Pharmacotherapeutic value of inflammatory and neurotrophic biomarkers in bipolar disorder: A systematic review.

Fernando Rodríguez de Fonseca, Juan Suárez, Jaime Martín-Martín, Fermín Mayoral-Cleries, Paloma Ruiz-Sastre, Carlos Gómez-Sánchez-Lafuente, Jesús Herrera-Imbroda, Ignacio Santos-Amaya, José Guzmán-Parra, Patricia Rivera

Journal: Progress in neuro-psychopharmacology & biological psychiatry 2024;134():111056

PMID: 38879067

Abstract

BACKGROUND

The various pharmacological interventions, ranging from mood stabilizers and antipsychotics to antidepressants, reflect the diff/iculty of treating depressive/manic symptomatology of bipolar disorder (BD). Among a broad range of mechanisms implicated, immune dysregulation may contribute to the increased inflammation that influences the course of BD. Inflammatory, neurotrophic and oxidative stress factors may be identified as promising peripheral biomarkers in brain functioning, perhaps serving as predictors of an effective response to treatment for BD. The present systematic review aimed to examine the evidence supporting the pharmacotherapeutic value of inflammatory and neurotrophic biomarkers in BD.

METHODS

PubMed, PsychINFO, Scopus and Web of Science were searched from inception to May 2024 by two independent reviewers. A total of 40 studies with 3371 patients with diagnosis and intervention of BD were selected.

RESULTS

Inconsistencies in the effects of pharmacological treatments on the connection between the expected anti-inflammatory response and symptomatologic improvement were identified. Mood stabilizers (lithium), antipsychotics (quetiapine), antidepressants (ketamine) or their combination were described to increase both pro-inflammatory (TNFα, IL-6) and anti-inflammatory (IL-4, IL-8) factors. Other medications, such as memantine and dextromethorphan, autoimmune (infliximab) non-steroidal anti-inflammatory (aspirin, celecoxib) drugs, antidiabetics (pioglitazone), and even dietary supplementation (omega-3), or their combination, clearly decrease inflammatory factors (TNFα, IL-6, IL-1β, C-reactive protein) and/or increase the neurotrophic factor BDNF in BD patients.

CONCLUSION

Inflammation in BD requires further investigation to understand the underlying immunologic mechanism, to identify predictors of treatment response, and to make informed decisions about the use and development of more effective pharmacological interventions for BD.

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Address: Instituto de Investigación Biomédica de Málaga (IBIMA)-Plataforma BIONAND, Calle Severo Ochoa 35, 29590 Málaga, Spain; Facultad de Medicina, Universidad de Málaga, Andalucia Tech, Campus de Teatinos, 29071 Málaga, Spain; UGC Salud Mental, Hospital Regional Universitario de Málaga, 29010 Málaga, Spain.; Instituto de Investigación Biomédica de Málaga (IBIMA)-Plataforma BIONAND, Calle Severo Ochoa 35, 29590 Málaga, Spain; UGC Salud Mental, Hospital Regional Universitario de Málaga, 29010 Málaga, Spain.; Instituto de Investigación Biomédica de Málaga (IBIMA)-Plataforma BIONAND, Calle Severo Ochoa 35, 29590 Málaga, Spain; Departamento de Anatomía Humana, Medicina Legal e Historia de la Ciencia, Universidad de Málaga, Bulevar Louis Pasteur 32, 29071 Málaga, Spain.; Instituto de Investigación Biomédica de Málaga (IBIMA)-Plataforma BIONAND, Calle Severo Ochoa 35, 29590 Málaga, Spain; Servicio Neurologia, Hospital Regional Universitario de Málaga, 29010 Málaga, Spain.; Instituto de Investigación Biomédica de Málaga (IBIMA)-Plataforma BIONAND, Calle Severo Ochoa 35, 29590 Málaga, Spain; UGC Salud Mental, Hospital Regional Universitario de Málaga, 29010 Málaga, Spain. Electronic address: [email protected].; Instituto de Investigación Biomédica de Málaga (IBIMA)-Plataforma BIONAND, Calle Severo Ochoa 35, 29590 Málaga, Spain; Departamento de Anatomía Humana, Medicina Legal e Historia de la Ciencia, Universidad de Málaga, Bulevar Louis Pasteur 32, 29071 Málaga, Spain. Electronic address: [email protected].
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