Abstract
A rapidly growing body of evidence supports that neuroinflammation plays a major role in epileptogenesis and disease progression. The capacity to identify pathological neuroinflammation in individuals with epilepsy is a crucial step on the timing of anti-inflammatory intervention and patient selection, which will be challenging aspects in future clinical studies. The discovery of noninvasive biomarkers that are accessible in the blood or molecular neuroimaging would facilitate clinical translation of experimental findings into humans. These innovative and noninvasive approaches have the advantage of monitoring the dynamic changes of neuroinflammation in epilepsy. Here, we will review the available evidence for the measurement of neuroinflammation in patients with epilepsy using noninvasive techniques and critically analyze the major scientific challenges of noninvasive methods. Finally, we propose the potential for use in clinical applications.
Highlights
Epilepsy is a common heterogeneous disease with a complex pathophysiology
Increasing evidence suggests that dynamic changes of neuroinflammation processes in epilepsy with a range of etiologies lead to the development and progression of this disease
The discovery of noninvasive biomarkers of maladaptive neuroinflammation in epilepsy would facilitate clinical translation of anti-inflammatory treatments as they would enable the identification of patients who could benefit from the treatments and would provide pharmacodynamic markers of the therapeutic response
Summary
Epilepsy is a common heterogeneous disease with a complex pathophysiology. Increasing evidence suggests that dynamic changes of neuroinflammation processes in epilepsy with a range of etiologies lead to the development and progression of this disease. Initiation of inflammatory pathways exacerbates blood-brain barrier damage (BBBD) and fuels the innate and adaptive immune response within the brain and the periphery These inflammatory processes often occur and last throughout the development of epilepsy, which contribute to the progression and severity of epilepsy. The causal and reciprocal link between neuroinflammation and epilepsy may contribute to neuronal hyperexcitability and drug resistance [1] Modulation of these inflammation mechanisms could be a potential therapeutic target for epilepsy, which fostered interest in developing drugs targeting pathologic inflammatory pathways for selected epilepsy syndromes [2]. Inflammatory mediator measurement in the blood sample and brain imaging of neuroinflammation could provide noninvasive methodologies to detect and quantify brain inflammation in humans.
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