Neuroinflammation as a shared mechanism linking epilepsy and psychiatric comorbidities
Abstract
Although epilepsy arises from diverse etiologies, neuroinflammatory processes have emerged as a key factor in epileptogenesis. Neuroinflammation activates a complex network of cellular and molecular mechanisms involving microglia and astrocytes, as well as the production of pro-inflammatory mediators such as interleukin IL-1β, IL-6, and TNF-α, with inflammasome signaling representing a major upstream driver of these responses. These inflammatory processes contribute to increased seizure susceptibility and facilitate seizure propagation. Beyond their role in seizure generation, inflammatory mechanisms have also been implicated in the development of psychiatric disorders commonly associated with epilepsy. Depression, anxiety, and psychotic disorders occur at disproportionately high rates in people with epilepsy, particularly in those with temporal lobe epilepsy. Notably, many of these psychiatric conditions are associated with inflammatory alterations. This convergence suggests that neuroinflammatory signaling may represent a shared pathophysiological mechanism linking epileptic network dysfunction and psychiatric symptomatology. In this review, we synthesize clinical and experimental evidence supporting the involvement of inflammatory pathways in both epilepsy and its major psychiatric comorbidities. We discuss the molecular mediators, cellular mechanisms, and neural circuit alterations that may underlie this association and evaluate their potential utility as biomarkers and therapeutic targets for improving neuropsychiatric outcomes in epilepsy. Keywords: Neuroinflammation; Seizure; Epilepsy; Depression; Anxiety; Psychosis.
Related
- Economic burden of immune-mediated and psychiatric comorbidities in patients with newly diagnosed vitiligo
- Neuroinflammation: an important mechanism of sevoflurane-induced developmental neurotoxicity
- Cooperative care as a candidate mechanism linking prolonged childhood and brain expansion in human evolution
- Disrupted Enteric Glial Cell Circadian Oscillation: A Proposed Mechanism Linking CMM-Axis Desynchronization, Gut Jet Lag, and Chronic Functional Constipation
- T1R2/T1R3 Identified as the Aβ Receptor: A New Mechanism Linking Aβ42/40 Ratio to Neuronal Hyperexcitability in Alzheimer's Disease
BibTeX
@misc{eiris2026neuroinflammation,
title = {{Neuroinflammation as a shared mechanism linking epilepsy and psychiatric comorbidities}},
author = {Beatriz Eiris and Tamiris Prizon and Ana Carolina Medeiros and Thais Forner Batelli and José Eduardo Peixoto-Santos and Joao Pereira Leite and Rafael Naime Ruggiero},
howpublished = {PsyArXiv},
year = {2026},
month = oct,
doi = {10.31234/osf.io/evkw2_v1},
url = {https://osf.io/preprints/psyarxiv/evkw2_v1/},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - Neuroinflammation as a shared mechanism linking epilepsy and psychiatric comorbidities
AU - Beatriz Eiris
AU - Tamiris Prizon
AU - Ana Carolina Medeiros
AU - Thais Forner Batelli
AU - José Eduardo Peixoto-Santos
AU - Joao Pereira Leite
AU - Rafael Naime Ruggiero
PY - 2026
DA - 2026/10/01
PB - PsyArXiv
DO - 10.31234/osf.io/evkw2_v1
UR - https://osf.io/preprints/psyarxiv/evkw2_v1/
AB - Although epilepsy arises from diverse etiologies, neuroinflammatory processes have emerged as a key factor in epileptogenesis. Neuroinflammation activates a complex network of cellular and molecular mechanisms involving microglia and astrocytes, as well as the production of pro-inflammatory mediators such as interleukin IL-1β, IL-6, and TNF-α, with inflammasome signaling representing a major upstream driver of these responses. These inflammatory processes contribute to increased seizure susceptibility and facilitate seizure propagation. Beyond their role in seizure generation, inflammatory mechanisms have also been implicated in the development of psychiatric disorders commonly associated with epilepsy. Depression, anxiety, and psychotic disorders occur at disproportionately high rates in people with epilepsy, particularly in those with temporal lobe epilepsy. Notably, many of these psychiatric conditions are associated with inflammatory alterations. This convergence suggests that neuroinflammatory signaling may represent a shared pathophysiological mechanism linking epileptic network dysfunction and psychiatric symptomatology. In this review, we synthesize clinical and experimental evidence supporting the involvement of inflammatory pathways in both epilepsy and its major psychiatric comorbidities. We discuss the molecular mediators, cellular mechanisms, and neural circuit alterations that may underlie this association and evaluate their potential utility as biomarkers and therapeutic targets for improving neuropsychiatric outcomes in epilepsy. Keywords: Neuroinflammation; Seizure; Epilepsy; Depression; Anxiety; Psychosis.
ER -