Depression Wheel

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Bibliography (by units of analysis)

Molecular

(1) Anacker, Christoph et al. “The Glucocorticoid Receptor: Pivot of Depression and of Antidepressant Treatment?” Psychoneuroendocrinology 36.3 (2011): 415–425. PMC. Web. 8 Oct. 2015.

• Shows that GR involvement is tied to neurobiological correlates that underlie depression, ranging from glucocorticoid resistance to HPA-axis hyperactivity. Because GR function can be modified through antidepressants, GRs could be involved in depression.

(2) Lee, Heon-Jin, et al. "Oxytocin: The great facilitator of life." Progress in Neurobiology 88.2 (2009): 127-51. Print.

• Provides a review on the role of oxytocin in non-social and social behaviors and in disorders characterized by abnormal affect regulation.

(3) Svenningsson, Per, et al. "Alterations in 5-HT1B Receptor Function by p11 in Depression-Like States." Science 311.5757 (2006): 77-80. Print.

• Highlights the role of serotonin receptors (5-HT1B) and their interaction with p11, which is increased in rodent brains by antidepressants. Shows that modulation of serotonin receptors by p11 gene can change molecular adaptations involved in the depressed brain.

Genetic

(4) Felten, Andrea, et al. "Genetically determined dopamine availability predicts disposition for depression." Brain and Behavior 1.2 (2011): 109-18. Print.

• Focuses on dopaminergic gene loci related to traits of positive and negative emotionality. Shows influence of two DA gene polymorphisms on Sadness.

(5) Bufalino, Chiara, et al. "The role of immune genes in the association between depression and inflammation: A review of recent clinical studies." Brain, Behavior, and Immunity 31 (2013): 31-47. Print.

• Shows that gene variants related to cytokines, enzymes and the serotonin pathway may increase the risk for depression and that these can influence the mechanisms by which the immune system contributes to depression.

(6) Lewis, Cathryn M., et al. "Genome-Wide Association Study of Major Recurrent Depression in the U.K. Population." The American Journal of Psychiatry 167.8 (2010): 949-57. Print.

• Describes a SNP in BICC1 that was found to be associated with female depression though a GWAS done in the U.K. Most importantly, it restates that individual genes tied to depression are likely to have a minor effect but by large genetic analysis we can identify them.

(7) Thompson, Renee J., et al. "Oxytocin receptor gene polymorphism (rs2254298) interacts with familial risk for psychopathology to predict symptoms of depression and anxiety in adolescent girls." Psychoneuroendocrinology 36.1 (2011): 144-47. Print.

• Shows that being heterozygous for the OXTR rs2254298 gene plus having a mother’s history of recurrent MDD increased the risk of offspring in having depression and anxiety symptoms. These findings highlight the potential importance of the OXTR gene polymorphism in the etiology of depression and anxiety disorders.

(8) Woody, Mary L., John E. McGeary, and Brandon E. Gibb. "Brooding rumination and heart rate variability in women at high and low risk for depression: Group differences and moderation by COMT genotype." Journal of Abnormal Psychology 123.1 (2014): 61-67. Print.

• Shows that several COMT gene polymorphisms have been linked to a heightened amygdala reactivity and deficit in PFC function, both depression-related abnormalities.

Circuit

(9) Avery, Jason A., et al. "Major Depressive Disorder Is Associated With Abnormal Interoceptive Activity and Functional Connectivity in the Insula." Biological Psychiatry 76.3 (2014): 258-66. Print.

• Highlights that MDD is associated with abnormal interoceptive representation within the insula, which is known as a structure that regulates “gut feelings.”

(10) Mayberg, Helen S., et al. "Deep Brain Stimulation for Treatment-Resistant Depression." Neuron 45.5 (2005): 651-60. Print.

• Associates DBS of white matter adjacent to subgenual cingulate gyrus with sustained remission of depression. Relevant in treating depression because it shows the efficacy of deep brain stimulation in a certain brain region to treat depression.

(11) Scheuerecker, Johanna, et al. "Orbitofrontal volume reductions during emotion recognition in patients with major depression." Journal of Psychiatry and Neuroscience 35 (2010): 311+. Print.

• Provides evidence that the orbitofrontal cortex is a key area in major depression and that structural changes in it result in alteration within the emotional circuit.

(12) Siegle, Greg J., et al. "Increased Amygdala and Decreased Dorsolateral Prefrontal BOLD Responses in Unipolar Depression: Related and Independent Features." Biological Psychiatry 61.2 (2007): 198-209. Print.

• Shows depression to be associated with increased limbic activity in response to emotional information and decreased DLPFC activity in response to cognitive tasks.

(13) Treadway, Michael T., et al. "Early Adverse Events, HPA Activity and Rostral Anterior Cingulate Volume in MDD." PLoS ONE 4.3 (2009): e4887. Print.

• Finds the grey matter volume of the rostral ACC to correlate with cortisol and early adverse events, which hints to a relationship between ACC morphology and pathophysiology of MDD.

Physiology

(14) Dowlati, Yekta, et al. "A Meta-Analysis of Cytokines in Major Depression." Biological Psychiatry 67.5 (2010): 446-57. Print.

• Reports a meta-analysis of findings that highlight the role of proinflammatory cytokines in depressed subjects compared to controls.

(15) Vreeburg, S. A., et al. "Major depressive disorder and hypothalamic-pituitary-adrenal axis activity: Results from a large cohort study." Archives of General Psychiatry 66.6 (2009): 617-26. Print.

• Shows associations between MDD and specific HPA axis indicators, which could be an indicative of an increased biological vulnerability for depression.

Behavior

(16) Joormann, Jutta, Marco Dkane, and Ian H. Gotlib. "Adaptive and Maladaptive Components of Rumination? Diagnostic Specificity and Relation to Depressive Biases." Behavior Therapy 37.3 (2006): 269-80. Print.

• Supports the idea that rumination is composed of an adaptive reflective factor and a maladaptive brooding factor and shows a correlation between attention to sad faces and depression.

(17) Matos, Marcela, José Pinto-Gouveia, and Vânia Costa. "Understanding the Importance of Attachment in Shame Traumatic Memory Relation to Depression: The Impact of Emotion Regulation Processes." Clinical Psychology & Psychotherapy 20.2 (2013): 149-65. Print.

• Highlights the relationship between shame traumatic memory and depressive symptoms and highlights that shame can be an obstacle for patients that seek recovery. Highlights the importance of scientific studies to understand how to treat depression and accelerate recovery.

(18) Treadway, Michael T., and David H. Zald. "Reconsidering anhedonia in depression: Lessons from translational neuroscience." Neuroscience & Biobehavioral Reviews 35.3 (2011): 537-55. Print.

• Moves away from the idea that anhedonia is a steady-state mood-like phenomena and reframes anhedonia in terms of decision-making. Important to understand how depression can affect essential behaviors such as decision-making.