Severe depression linked with inflammation in the brain
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Clinical depression is associated with a 30% increase of
inflammation in the brain, according to a new study published in JAMA
Psychiatry.
illustration depicting brain of depressed person
The new study is the first to find definitive evidence of
inflammation in the brain of depressed patients.
Inflammation is the immune system's natural response to
infection or disease. The body often uses inflammation to protect itself, such
as when an ankle is sprained and becomes inflamed, and the same principle also
applies to the brain. However, too much inflammation is unhelpful and can be
damaging.
Increasingly, evidence is suggesting that inflammation may
drive some depressive symptoms, such as low mood, loss of appetite and reduced
ability to sleep.
What the new study set out to investigate was whether
inflammation is a driver of clinical depression independent of other physical
illness.
Researchers from the Centre for Addiction and Mental
Health's (CAMH) Campbell Family Mental Health Research Institute in Toronto,
Canada, used positron emission tomography (PET) to scan the brains of 20
patients with depression and 20 healthy control participants.
In particular, the team closely measured the activation of
microglia - immune cells that play a key role in the brain's inflammatory
response
The PET scans showed significant inflammation in the brains
of the people with depression, and the inflammation was most severe among the
participants with the most severe depression. The brains of people who were
experiencing clinical depression exhibited an inflammatory increase of 30%.
Previous studies have examined markers of inflammation in
the blood of depressed people, in an attempt to solve the "chicken or
egg" debate of whether inflammation is a consequence of or contributor to
major depression.
For instance, in 2012, a study conducted by Duke University
Medical Center researchers and published in Biological Psychiatry found an
association between the number of cumulative depressive episodes experienced by
study participants and increased levels of an inflammation marker in their
blood called C-reactive protein (CRP).
"Our results support a pathway from childhood
depression to increased levels of CRP, even after accounting for other
health-related behaviors that are known to influence inflammation. We found no
support for the pathway from CRP to increased risk for depression," said
Duke study leader Dr. William Copeland.
The Duke team concluded that depression, therefore, is more
likely to contribute to inflammation in the body as opposed to arising as a
consequence of inflammation.
Medical News Today did not have access to data on whether
the patients in the CAMH study exhibited brain inflammation prior to developing
depression or after symptom onset. However, the CAMH researchers claim that
their study is the first to find definitive evidence of inflammation in the
brains of depressed patients.
Should future depression therapies target inflammation?
"This finding provides the most compelling evidence to
date of brain inflammation during a major depressive episode," says senior
author Dr. Jeffrey Meyer, who holds a Canada Research Chair in the
neurochemistry of major depression. He adds:
"This discovery has important implications for
developing new treatments for a significant group of people who suffer from
depression. It provides a potential new target to either reverse the brain
inflammation or shift to a more positive repair role, with the idea that it
would alleviate symptoms."
Severe depression affects 4% of the general population.
However, more than half of people with major depression do not respond to
antidepressants. Dr. Meyer suggests that future studies should investigate the
possible impact of anti-inflammatory drugs on depression symptoms.
"Depression is a complex illness and we know that it
takes more than one biological change to tip someone into an episode,"
says Dr. Meyer. "But we now believe that inflammation in the brain is one
of these changes and that's an important step forward."
C. Gilman Jones
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