The Evolution of the Cognitive Model of Depression and Its Neurobiological Correlates

• Published in: The American journal of psychiatry Vol. 165; no. 8; pp. 969 - 977
• Main Author: Beck, Aaron T.
• Format: Journal Article
• Language: English
• Published: Washington, DC American Psychiatric Association 01.08.2008
• Subjects: Adult and adolescent clinical studies; Attention - physiology; Biological and medical sciences; Brain; Brain - physiopathology; Cognition & reasoning; Cognition Disorders - epidemiology; Cognition Disorders - physiopathology; Depression; Depressive Disorder, Major - epidemiology; Depressive Disorder, Major - genetics; Depressive Disorder, Major - physiopathology; Dreams; Genotype; Humans; Information processing; Medical imaging; Medical sciences; Mood disorders; Problem Solving; Psychology; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Serotonin Plasma Membrane Transport Proteins - genetics; Social research; Mood disorder; Human; Central nervous system; Neuroendocrine regulation; Depression; Cognition; Basal ganglion; Vulnerability; Review; Prefrontal cortex; Genetic determinism; Stress; Encephalon; Cognitive theory; Theoretical model; Genetics; Evolution; Amygdaloid nucleus; Cognitive bias; Polymorphism
• ISSN: 0002-953X; 1535-7228
• DOI: 10.1176/appi.ajp.2008.08050721

Although the cognitive model of depression has evolved appreciably since its first formulation over 40 years ago, the potential interaction of genetic, neurochemical, and cognitive factors has only recently been demonstrated. Combining findings from behavioral genetics and cognitive neuroscience with the accumulated research on the cognitive model opens new opportunities for integrated research. Drawing on advances in cognitive, personality, and social psychology as well as clinical observations, expansions of the original cognitive model have incorporated in successive stages automatic thoughts, cognitive distortions, dysfunctional beliefs, and information-processing biases. The developmental model identified early traumatic experiences and the formation of dysfunctional beliefs as predisposing events and congruent stressors in later life as precipitating factors. It is now possible to sketch out possible genetic and neurochemical pathways that interact with or are parallel to cognitive variables. A hypersensitive amygdala is associated with both a genetic polymorphism and a pattern of negative cognitive biases and dysfunctional beliefs, all of which constitute risk factors for depression. Further, the combination of a hyperactive amygdala and hypoactive prefrontal regions is associated with diminished cognitive appraisal and the occurrence of depression. Genetic polymorphisms also are involved in the overreaction to the stress and the hypercortisolemia in the development of depression-probably mediated by cognitive distortions. I suggest that comprehensive study of the psychological as well as biological correlates of depression can provide a new understanding of this debilitating disorder.