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MPBD: Depression Lectures summary
This document contains a summary of the lectures and powerpoints about depression.
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MPBD: DepressionPeople that did not experience depression Psychopathology and brain circuits
made up a social construct stating that New paradigm: depressive symptoms are
depression occurs when there are a lot of increasingly linked to malfunctioning specific
negative things happening in the brain circuits. Genes + environmental risk
environment, which causes someone to be factors conspire to produce inefficient
more negative. This is not always true. information processing in neural circuitry.
Depression can occur in people even though
their life seems “great” and there is not much Etiology ideas depression
to complain about. They feel like they are • Overactive amygdala
seeing life through grey glasses and feel/ • Decreased activity in the prefrontal cortex
experience everything darker, more fearful • Decreased hippocampal volume (neurogenic
and threatening than it is. It is their brain hypothesis)
that filters reality in another way and • Overactive HPA-axis
presents it to them as being more negative, • Decreased levels of brain-derived neurotrophic
fearful, and threatening, making them believe factors (BDNF)
that this grey-filtered life is true.
* These are all connected in complex interactions
Depression diagnosis
DSM-5 diagnostic criteria for depression, one Neuroimaging findings
of these symptoms are present: Researchers found that in people with depression
• Depressed or irritable mood the amygdala is overreactive. They measured
• Decreased interest in pleasurable activities this via an MRI. The depressed group as well as
and anhedonia the control group heard positive and negative
associated words and they saw that the amygdala
Other symptoms are: response to negative words was much stronger in
• Significant weight gain or loss (>5% change depressed people. But even with neutral and
in a month) positive words, there was a higher amygdala
• Insomnia or hypersomnia response in depressed people.
• Psychomotor agitation or retardation
• Fatigue or loss of energy
• Feelings of worthlessness or excessive guilt
• Diminished ability to think or concentrate
• Recurrent thoughts of death or suicide
To be diagnosed with depression you must
have at least 5+ symptoms listed above, which
are experienced daily for approximately 2
weeks.
Next, they looked at the prefrontal cortex. The
10-20% of people will experience depression depressed and the control group had to
in their life and it occurs twice as much in remember 5 digits and they saw that in
females. According to WHO depression is in depressed people they have decreased activity in
the top 10 causes of mortality (factors you die the prefrontal cortex compared to the control
from) and morbidity (anxiety, ADHD, group. Even though the depressed group had a
addiction and other psychiatric disorders). decreased activity the performance was the same
as in the control group.
In the past, the monoamine hypothesis of
depression was thought of as a low
concentration of serotonin in the brain.
Researchers thought this because drugs that
act on serotonin or norepinephrine pathways
relieve the symptoms of depression within a
few weeks. But this is an overly simplistic
paradigm, there is more to this.
, So, depression is characterized by increased Hippocampal volume
and sustained emotional reactivity, especially Some studies found reduced hippocampal volume
to negative emotions, because of the reactivity in patients with major depressive disorder and
of the amygdala to hearing emotional others did not. Possible explanations for these
information. But also the decreased activity of results could be that it is dependent on the
the prefrontal cortex. subtype of depression. Another explanation could
be that you see reduced hippocampal volume
What is the interaction between the amygdala when people feel acutely depressed and that it is
and the prefrontal cortex? normalized after treatment. But it could also be
In normal people, the prefrontal cortex possible that reduced hippocampal volume is an
inhibits the activity of the amygdala keeping indicator of vulnerability to depression in
emotions under control. In depressed people, healthy people.
you see an overactive amygdala and a
decrease in prefrontal cortex activity, which A study looked at girls between 9 and 15 years
means that the communication between the old that are daughters of mothers with recurrent
amygdala and prefrontal cortex is insufficient. episodes of depression and a control group. None
To test this they used two groups, one healthy of the girls had any past or current symptoms.
group and one group with people with They looked at the volume of the girls in the risk
depression. They showed 8 pictures to them group to see if they have a reduced hippocampal
with sad facial expressions going from neutral volume, and the results showed that this is true.
to extremely sad faces. Results showed that
the amygdala activity increased in picture 3 A second study looked at the structure of the
for depressed people, and picture 5 for healthy hippocampus. The hippocampus consists of a
people. After this, they started to treat small hippocampal head, a larger hippocampal
depressed people with antidepressants, which body, and a smaller hippocampal tail. This study
showed a normalization of amygdala activity. measured all these subregions and found that a
They also tested this after cognitive decrease in the hippocampal tail and head
behavioural therapy. What this therapy does is volumes could be vulnerability markers. The
training the brain by using certain synapses hippocampal tail and head tend to be smaller in
more often so they become stronger. It people at risk of depression. They also discovered
increases certain thought patterns and that the hippocampal body changes may depend
decreases others, so the synapses of the neural on the mood state/treatment (if they are
circuit change. depressed or non-depressed at that moment).
Long-term antidepressant use may affect
hippocampal volume in patients with major
depressive disorder.
Several different etiological pathways can
contribute to the decreased hippocampal volume.
Reduction in volume in the prefrontal cortex as
well as the hippocampus can be caused by loss of
volume of the neurons, such as dendritic atrophy,
spine loss and decreased neuronal synapses. A
reduction in the hippocampus only can be due to
a loss in the number of neurons in the
hippocampus. There could be an inhibition of
neurogenesis, which means that neurons are
being inhibited from being born.
So, pharmacotherapy and behavioural therapy
can normalize amygdala and prefrontal cortex
functioning.
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