Migraine is a prevalent neurological condition characterized by recurrent headaches and sensory disturbances. Despite its high global burden, the molecular pathways contributing to migraine pathogenesis remain unclear. To better understand its biological basis, transcriptomic profiling was performed on peripheral blood mononuclear cells from 102 migraine patients and 95 healthy controls using next-generation RNA sequencing technology.
Analysis of the data revealed substantial dysregulation of genes associated with neuroinflammatory and pain signaling pathways. The most prominent molecular signature involved upregulation of microglial activation markers, including CX3CR1 and TREM2, suggesting persistent neuroinflammatory activity in migraine patients. Additionally, increased expression of cytokine-related genes such as IL6, TNF, and CCL2 was observed, confirming the role of immune-mediated inflammation in migraine attacks.
Interestingly, downregulation of GABA receptor-associated genes and altered calcium channel subunits were detected, indicating an imbalance between excitatory and inhibitory neurotransmission within the central nervous system. This disruption may underlie the heightened neuronal sensitivity and pain perception characteristic of migraines.
Pathway analysis further identified alterations in serotonin and glutamate signaling, implicating neurotransmitter dysregulation as a key contributor to migraine pathophysiology. Collectively, these findings support the hypothesis that migraine is not merely a vascular disorder but a neuroinflammatory condition involving complex immune and neural interactions.
The identified gene expression signatures provide valuable insight into potential therapeutic targets aimed at modulating neuroinflammation and restoring neurotransmitter balance. Future research integrating genomics, proteomics, and metabolomics will be essential to develop precise diagnostic biomarkers and personalized treatment strategies for migraine management.
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