Stress and Anxiety

Neurobiology of Depression

Depression's neurobiology contains dichotomous deviations in corticolimbic brain areas. Neuronal shrinkage and synaptic dysfunction are shown in the prefrontal cortex and hippocampus, but neuronal hypertrophy and enhanced synaptic activity are seen in the nucleus accumbens and amygdala.

Different brain areas exhibit abnormal activity in persons with major depressive disorder (MDD), according to scientific investigations, which has fueled advocates of numerous theories that seek to find a physiological genesis of the disease rather than psychological or social factors. Nutritional deficiencies in magnesium, vitamin D, and tryptophan, which have a situational origin but a biological consequence, are among the factors that span these causal groupings.

Several ideas have been proposed throughout the years regarding the molecular origin of depression, including theories involving monoamine neurotransmitters, neuroplasticity, neurogenesis, inflammation, and the circadian rhythm. Depressive symptoms can also be triggered by physical conditions such as hypothyroidism and mitochondrial disease. Neural pathways involved in the creation and regulation of emotion, as well as reward, have been linked to depression. The lateral prefrontal cortex, whose putative role is usually thought to involve emotion regulation, is prone to abnormalities. The peripheral and central immune systems, which are important in the neurobiology of depression, are dysregulated in subsets of depressed people. Immune impairment in mice subjected to environmental and psychosocial stress is similar to that seen in human populations.

Typical antidepressant agents improve mood by regulating the levels of the monoamines serotonin and noradrenaline, but also partially through attenuation of immune dysregulation. Other antidepressant therapies that limit neuroimmune activation and promote anti-inflammatory pathways may provide alternative treatment options for subsets of depressed individuals.