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Enhancing NADPH to restore redox homeostasis and lysosomal function in G6PD-deficient microglia

Abir Mondal1, Soumyadeep Mukherjee1, Prince Upadhyay1

  • 1Department of Life Sciences, School of Natural Sciences, Shiv Nadar Institution of Eminence, Delhi NCR, India.

Heliyon
|March 14, 2025
PubMed

Insights

Glucose-6-phosphate dehydrogenase (G6PD) deficiency in microglia impairs redox balance. Targeting alternative pathways with metabolites and small molecules restored NADPH levels and lysosomal function, offering therapeutic potential.

Area of Science:

  • Neuroscience
  • Immunology
  • Metabolic pathways

Background:

  • Microglia are central nervous system immune cells vital for brain function.
  • Microglial inflammation contributes to neurodegenerative diseases like Alzheimer's and Parkinson's.
  • Glucose-6-phosphate dehydrogenase (G6PD) is crucial for producing NADPH, which combats oxidative stress.

Purpose of the Study:

  • To investigate the impact of G6PD deficiency on microglial redox balance and lysosomal function.
  • To explore alternative metabolic strategies for restoring NADPH levels in G6PD-deficient microglia.

Main Methods:

  • Examined G6PD deficiency effects on microglial NADPH levels, redox balance, and lysosomal function.
  • Targeted alternative NADPH-producing enzymes: isocitrate dehydrogenase 1 (IDH1) and malic enzyme 1 (ME1).
  • Administered metabolic supplements (citric acid, malic acid) and small molecules (dieckol, resveratrol).

Main Results:

  • G6PD deficiency in microglia reduced NADPH, disrupting redox and lysosomal homeostasis.
  • Targeting IDH1 and ME1 with metabolites and small molecules increased NADPH levels.
  • Combined interventions successfully restored redox balance and lysosomal function.

Conclusions:

  • G6PD deficiency severely impacts microglial metabolic function and redox homeostasis.
  • Alternative metabolic targeting offers a promising therapeutic avenue for G6PD deficiency-related neurological disorders.
  • Restoring NADPH production is key to mitigating neuroinflammation and neurodegeneration in G6PD deficiency.
Keywords:
G6PD deficiencyMetabolitesOxidative stressPhytochemicalsTherapeutics

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