Abstract
Background
Although the peak onset of depressive symptoms occurs during adolescence, very few
studies have directly examined depression-related changes in resting-state (RS) default
mode network activity during adolescence, controlling for potential neural markers
of risk.
Methods
This study used data from a longitudinal adolescent cohort to investigate age-specific,
persistent (i.e., lagged), and dynamic associations between RS functional connectivity
within the default mode network and depressive symptoms during adolescence using a
random intercept cross-lagged panel framework. The Neuroventure sample consisted of
151 adolescents ages 12–14 at study entry without any neurological illness who were
assessed three times during a 5-year follow-up with 97% follow-up across the three
assessments. Depressive symptoms were measured using the depression subscale of the
Brief Symptoms Inventory. RS functional magnetic resonance imaging data were collected
using a 3T Siemens Magnetom Trio scanner in a single 6-minute sequence.
Results
After controlling for relationships between random intercepts, future depression risk
was predicted by RS couplings in the perigenual anterior cingulate cortex and anterior
dorsomedial prefrontal cortex (β = −0.69, p = .014) and in the left inferior parietal lobule and anterior superior frontal gyrus
(β = −0.43, p = .035). Increases in depressive symptoms at previous time points significantly predicted
changes in functional connectivity between the posterior cingulate cortex and the
precuneus and posterior middle temporal gyrus (β = 0.37, p = .039) and between the dorsal precuneus and posterior middle temporal gyrus (β =
0.47, p = .036).
Conclusions
This study was able to disassociate the RS brain markers of depression from those
that appear to follow early-onset depression.
Keywords
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Article Info
Publication History
Published online: December 17, 2021
Accepted:
October 28,
2021
Received in revised form:
October 5,
2021
Received:
June 21,
2021
Identification
Copyright
© 2022 Published by Elsevier Inc on behalf of Society of Biological Psychiatry.
