Molecular and behavioural abnormalities in the FUS-tg mice mimic frontotemporal lobar degeneration: Effects of old and new anti-inflammatory therapies

J Cell Mol Med. 2020 Sep;24(17):10251-10257. doi: 10.1111/jcmm.15628. Epub 2020 Jul 15.

Abstract

Genetic mutations in FUS, a DNA/RNA-binding protein, are associated with inherited forms of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). A novel transgenic FUS[1-359]-tg mouse line recapitulates core hallmarks of human ALS in the spinal cord, including neuroinflammation and neurodegeneration, ensuing muscle atrophy and paralysis, as well as brain pathomorphological signs of FTLD. However, a question whether FUS[1-359]-tg mouse displays behavioural and brain pro-inflammatory changes characteristic for the FTLD syndrome was not addressed. Here, we studied emotional, social and cognitive behaviours, brain markers of inflammation and plasticity of pre-symptomatic FUS[1-359]-tg male mice, a potential FTLD model. These animals displayed aberrant behaviours and altered brain expression of inflammatory markers and related pathways that are reminiscent to the FTLD-like syndrome. FTLD-related behavioural and molecular Journal of Cellular and Molecular Medicine features were studied in the pre-symptomatic FUS[1-359]-tg mice that received standard or new ALS treatments, which have been reported to counteract the ALS-like syndrome in the mutants. We used anti-ALS drug riluzole (8 mg/kg/d), or anti-inflammatory drug, a selective blocker of cyclooxygenase-2 (celecoxib, 30 mg/kg/d) for 3 weeks, or a single intracerebroventricular (i.c.v.) infusion of human stem cells (Neuro-Cells, 500 000-CD34+ ), which showed anti-inflammatory properties. Signs of elevated anxiety, depressive-like behaviour, cognitive deficits and abnormal social behaviour were less marked in FUS-tg-treated animals. Applied treatments have normalized protein expression of interleukin-1β (IL-1β) in the prefrontal cortex and the hippocampus, and of Iba-1 and GSK-3β in the hippocampus. Thus, the pre-symptomatic FUS[1-359]-tg mice demonstrate FTLD-like abnormalities that are attenuated by standard and new ALS treatments, including Neuro-Cell preparation.

Keywords: FUS[1-359]-tg mice; amyotrophic lateral sclerosis; animal model; celecoxib; emotionality and cognition; frontotemporal lobar degeneration; neuroinflammation; riluzole; stem cell therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyotrophic Lateral Sclerosis / drug therapy
  • Amyotrophic Lateral Sclerosis / metabolism
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Behavior, Animal / drug effects
  • Brain / drug effects*
  • Brain / metabolism
  • Cyclooxygenase 2 / metabolism
  • Frontotemporal Lobar Degeneration / drug therapy*
  • Frontotemporal Lobar Degeneration / metabolism*
  • Glycogen Synthase Kinase 3 beta / metabolism
  • Inflammation / drug therapy
  • Inflammation / metabolism
  • Interleukin-1beta / metabolism
  • Male
  • Mice
  • Mutation / drug effects
  • Neurons / drug effects
  • Neurons / metabolism
  • RNA-Binding Protein FUS / metabolism*
  • Social Behavior
  • Spinal Cord / drug effects
  • Spinal Cord / metabolism

Substances

  • Anti-Inflammatory Agents
  • FUS protein, mouse
  • Interleukin-1beta
  • RNA-Binding Protein FUS
  • Cyclooxygenase 2
  • Glycogen Synthase Kinase 3 beta