Neuroprotective Effects of Anodal tDCS on Oxidative Stress and Neuroinflammation in Temporal Lobe Epilepsy.

Background

Epilepsy affects over 50 million people worldwide, and about 30% remain drug-resistant-underscoring the urgent need for new therapies. This study evaluated the neuroprotective effects of anodal transcranial direct current stimulation (tDCS) in PTZ-induced epilepsy at acute and chronic stages in rats.

Methods

Sixty male Wistar Albino rats (12 per group) were randomly assigned to five groups: control, acute epilepsy, acute epilepsy+ tDCS, chronic epilepsy, and chronic epilepsy+ tDCS. Behavioral tests-including the open-field, novel-object recognition, and Y-maze-assessed locomotion, recognition, and spatial memory. Hippocampal tissues were analyzed for oxidative stress markers (SOD, MDA), inflammatory cytokines (IL-1β, TNF-α), histopathology, and mechanistic markers of astrocytic and nitric oxide-mediated neuronal damage (GFAP and nNOS immunohistochemistry).

Results

PTZ-induced epilepsy resulted in cognitive deficits, increased oxidative stress, neuroinflammation, neuronal degeneration, and astrocytic activation. Specifically, SOD decreased, while MDA, IL-1β, and TNF-α increased; GFAP and nNOS upregulation indicated activation of astrocytes and nitric oxide-mediated neuronal damage. tDCS mitigated these effects by enhancing SOD, reducing MDA, IL-1β, and TNF-α, and modulating the NO/GFAP axis, which corresponded to decreased neuronal degeneration and vascular hyperemia. Behaviorally, tDCS improved recognition memory and partially rescued spatial memory deficits.

Conclusions

Anodal tDCS exerts neuroprotective effects in acute and chronic epilepsy by modulating oxidative stress, neuroinflammation, and the astrocytic/nitric oxide pathways, supporting its potential as a non-invasive adjunct therapy for cognitive and cellular protection. Future studies should investigate its effects on hippocampal glutamatergic and GABAergic pathways, as well as calcium homeostasis.