. Ittner*, Thomas Fath

*Corresponding author for this work

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease and familial ALS accounts for 10% of cases. The identification of familial ALS mutations in the actin-binding protein profilin 1 directly implicates actin dynamics and regulation in the pathogenesis of ALS. The mechanism by which these mutations cause ALS is unknown. In this study we show that expression of the ALS-associated actin-binding deficient mutant of PFN1 (PFN1C71G) results in increased dendritic arborisation and spine formation, and cytoplasmic inclusions in cultured mouse hippocampal neurons.

Original languageEnglish
Pages (from-to)223-228
Number of pages6
JournalNeuroscience Letters
Volume609
DOIs
Publication statusPublished - 16 Nov 2015
Externally publishedYes

Keywords

  • Actin cytoskeleton
  • Amyotrophic lateral sclerosis
  • Profilin 1

Fingerprint Dive into the research topics of 'Amyotrophic lateral sclerosis-associated mutant profilin 1 increases dendritic arborisation and spine formation in primary hippocampal neurons'. Together they form a unique fingerprint.

  • Cite this