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Published on: August 15, 2017
Inflammatory markers and electroconvulsive therapy-related cognitive outcomes in Depressive Disorders: A systematic
Hanie Karimi1, Anahita Najafi2, Kimia Farahmand1
1Psychiatric Research Center, Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Background:
Electroconvulsive therapy (ECT) is an effective treatment for severe mood disorders. However, its cognitive side effects limit the widespread use. This systematic review evaluates the role of inflammatory markers in ECT-induced cognitive changes and identifies potential predictors of cognitive outcomes.
Methods:
A comprehensive search was conducted in four databases (ISI Web of Science, Scopus, PubMed, and Embase), following PRISMA guidelines. We included studies investigating the association between inflammatory biomarkers and cognitive performance before and after ECT in unipolar or bipolar depression, as well as animal models.
Results:
Eight studies met the inclusion criteria, comprising five human and three animal studies. Key inflammatory markers examined included interleukin (IL)-6, IL-10, IL-1β, tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP). In human studies, higher baseline IL-10 levels were associated with lower cognitive impairment post-ECT. In contrast, the relationship between CRP and cognition was inconsistent, and no significant association was found between baseline IL-6 or TNF-α levels and cognitive changes. In animal models, elevated inflammatory markers such as IL-1β and TNF-α were associated with cognitive impairments following electroconvulsive shock, the animal analog of ECT.
Conclusions:
Inflammatory markers may play a role in ECT-induced cognitive impairment, with specific cytokines showing significant correlations with cognitive outcomes. However, evidence remains preliminary, and further prospective research is required before these markers can serve as clinically validated predictors that could inform targeted strategies to mitigate ECT-related cognitive adverse effects.
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