The potential pathological role of NLRP3 inflammasome activation in pediatric tic disorders and its therapeutic implications
- 1The Second Clinical College, Liaoning University of Traditional Chinese Medicine, Shenyang, China
- 2The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, China
Abstract
Tic disorders (TDs) are common neurodevelopmental disorders in children and adolescents, with pathophysiology involving abnormalities in cortico-striato-thalamo-cortical (CSTC) circuits, neurotransmitter imbalance, and neuroimmune dysregulation. In recent years, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has attracted increasing attention because of its role in linking cellular stress, innate immunity, and inflammatory responses. Current human TD/Tourette syndrome (TS) studies primarily support striatal neuroimmune abnormalities and microglial inflammatory changes, whereas more direct evidence for NLRP3-, caspase-1-, and gasdermin D (GSDMD)-related alterations is derived mainly from animal models. Mechanistic evidence that NLRP3-related inflammation can influence synaptic function and neural circuits largely comes from non-TD experimental models. This review summarizes the activation mechanisms and biological effects of the NLRP3 inflammasome, with particular emphasis on its potential links to striatal neuroinflammation, pyroptosis-related effects, neurotransmitter regulation, and CSTC network abnormalities. We also discuss the pharmacological feasibility and evidentiary limitations of upstream modulation, direct NLRP3 inhibition, and blockade of downstream inflammatory effectors. At present, disease-specific causal validation of NLRP3 and direct evidence for NLRP3-targeted interventions in pediatric TDs remain lacking. Future studies integrating disease-specific mechanistic validation, biomarker development, and patient stratification are needed to clarify the pathological relevance and potential translational significance of NLRP3 in pediatric TDs.
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BibTeX
@article{zhang2026potential,
title = {{The potential pathological role of NLRP3 inflammasome activation in pediatric tic disorders and its therapeutic implications}},
author = {Siyu Zhang and Zhuoyu Meng and Huiyang Shi and Chushi Zhang},
journal = {Frontiers in Medicine},
year = {2026},
month = oct,
doi = {10.3389/fmed.2026.1968624},
url = {https://doi.org/10.3389/fmed.2026.1968624},
note = {CC BY},
}
RIS
TY - JOUR
TI - The potential pathological role of NLRP3 inflammasome activation in pediatric tic disorders and its therapeutic implications
AU - Siyu Zhang
AU - Zhuoyu Meng
AU - Huiyang Shi
AU - Chushi Zhang
PY - 2026
DA - 2026/10/23
JO - Frontiers in Medicine
DO - 10.3389/fmed.2026.1968624
UR - https://doi.org/10.3389/fmed.2026.1968624
AB - Tic disorders (TDs) are common neurodevelopmental disorders in children and adolescents, with pathophysiology involving abnormalities in cortico-striato-thalamo-cortical (CSTC) circuits, neurotransmitter imbalance, and neuroimmune dysregulation. In recent years, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has attracted increasing attention because of its role in linking cellular stress, innate immunity, and inflammatory responses. Current human TD/Tourette syndrome (TS) studies primarily support striatal neuroimmune abnormalities and microglial inflammatory changes, whereas more direct evidence for NLRP3-, caspase-1-, and gasdermin D (GSDMD)-related alterations is derived mainly from animal models. Mechanistic evidence that NLRP3-related inflammation can influence synaptic function and neural circuits largely comes from non-TD experimental models. This review summarizes the activation mechanisms and biological effects of the NLRP3 inflammasome, with particular emphasis on its potential links to striatal neuroinflammation, pyroptosis-related effects, neurotransmitter regulation, and CSTC network abnormalities. We also discuss the pharmacological feasibility and evidentiary limitations of upstream modulation, direct NLRP3 inhibition, and blockade of downstream inflammatory effectors. At present, disease-specific causal validation of NLRP3 and direct evidence for NLRP3-targeted interventions in pediatric TDs remain lacking. Future studies integrating disease-specific mechanistic validation, biomarker development, and patient stratification are needed to clarify the pathological relevance and potential translational significance of NLRP3 in pediatric TDs.
SN - 2296-858X
ER -