Post-stroke depression (PSD) affects about one-third of the ischemic stroke survivors and it is one of the world’s most significant health problems. Vascular dysregulation is often met in late-life depression (LLD) and cerebral blood flow (CBF) reduction can influence regional brain functions, contributing to affective and cognitive symptoms. However, it is not clear if perfusion deficits can cause secondary degenerative changes in the brain or that ongoing degenerative changes of the aged brain will be simply aggravated by stroke. A brain injury is accompanied by an exaggerated neuroinflammation by activation of immune-reactive microglial population and is considered a trigger mechanism for depressive-like behavior after injury that may last for weeks or months after stroke and is precipitated by advanced age. Research using animal models and clinical studies of mood disorders highlighted that an increased level of proinflammatory molecules and increased levels of reactive oxygen species (ROS) along with alteration of 5-hydroxytryptamine system (5-HT) are associated with decreased neurogenesis. Treatment of PSD includes psychotherapy (CBT-cognitive behavioral therapy) and selective serotonin reuptake inhibitor (SSRI) and selective norepinephrine reuptake inhibitor (SNRI) drugs. More recently, transcranial magnetic stimulation (TMS) has been used to treat depressive patients. Its efficacy is however, questionable. More basic and clinical research is needed to uncover mechanisms underlying depressive behaviour in the elderly caused by perfusion deficits or brain lesioning.
Keywords: Aging, cognitive behavioral therapy (CBT), depression, late-life depression, Major depressive disorder, neuroinflammation, oxidative stress, post stroke depression, psychotherapy, SSRI, transcranial magnetic stimulation (TMS).