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).
