SAGE Journal Articles

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Journal Article 1: Kim, J. H. (2017). Reducing Fear During Childhood to Prevent Anxiety Disorders Later: Insights From Developmental Psychobiology. Policy Insights from the Behavioral and Brain Sciences, 4(2), 131-138. doi:10.1177/2372732217719544

Abstract: Anxiety disorders are neurodevelopmental with the median age of onset 10 to 11 years, but developmental processes underlying fear and anxiety are rarely investigated. In the last decade, however, developmental rodent studies have increased our understanding of how to treat and prevent the persistence of anxiety. Behavioral findings from rodent studies match the observations in anxious children, and the neural and molecular findings help explain why anxiety disorders are indeed neurodevelopmental. Extinction processes that are involved in cognitive-behavioral therapy appear particularly effective in children compared with older populations. Policy should mandate school psychologists and government subsidies for therapy sessions to increase children’s mental-health-service utilization. Funding bodies also should challenge anxiety studies exclusively targeting adults to include younger people to investigate why anxiety disorders are developmental disorders and focus more on preventing their persistence later in life.

Journal Article 2: Cousins, L.,& Goodyer, I. M. (2015). Antidepressants and the adolescent brain. Journal of Psychopharmacology, 29(5), 545-555.


Abstract: Major unipolar depression is a significant global health problem, with the highest incident risk being during adolescence. A depressive illness during this period is associated with negative long-term consequences including suicide, additional psychiatric comorbidity, interpersonal relationship problems, poor educational performance and poor employment attainment well into adult life. Despite previous safety concerns, selective serotonin reuptake inhibitors (SSRIs) remain a key component of the treatment of moderate to severe depression episodes in adolescents. The impact of SSRIs on the developing adolescent brain, however, remains unclear. In this review we first consider what is currently known about the developing brain during adolescence and how these development processes may be affected by a depressive illness. We then review our understanding of the action of SSRIs, their effects on the brain and how these may differ between adults and adolescents. We conclude that there is currently little evidence to indicate that the human adolescent brain is at developmental risk from SSRIs. Furthermore, there is no clear-cut evidence to support the concerns of marked suicidal adverse side effects accruing in depressed adolescents being treated with SSRIs. Neither, however, is there irrefutable evidence to dismiss all such concerns. This makes SSRI prescribing a matter of medical judgement, ensuring the benefits outweigh the risks for the individual patients, as with so much in therapeutics. Overall, SSRIs show clinical benefits that we judge to outweigh the risks to neurodevelopment and are an important therapeutic choice in the treatment of moderate to severe adolescent depression.

Journal Article 3: Nestler, E. J., Peña, C. J., Kundakovic, M., Mitchell, A.,& Akbarian, S. (2016). Epigenetic basis of mental illness. Neuroscientist, 22(5), 447-463.
doi: 10.1177/1073858415608147.

Abstract: Psychiatric disorders are complex multifactorial illnesses involving chronic alterations in neural circuit structure and function as well as likely abnormalities in glial cells. While genetic factors are important in the etiology of most mental disorders, the relatively high rates of discordance among identical twins, particularly for depression and other stressrelated syndromes, clearly indicate the importance of additional mechanisms. Environmental factors such as stress are known to play a role in the onset of these illnesses. Exposure to such environmental insults induces stable changes in gene expression, neural circuit function, and ultimately behavior, and these maladaptations appear distinct between developmental versus adult exposures. Increasing evidence indicates that these sustained abnormalities are maintained by epigenetic modifications in specific brain regions. Indeed, transcriptional dysregulation and the aberrant epigenetic regulation that underlies this dysregulation is a unifying theme in psychiatric disorders. Here, we provide a progress report of epigenetic studies of the three major psychiatric syndromes, depression, schizophrenia, and bipolar disorder. We review the literature derived from animal models of these disorders as well as from studies of postmortem brain tissue from human patients. While epigenetic studies of mental illness remain at early stages, understanding how environmental factors recruit the epigenetic machinery within specific brain regions to cause lasting changes in disease susceptibility and pathophysiology is revealing new insight into the etiology and treatment of these conditions.

JournalArticle 4: Lee, J. H., Lee, S., & Kim, J.-H. (in press). Amygdala circuits for fear memory. Neuroscientist. doi:10.1177/1073858416679936.

Abstract: In addition to modulating a number of cognitive functions including reward, punishment, motivation, and salience, dopamine (DA) plays a pivotal role in regulating threat-related emotional memory. Changes in neural circuits of the amygdala nuclei are also critically involved in the acquisition and expression of emotional memory. In this review, we summarize the regulation of amygdala circuits by DA. Specifically, we describe DA signaling in the amygdala, and DA regulation of synaptic transmission and synaptic plasticity of the amygdala neurons. Finally, we discuss a potential contribution of DA-related mechanisms to the pathogenesis of posttraumatic stress disorder.

Journal Article 5: Keightley, P. C., Koloski, N. A., & Talley, N. J. (2015). Pathways in gut-brain communication: Evidence for distinct gut-to-brain and brain-to-gut syndromesAustralian & New Zealand Journal of Psychiatry, 49(3), 207-214.

Abstract: Objective: The rich interconnectedness between gut and brain is increasingly being identified. This article reviews the evidence for brain-gut and gut-brain syndromes, particularly recent epidemiological evidence, and animal studies demonstrating bi-directionality at the formative stage of development. Method: Narrative literature review with selection for relevance and quality. Results: Population surveys show a strong correlation between anxiety, depression, and functional gastrointestinal disorders, contradicting early suspicions that the high prevalence of anxiety and depression in the clinic was mainly due to neurotic health seeking behavior. Five and 12 year follow-up shows that psychological distress can predict later onset of a functional gastrointestinal disorder and vice versa. Brain-gut pathways include the autonomic nervous system, hypothalamic-pituitary-adrenal axis including corticotrophin releasing factor directly acting on the gut. Gut-brain pathways include ascending pain pathways, cytokines including tumor necrosis factor alpha in response to bacterial translocation and inflammation, 5-hydroxytryptamine secretion by entero-endocrine cells and psychoactive chemicals of bacterial origin which may enter the blood stream, such as gamma-aminobutyric acid, fatty acids and 5-hydroxytryptamine precursors. The ability to control rodent temperament and HPA responsiveness with early modification of gastrointestinal flora, and the effects of early stress on the barrier function of the gastrointestinal tract and flora, suggests an ability of both systems to prime each other in early life for later problems. This hypothesis seems to be supported by a possible protective effect of a probiotic strain of bacteria in a model of early rat psychological trauma.