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Fos regulates age-dependent neuroinflammation in VAPBALS.

Namrata Pramod Kulkarni1, Aparna Thulasidharan1, Amarendranath Soory1

  • 1Department of Biology, Indian Institute of Science Education and Research, Pune-411008, India.

Disease Models & Mechanisms
|June 4, 2026
PubMed
Summary

We developed a Drosophila model for Amyotrophic Lateral Sclerosis type 8 (ALS8) and found that glial-modulated neuroinflammation accelerates disease progression. Kayak, a Drosophila Fos protein, acts as a key regulator, with its modulation impacting motor function and lifespan.

Keywords:
Amyotrophic Lateral SclerosisCRISPR/Cas9KayakNeuroinflammationVesicle-associated membrane protein-associated protein B

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Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease causing progressive motor function loss.
  • The VAPB P58S mutation is linked to ALS8, a specific subtype of the disorder.
  • Intracellular membrane contact sites and ER-based adapter proteins like VAPB play roles in cellular regulation.

Purpose of the Study:

  • To establish a Drosophila melanogaster model for studying ALS8 (VAPBP58S).
  • To investigate the role of neuroinflammation in ALS8 pathogenesis.
  • To identify key regulators of age-dependent neuroinflammation in the context of ALS8.

Main Methods:

  • CRISPR/Cas9 genome editing to create the VAPBP58S Drosophila model.
  • Whole-transcriptome quantitative mRNA sequencing to analyze brain gene expression.
  • Genetic manipulation (overexpression and knockdown) of Drosophila Fos (Kayak) in glial cells.

Main Results:

  • VAPBP58S flies exhibit age-dependent motor deficits and reduced lifespan, mirroring human ALS.
  • Age-dependent neuroinflammation involving multiple immune pathways (Toll, IMD, Jak-STAT, Jun-kinase) was observed in VAPBP58S fly brains.
  • Kayak in glial cells was identified as a crucial negative regulator of neuroinflammation; its modulation affected motor function and inflammation levels.

Conclusions:

  • Glial-modulated neuroinflammation is a critical factor in ALS8 progression.
  • Kayak acts as a central regulator of age-dependent neuroinflammation in this ALS model.
  • Targeting glial-mediated inflammation pathways, potentially involving Kayak, could offer therapeutic strategies for ALS8.