Public Release: 

Brain inflammation linked to depression in multiple sclerosis

Reports new study in Biological Psychiatry


Philadelphia, PA, July 7, 2016 - Patients with multiple sclerosis have higher rates of depression than the general population, including people with other life-long disabling diseases. Symptoms of multiple sclerosis arise from an abnormal response of the body's immune system. Immune response has also been linked to depression, leading researchers to think it could be a shared pathological mechanism that leads to the increased rates of depressive symptoms in patients with multiple sclerosis.

A new study in Biological Psychiatry supports this hypothesis, providing evidence that inflammation of the hippocampus, a region of the brain implicated in the genesis and maintenance of depression and in the pathology of multiple sclerosis, alters its function and contributes to symptoms of depression.

"This study elegantly links hippocampal inflammation to depression," said Dr. John Krystal, Editor of Biological Psychiatry.

The research was a collaboration between King's College London, Imperial College London, and Imanova Center for Imaging Sciences. Led by senior authors Paul Matthews and Eugenii Rabiner, the research team combined two complementary brain imaging techniques to study the relationship between hippocampal immune response, functional connections, and depressive symptoms in 13 patients with multiple sclerosis and 22 healthy control subjects. Positron emission tomography (PET) allowed for quantification of activated microglia, a measure of immune response. Functional magnetic resonance imaging (fMRI) assessed the strength of hippocampal connections to an extensive network of brain regions involved in emotion.

First author Dr. Alessandro Colasanti, of King's College London, explained that PET imaging revealed immune activation in the hippocampus of patients with multiple sclerosis. "We also discovered that more inflammation was associated to more severe symptoms of depression," said Colasanti.

Measurements of functional brain connections with fMRI during rest showed that immune activation in the hippocampus altered its connections with other brain regions. "This study, combining two advanced complementary brain imaging methods, suggests that the inflammation of the hippocampus affects the brain function and causes depression," said Colasanti.

The findings suggest that hippocampal inflammation could be the contributing cause of high rates of depression in multiple sclerosis. The authors predict that an effective and targeted treatment of brain inflammation would help to restore brain function and protect against depression in multiple sclerosis.


Notes for editors

The article is "Hippocampal Neuroinflammation, Functional Connectivity, and Depressive Symptoms in Multiple Sclerosis," by Alessandro Colasanti, Qi Guo, Paolo Giannetti, Matthew B. Wall, Rexford D. Newbould, Courtney Bishop, Mayca Onega, Richard Nicholas, Olga Ciccarelli, Paolo A. Muraro, Omar Malik, David R. Owen, Allan H. Young, Roger N. Gunn, Paola Piccini, Paul M. Matthews, and Eugenii A. Rabiner (doi: 10.1016/j.biopsych.2015.11.022). It appears in Biological Psychiatry, volume 80, issue 1 (2016), published by Elsevier.

Copies of this paper are available to credentialed journalists upon request; please contact Rhiannon Bugno at +1 214 648 0880 or Journalists wishing to interview the authors may contact Alessandro Colasanti at

The authors' affiliations, and disclosures of financial and conflicts of interests are available in the article.

John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine, Chief of Psychiatry at Yale-New Haven Hospital, and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.

About Biological Psychiatry

Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.

The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.

Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 5th out of 140 Psychiatry titles and 11th out of 256 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2015 Impact Factor score for Biological Psychiatry is 11.212.

About Elsevier

Elsevier is a world-leading provider of information solutions that enhance the performance of science, health, and technology professionals, empowering them to make better decisions, deliver better care, and sometimes make groundbreaking discoveries that advance the boundaries of knowledge and human progress. Elsevier provides web-based, digital solutions -- among them ScienceDirect, Scopus, Elsevier Research Intelligence and ClinicalKey -- and publishes over 2,500 journals, including The Lancet and Cell, and more than 35,000 book titles, including a number of iconic reference works. Elsevier is part of RELX Group, a world-leading provider of information and analytics for professional and business customers across industries.

Media contact

Rhiannon Bugno
Editorial Office, Biological Psychiatry
+1 214 648 0880

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.