The enigma of vascular depression in old age: a critical update.

Abstract

Depression is common in older individuals and is associated with high disability and increased mortality, yet the factors predicting late-life depression (LLD) are poorly understood. The relationship between of depressive disorder, age- and disease-related processes have generated pathogenic hypotheses and provided new treatment options. LLD syndrome is often related to a variety of vascular mechanisms, in particular hypertension, cerebral small vessel disease, white matter lesions, subcortical vascular impairment, and other processes (e.g., inflammation, neuroimmune regulatory dysmechanisms, neurodegenerative changes, amyloid accumulation) that may represent etiological factors by affecting frontolimbic and other neuronal networks predisposing to depression. The "vascular depression" hypothesis suggests that cerebrovascular disease (CVD) and vascular risk factors may predispose, induce or perpetuate geriatric depressive disorders. It is based on the presence of various cerebrovascular risk factors in many patients with LLD, its co-morbidity with cerebrovascular lesions, and the frequent development of depression after stroke. Other findings related to vascular depression are atrophy of the medial temporal cortex or generalized cortical atrophy that are usually associated with cognitive impairment. Other pathogenetic hypotheses of LLD, such as metabolic or inflammatory ones, are briefly discussed. Treatment planning should consider there may be a modest response to antidepressants, but several evidence-based and novel treatment options for LLD exist, such as electroconvulsive therapy, transcranial magnetic stimulation, neurobiology-based psychotherapy, as well as antihypertension and antiinflammatory drugs. However, their effectiveness needs further investigation, and new methodologies for prevention and treatment of depression in older individuals should be developed.