Precision medicine

The Role of Microglia in Multiple Sclerosis: Implications for Treatment with Bruton’s Tyrosine Kinase Inhibitors

The presentation explores sphingosine-1-phosphate receptor modulators in Multiple Sclerosis, emphasizing receptor selectivity, pharmacokinetics, and class-related adverse effects. These factors are discussed in relation to clinical decision-making, treatment sequencing, and patient safety.

Microglia are increasingly recognised as central regulators of neuroinflammation in Multiple Sclerosis (MS). Beyond their traditional classification, advances in molecular biology have revealed a spectrum of functional states that influence both tissue damage and repair. This lecture provides a concise overview of microglial biology in MS and explores how emerging therapeutic strategies, particularly Bruton tyrosine kinase (BTK) inhibitors, may modulate these cells to impact disease progression.

Key Insights from the Lecture:

Microglia as central orchestrators of CNS immunity: Microglia act as resident immune cells coordinating innate and adaptive responses within the central nervous system.
Functional diversity beyond simple classification: Microglial states extend beyond a simple pro- and anti-inflammatory dichotomy, reflecting diverse roles in health and disease.
Sustained activation drives disease progression: Chronic microglial activation persists across MS stages and contributes to ongoing, smouldering disease pathology.
Microglia as biomarkers and prognostic indicators: In vivo imaging of microglial activation may serve as a biomarker to predict disease progression in MS.
Dual role: neurotoxicity and repair: Microglia contribute to both tissue damage through inflammation and repair through remyelination processes.
BTK inhibition as a therapeutic strategy: BTK inhibitors modulate microglial and B-cell activity to reduce inflammation and support regulatory mechanisms.
Clinical evidence emerging for BTK inhibitors: Emerging clinical data suggest BTK inhibitors may reduce disability progression, particularly in progressive MS.