Jane A Foster1, Glenda MacQueen. 1. Department of Psychiatry and Behavioural Neurosciences, McMaster University.
Abstract
OBJECTIVE: To examine the neurobiological basis of personality and depression. METHOD: We examined preclinical and clinical studies related to neuroanatomy, neuroendocrine, molecular, and genetic alterations in depressed patients. We considered whether common neurobiological factors might be shared between personality and depression. RESULTS: Preclinical studies provide insights into the neurobiological mechanisms underlying the pathophysiology of depression including neuroendocrine alterations in hypothalamic-pituitary-adrenal (HPA) function, neuroanatomical alterations in key brain regions, and alterations in neurotrophin and serotonergic signalling systems. Clinical studies show similar alterations in depressed patients. Evidence suggests that neuroendocrine alterations in HPA function may contribute to personality traits. Brain regions implicated in depression, including the hippocampus and the anterior cingulate cortex, might play a role in personality. Key molecules implicated in depression have been extensively studied with reference to personality traits, particularly neuroticism. To date, physiological measures (serum and positron emission tomography) provide the strongest evidence implicating brain-derived neurotrophic factor and serotonin in personality, while genetic evidence is less convincing. CONCLUSIONS: A neurobiological link exists between personality and depression; however, more work is needed to provide an understanding of the nature of this relation and to link this work with clinical studies examining the influence of personality factors on depression.
OBJECTIVE: To examine the neurobiological basis of personality and depression. METHOD: We examined preclinical and clinical studies related to neuroanatomy, neuroendocrine, molecular, and genetic alterations in depressedpatients. We considered whether common neurobiological factors might be shared between personality and depression. RESULTS: Preclinical studies provide insights into the neurobiological mechanisms underlying the pathophysiology of depression including neuroendocrine alterations in hypothalamic-pituitary-adrenal (HPA) function, neuroanatomical alterations in key brain regions, and alterations in neurotrophin and serotonergic signalling systems. Clinical studies show similar alterations in depressedpatients. Evidence suggests that neuroendocrine alterations in HPA function may contribute to personality traits. Brain regions implicated in depression, including the hippocampus and the anterior cingulate cortex, might play a role in personality. Key molecules implicated in depression have been extensively studied with reference to personality traits, particularly neuroticism. To date, physiological measures (serum and positron emission tomography) provide the strongest evidence implicating brain-derived neurotrophic factor and serotonin in personality, while genetic evidence is less convincing. CONCLUSIONS: A neurobiological link exists between personality and depression; however, more work is needed to provide an understanding of the nature of this relation and to link this work with clinical studies examining the influence of personality factors on depression.
Authors: Didier L Schrijvers; Ellen R A De Bruijn; Marianne Destoop; Wouter Hulstijn; Bernard G C Sabbe Journal: J Neural Transm (Vienna) Date: 2010-05-16 Impact factor: 3.575
Authors: Aron S Buchman; Patricia A Boyle; Robert S Wilson; Sue E Leurgans; Steven E Arnold; David A Bennett Journal: Am J Geriatr Psychiatry Date: 2013-01-22 Impact factor: 4.105
Authors: Frank M Schmidt; Christian Sander; Juliane Minkwitz; Roland Mergl; Bethan Dalton; Lesca M Holdt; Daniel Teupser; Ulrich Hegerl; Hubertus Himmerich Journal: Front Psychiatry Date: 2018-11-20 Impact factor: 4.157
Authors: Man K Xu; Darya Gaysina; Roula Tsonaka; Alexandre J S Morin; Tim J Croudace; Jennifer H Barnett; Jeanine Houwing-Duistermaat; Marcus Richards; Peter B Jones Journal: Front Psychol Date: 2017-10-11