Brain-immune crosstalk in the treatment of major depressive disorder
European Neuropsychopharmacology. 2021-04-01; 45: 89-107
DOI: 10.1016/j.euroneuro.2020.11.016
Lire sur PubMed
1. Eur Neuropsychopharmacol. 2021 Apr;45:89-107. doi:
10.1016/j.euroneuro.2020.11.016. Epub 2020 Dec 29.
Brain-immune crosstalk in the treatment of major depressive disorder.
Branchi I(1), Poggini S(2), Capuron L(3), Benedetti F(4), Poletti S(4), Tamouza
R(5), Drexhage HA(6), Penninx BWJH(7), Pariante CM(8); European College of
Neuropsychopharmacology (ECNP) ImmunoNeuroPsychiatry Thematic Working Group and
Marion Leboyer(5).
Author information:
(1)Center for Behavioral Sciences and Mental Health, Istituto Superiore di
Sanità, Viale Regina Elena, 299, 00161 Rome, Italy. Electronic address:
.
(2)Center for Behavioral Sciences and Mental Health, Istituto Superiore di
Sanità, Viale Regina Elena, 299, 00161 Rome, Italy.
(3)University of Bordeaux, INRAE, Bordeaux INP, NutriNeuro, UMR 1286, Bordeaux,
France.
(4)Division of Neuroscience, Psychiatry and Clinical Psychobiology Unit, IRCCS
San Raffaele Scientific Institute, Milano, Italy; University Vita-Salute San
Raffaele, Milano, Italy.
(5)Département Medico-Universitaire de Psychiatrie et d’Addictologie (DMU
ADAPT), Laboratoire Neuro-psychiatrie translationnelle, AP-HP, Université Paris
Est Créteil, INSERM U955, IMRB, Hôpital Henri Mondor, Fondation FondaMental,
F-94010 Créteil, France.
(6)Department of Immunology, ErasmusMC, University Medical Center Rotterdam,
Rotterdam, the Netherlands.
(7)Department of Psychiatry, Amsterdam UMC, Department of Amsterdam Public
Health Research Institute and Amsterdam Neuroscience, Vrije Universiteit
Amsterdam, Amsterdam, the Netherlands.
(8)Department of Psychological Medicine, King’s College London, Institute of
Psychiatry, Psychology and Neuroscience, London, UK.
A growing number of studies are pointing out the need for a conceptual shift
from a brain-centered to a body-inclusive approach in mental health research. In
this perspective, the link between the immune and the nervous system, which are
deeply interconnected and continuously interacting, is one of the most important
novel theoretical framework to investigate the biological bases of major
depressive disorder and, more in general, mental illness. Indeed, depressed
patients show high levels of inflammatory markers, administration of
pro-inflammatory drugs triggers a depressive symptomatology and antidepressant
efficacy is reduced by excessive immune system activation. A number of molecular
and cellular mechanisms have been hypothesized to act as a link between the
immune and brain function, thus representing potential pharmacologically
targetable processes for the development of novel and effective therapeutic
strategies. These include the modulation of the kynurenine pathway, the
crosstalk between metabolic and inflammatory processes, the imbalance in
acquired immune responses, in particular T cell responses, and the interplay
between neural plasticity and immune system activation. In the personalized
medicine approach, the assessment and regulation of these processes have the
potential to lead, respectively, to novel diagnostic approaches for the
prediction of treatment outcome according to the patient’s immunological
profile, and to improved efficacy of antidepressant compounds through immune
modulation.
Copyright © 2020 Elsevier B.V. and ECNP. All rights reserved.
DOI: 10.1016/j.euroneuro.2020.11.016
PMID: 33386229 [Indexed for MEDLINE]
Conflict of interest statement: Conflict of Interest BP has received
(non-related) research funding from Boehringer Ingelheim and Jansen Research.
CMP is funded by the National Institute for Health Research (NIHR) Biomedical
Research Center at South London and Maudsley NHS Foundation Trust and King’s
College London, and is a NIHR Senior Investigator; moreover, he has received
research funding from Johnson & Johnson for research on depression and
inflammation, and by the Wellcome Trust strategy award to the Neuroimmunology of
Mood Disorders and Alzheimer’s Disease (NIMA) Consortium (104025), which is also
funded by Janssen, GlaxoSmithKline, Lundbeck and Pfizer, but this paper is
independent from this funding. IB, SP, LC, FB, SP, RT, ML and HAD declare no
competing financial interests. Funders had no role in the preparation, review,
or approval of the manuscript and decision to submit the manuscript for
publication.