노인 우울증의 신경생물학

The Neurobiology of Late-Life Depression

Late-life depression is a mental disease common in the elderly that is multifaceted and difficult to understand and approach because many pathological factors are involved. Inflammation plays an important role in the pathogenesis of depression in elderly people, and an increase in cytokines and activation of the microglia can cause depression. In the field of genetics, genes such as APOE, SLC6A4, Val66Met, and MTHFR are involved in the pathogenesis of depression in the elderly. Disorders of the serotonin system and dopamine function in late-life depression have been reported. Cerebral microvascular disease and endothelial dysfunction impair the frontallimbic system and other important neural networks, causing subcortical white matter and gray matter lesions, which can lead to late-life depression. Depression in the elderly is associated with the severity or volume of white matter hyperintensities, and the reduced cortical volume and cortical thickness are also associated with late-life depression. Hyperactivity of the hypothalamus–pituitary–adrenal axis has been reported in late-life depression, and metabolic risk factors such as hypertension, dyslipidemia, and diabetes contribute to the development of depression in the elderly. Additional neurobiological mechanisms, including brain-derived neurotrophic factor (BDNF) dysfunction and amyloid pathology, are currently being explored.