Major depression disorder is a leading cause of disability worldwide, and affects more than 17% of the populations, making it one of the most prevalent health-related causes of human suffering. However, the mechanisms of depression are far from clear. The most widely accepted theory about depression points to stress, especially early life stress. Even though compelling evidences from genetic studies and pharmacological studies points to dysfunction of hypothalamus-pituitary-adrenal axis (HPA) hormones and their related the central monoamine network, the exact mechanisms about how do early life stress affects the adult depression are still not clear?
The mechanisms whereby external stressors affect brain function have been the subject of extensive study over the past 60 years. During the early to mid twentieth century, Freud already mentioned that it is the early life stressful event hidden in the unconscious minds that causes mental disorders. And later John Bowlby proposed that life stress between kids and parents are the most important events, which might induce many life style changes, especially attachments. He proposed two types of attachments: secured attachment, unsecured attachment, with the latter including anxiety attachment, avoidance attachment, is related to mental disorders. From a neuroscience point, the neural plasticity underlying stress undoubtedly affects the brain function and may prompt functional alternations in mental disorders. Corticotropin-releasing hormone (CRH), which was named the stress hormone, in both animals and humans, can simulate norepinephrine (NE) synthesis, dopamine and 5-HT. These monoamines are the substrates of many mental disorders, such as depression. CRH release also activates the hypothalamic-pituitary-adrenal (HPA) axis, which has been widely accepted as one of the central mechanisms involved in stress. The CRH induces release of ACTH (adrenocorticotropic hormone), which can in turn alter function of the neural network by altering building blocks in the networks and by altering the integrative properties, and thus the behavioral or emotional changes. Indeed, some early life events can induce epigenetic changes, which are related to depression, such as methylation DNA of MAO (monoamine oxidase), or through miRNA changes. In this Research Topic, we invite research studies on early life traumatic events with depression. We welcome the following submission formats: original quantitative or qualitative research, review, perspective, and case studies. The topics might include but not limited to:
1. Psychological mechanisms about early life stress leading to depression, such as attachment, life style changes after early life stress.
2. Early life stress induced emotional changes, cognitive changes, and life style changes which might related to depression.
3. Neurobiological mechanisms about early life stress with adult depression, such as epigenetics.
4. Early life stress induced brain functional changes, such as ERP changes, fMRI changes.
Major depression disorder is a leading cause of disability worldwide, and affects more than 17% of the populations, making it one of the most prevalent health-related causes of human suffering. However, the mechanisms of depression are far from clear. The most widely accepted theory about depression points to stress, especially early life stress. Even though compelling evidences from genetic studies and pharmacological studies points to dysfunction of hypothalamus-pituitary-adrenal axis (HPA) hormones and their related the central monoamine network, the exact mechanisms about how do early life stress affects the adult depression are still not clear?
The mechanisms whereby external stressors affect brain function have been the subject of extensive study over the past 60 years. During the early to mid twentieth century, Freud already mentioned that it is the early life stressful event hidden in the unconscious minds that causes mental disorders. And later John Bowlby proposed that life stress between kids and parents are the most important events, which might induce many life style changes, especially attachments. He proposed two types of attachments: secured attachment, unsecured attachment, with the latter including anxiety attachment, avoidance attachment, is related to mental disorders. From a neuroscience point, the neural plasticity underlying stress undoubtedly affects the brain function and may prompt functional alternations in mental disorders. Corticotropin-releasing hormone (CRH), which was named the stress hormone, in both animals and humans, can simulate norepinephrine (NE) synthesis, dopamine and 5-HT. These monoamines are the substrates of many mental disorders, such as depression. CRH release also activates the hypothalamic-pituitary-adrenal (HPA) axis, which has been widely accepted as one of the central mechanisms involved in stress. The CRH induces release of ACTH (adrenocorticotropic hormone), which can in turn alter function of the neural network by altering building blocks in the networks and by altering the integrative properties, and thus the behavioral or emotional changes. Indeed, some early life events can induce epigenetic changes, which are related to depression, such as methylation DNA of MAO (monoamine oxidase), or through miRNA changes. In this Research Topic, we invite research studies on early life traumatic events with depression. We welcome the following submission formats: original quantitative or qualitative research, review, perspective, and case studies. The topics might include but not limited to:
1. Psychological mechanisms about early life stress leading to depression, such as attachment, life style changes after early life stress.
2. Early life stress induced emotional changes, cognitive changes, and life style changes which might related to depression.
3. Neurobiological mechanisms about early life stress with adult depression, such as epigenetics.
4. Early life stress induced brain functional changes, such as ERP changes, fMRI changes.
