ROLE OF HIPPOCAMPUS AND AMYGDALA IN MAJOR DEPRESSION
Department of Psychiatry, University of Occupational and Environmental Health, Fukuoka, Japan
*Corresponding Author:
Reiji Yoshimura, Department of Psychiatry, University of Occupational and Environmental Health,
Fukuoka,
Japan,
Email: yoshi621@med.uoeh-u.ac.jp
Received: 30-Jan-2023, Manuscript No. AJOPY-23-88195;
Editor assigned: 03-Feb-2023, Pre QC No. AJOPY-23-88195 (PQ);
Reviewed: 17-Feb-2023, QC No. AJOPY-23-88195;
Revised: 24-Feb-2023, Manuscript No. AJOPY-23-88195 (R);
Published:
03-Nov-2023, DOI: 10.54615/2231-7805.S3.001
Description
The amygdala and hippocampus have been
associated with social interactions. Memory is
thought to be dependent on the hippocampal
system. The amygdala is prominently involved in
producing emotional responses and memories.
However, our emotional state seems to
considerably affect the way and accuracy with
which we retain information. The amygdala and
hippocampus work synergistically to form longterm
memories of robust emotional events. These
brain structures are activated after emotional events
and communicate with each other during memory
consolidation, which are related to neuropsychiatric
diseases [1].
Major Depression (MD) is one of the most
common psychiatric disorders, with a total lifetime
prevalence of approximately 15%-18%. MD has a
significant impact on the patient’s quality of life,
social interaction, and occupational achievement
[2].
A report on the findings of the ENIGMA study, a
comprehensive investigation conducted using
Magnetic Resonance Imaging (MRI) to assess brain
structure, function, and disease, reported a
statistically significant reduction in hippocampal
and amygdala volumes in patients with MD
compared with that in Healthy Controls (HC) [3].
While chronic stress conditions are known to cause
an increase in cortisol levels, previous studies have
suggested that elevated cortisol levels can
contribute to hippocampal and amygdala atrophy
[4].
In our study, we reported no difference in total
hippocampal volume between patients with MD
and HC. However, the volumes of the
Hippocampal-Amygdala-Transitional Area
(HATA) in the left hemisphere and the Para hippocampal, anterior cerebellar and limbic
structures in the right hemisphere were
significantly smaller in the MD group than in the
HC group. Furthermore, the right hippocampal
fissure volume was significantly smaller in the HC
group than in the MD group. Additionally, we
established a positive linear correlation between
hippocampal volume in the left CA4 region and
plasma levels of the Brain-Derived Neurotrophic
Factor (BDNF) in the MD group. BDNF is a
neurotrophic factor involved in neuroplasticity and
is associated with neurogenesis and synaptic
plasticity in the hippocampus [5]. In other words,
several subfields of the hippocampus were
correlated with plasma BDNF levels, and an
association was established between the right
parafoveal cerebellar volumes in the MD and HC
groups with respect to plasma BDNF levels [6].
With regards to the amygdala volume, no
difference in amygdala subregion volume was
observed between the HC and MD groups.
However, when we examined the relationship
between the amygdala subregional volume and
depression severity in the MD group, we found that
the more severe the core symptoms of MD, the
smaller the volumes of the lateral nucleus and
anterior amygdala region of the right amygdala,
and the more severe the anxiety or agitation, the
smaller the volumes of lateral nucleus, anterior
amygdala region, transition, and total amygdala.
Furthermore, the volumes of lateral nucleus and
anterior amygdala regions were strongly associated
with the total Hamilton rating scale for depression
scores for clinical symptoms of MD [7].
Taking these findings into account, volume changes
in sub regions of the hippocampus and amygdala in
MD patients could be complicated, which might be
reflected by impairments in the connections
between the hippocampus and amygdala.
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