Affective disorders are the leading cause of disability worldwide. For example, major depressive disorder is a prevalent emotional disorder that affects more than 1/5 of the population worldwide, making it one of the most prevalent health-related causes of human suffering. In addition, it is a leading risk factor for the estimated one million deaths by suicide per year worldwide. However, the mechanisms of affective disorders are not precise. Thus the treatment is not as effective as expected.
Stress has been a critical causing factor for affective disorders. Stress is evolutionarily crucial for survival and benefits all lives. However, overwhelming stress is considered one of the main risk factors for developing affective disorders such as anxiety and depression. It is found that the onsets of significant depression correlate with stressful events in earlier lives.
How early life stress can induce long term changes in the brain to induce emotional disorders in adults is far from clear. However, there is compelling evidence of a causal link between chronic stress and monoamine neurotransmitters. So far, the first-line treatment for affective disorders has focused on the monoamine neurotransmitters (such as dopamine, serotonin and norepinephrine). Thus the early life stress-induced epigenetic changes for these neurotransmitters or oxidases might be the causes for the affective disorders. In addition, stress-induced changes in the HPA axis (hypothalamus-pituitary-adrenal axis) has been proved to associate with emotional disorders.
Furthermore, stress causes elevation of corticosteroids and other stress hormones, such as CRF (corticotropin-releasing factor), the known stress hormone. Thus, HPA dysregulation may be both a causative factor and a consequence of emotional disorders via long term changes in the endocrine systems, which induce behaviour changes that habitually deal with stressful situations. Moreover, cytokine might also be regarded as a causing mechanism for depression. Lymphocytes, mast cells and other immune system cells contain adrenoreceptors that respond to stress. It is reported that the level of lymphocyte activity dramatically reduced in depressed patients. Thus, there is evidence that sympathetic nervous, immune and endocrine systems are linked. Therefore, epigenetic changes in receptors for these cytokines might also involve in affective disorders.
Above all, early life stress-induced epigenetic changes on the receptors for these neuromodulators, neurotransmitters and cytokines might cause affective disorders in adults. So we set out this Research Topic to welcome recent studies on the epigenetics and neurotransmitter and cytokine changes induced by early life stress and their relationship with affective disorders, such as depression and anxiety. Potential topics include but are not limited to the following:
1. The epigenetic changes induced by early-life stress, such as methylation of DNA.
2. Neuromodulator changes (such as monoamine changes induced by early life stress) and epigenetics' possible role.
3. Molecular changes, such as neurotransmitters or genetic changes, for early life stress-induced emotional disorders,
4. The early life stress, or traumatic stress, induced cellular neuronal changes and their relationship with affective disorders.
5. Possible pathways involved in the cytokine changes after stress-induced affective disorders.
6. Drugs that affect the epigenetic changes involved in early life stress-induced affective disorders.
Affective disorders are the leading cause of disability worldwide. For example, major depressive disorder is a prevalent emotional disorder that affects more than 1/5 of the population worldwide, making it one of the most prevalent health-related causes of human suffering. In addition, it is a leading risk factor for the estimated one million deaths by suicide per year worldwide. However, the mechanisms of affective disorders are not precise. Thus the treatment is not as effective as expected.
Stress has been a critical causing factor for affective disorders. Stress is evolutionarily crucial for survival and benefits all lives. However, overwhelming stress is considered one of the main risk factors for developing affective disorders such as anxiety and depression. It is found that the onsets of significant depression correlate with stressful events in earlier lives.
How early life stress can induce long term changes in the brain to induce emotional disorders in adults is far from clear. However, there is compelling evidence of a causal link between chronic stress and monoamine neurotransmitters. So far, the first-line treatment for affective disorders has focused on the monoamine neurotransmitters (such as dopamine, serotonin and norepinephrine). Thus the early life stress-induced epigenetic changes for these neurotransmitters or oxidases might be the causes for the affective disorders. In addition, stress-induced changes in the HPA axis (hypothalamus-pituitary-adrenal axis) has been proved to associate with emotional disorders.
Furthermore, stress causes elevation of corticosteroids and other stress hormones, such as CRF (corticotropin-releasing factor), the known stress hormone. Thus, HPA dysregulation may be both a causative factor and a consequence of emotional disorders via long term changes in the endocrine systems, which induce behaviour changes that habitually deal with stressful situations. Moreover, cytokine might also be regarded as a causing mechanism for depression. Lymphocytes, mast cells and other immune system cells contain adrenoreceptors that respond to stress. It is reported that the level of lymphocyte activity dramatically reduced in depressed patients. Thus, there is evidence that sympathetic nervous, immune and endocrine systems are linked. Therefore, epigenetic changes in receptors for these cytokines might also involve in affective disorders.
Above all, early life stress-induced epigenetic changes on the receptors for these neuromodulators, neurotransmitters and cytokines might cause affective disorders in adults. So we set out this Research Topic to welcome recent studies on the epigenetics and neurotransmitter and cytokine changes induced by early life stress and their relationship with affective disorders, such as depression and anxiety. Potential topics include but are not limited to the following:
1. The epigenetic changes induced by early-life stress, such as methylation of DNA.
2. Neuromodulator changes (such as monoamine changes induced by early life stress) and epigenetics' possible role.
3. Molecular changes, such as neurotransmitters or genetic changes, for early life stress-induced emotional disorders,
4. The early life stress, or traumatic stress, induced cellular neuronal changes and their relationship with affective disorders.
5. Possible pathways involved in the cytokine changes after stress-induced affective disorders.
6. Drugs that affect the epigenetic changes involved in early life stress-induced affective disorders.