Lee and colleagues (2014) found
that adolescence is a peak period for clinical onset of most MDs. (ADHD, conduct disorder, anxiety disorders, mood disorders, ScZ and substance abuse)
because of the developmental phase of adolescence makes the brain more plastic it can be a peak time for clinical onset of most illnesses. (????)
(Paus et al., 2008)
Skosnik and colleagues (2012) found
- chronic exposure to exogenous cannibinoids can effect the ability to generate neural oscillations (especially gamma)
- implications for neurodevelopmental disorders
could disrupt ability to synchronize neural circuits - major risk factor for ScZ
Klein and colleagues (2014) found
- cortical folding patterns undergo pronounced change which involves a reduction in gyrification across large areas of the cerebral cortex, in particular in precentral, frontal and temporal regions.
- supports that adolescence involves fundamental changes in the architecture of the cerebral cortex
- aberrant gyrification in ScZ
There is emerging data that the type of abuse/neglect has specific neurobiological
consequences (????)
(Pechtel et al., 2014)
the course of psychiatric disorders in individuals exposed to childhood maltreatment
is more severe (????)
(Nemeroff, 2016)
Nemeroff, (2016) conducted a review and found
- Childhood maltreatment and trauma questionnaire scores positively correlated with right amygdala responsiveness to negative facial expressions (more activity)
- found that the higher the maltreatment score the lower hippocampal volume is
- Adolescents showed exaggerated amygdala activity relative to children and adults. This age-related difference decreased with repeated exposures to the stimuli.
- Individuals with higher trait anxiety showed less habituation over repeated exposures
- failure to habituate = less functional connectivity between ventral PFC and amygdala.
- suggests that exaggerated emotional reactivity during adolescence may increase the need for top-down control and put individuals with less control at greater risk for poor outcomes. (????)
(Hare et al., 2008)
- data show that the effects of traumatic stress on the developing brain may be severe and persistent and lead to adverse brain development.
- Environmental stress and adrenal steroids inhibit neurogenesis
- there is neurogenesis in the primate brain, effective psychosocial and medical treatments of abuse-related disorders and therapeutic reversibility are important areas for future investigations. (????)
(De Bellis et al., 2011)
Gee and colleagues (2013)
Relative to adults, adolescents experience more extreme and short-lived emotions in their everyday lives and show heightened amygdala reactivity to affective cues.
- fMRI study
- 56 pps (adult vs. adolescence)
- During active regulation, older = greater drops in negative affect and inverse rostrolateral prefrontal-amygdala connectivity.
- During re-presentation, older pps continued reduction in the amygdala response to aversive stimuli - mediated by rostrolateral PFC.
- suggests that one source of heightened emotionality in adolescence is a diminished ability to cognitively down-regulate aversive reactions.
(Silvers et al., 2015)
Cohen and colleagues (2013)
- mice and orphan study for trauma
- mouse study found type and timing of stressors result in alterations of amygdala circuitry
- orphans had diminished ability to suppress attention towards threatening info and to favor goal-directed behavior compared to non-institutionalized kids.
Studies have shown that the cannabinoid system has a key role in neurogeneisis, neural maturation, glia formation and others
Harkany et al., 2017
Patten and colleagues (2014)
- longitudinal study to address MDs
- episodes of MDs in adolescence often precedes into adult hood
- if episodes are brief, symptom remission is common
- early intervention could help tackle duration of episodes and onset
What is the synaptic pruning hypothesis
synaptic pruning takes place in adolescence, improper synaptic pruning could lead to the onset of ScZ
- Strongest risk factors for development of MDD in adolescence is family history of MDD and exposure to psycho-social stress.
Tharpar et al., 2012
