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Updated: May 20, 2026

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats
Published on: May 22, 2019
Cerebrovascular diseases and depression: epidemiology, mechanisms and treatment
F Göthe1, D Enache, L O Wahlund
1Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden. frida.gothe@ki.se
Insights
Elderly depression and cerebrovascular disease (CVD) have a two-way link. Treating CVD may reduce depression risk, while depression worsens stroke outcomes.
Area of Science:
- Gerontology
- Neurology
- Psychiatry
Background:
- Cerebrovascular disease (CVD) and depression are prevalent in older adults.
- A bidirectional relationship exists: depression can precipitate CVD, and subcortical CVD increases depression risk.
- Post-stroke depression is common, impacting prognosis and mortality.
Purpose of the Study:
- To explore the complex interplay between cerebrovascular disease and depression in the elderly.
- To identify risk factors and potential mechanisms linking CVD and depression.
- To review current and emerging treatment strategies for post-stroke depression.
Main Methods:
- Literature review and meta-analysis of existing studies on CVD and depression.
- Analysis of neuroimaging correlates, such as deep white matter lesions.
- Examination of potential biological pathways including neuroinflammation and HPA-axis dysregulation.
Main Results:
- Depression is linked to poorer functional outcomes and increased mortality post-stroke.
- Deep white matter lesions are consistently associated with depression.
- Neuroinflammation, HPA-axis activation, and serotonergic dysfunction are potential mediating mechanisms.
Conclusions:
- Antidepressants and vitamin B show efficacy in treating and preventing post-stroke depression.
- Psychotherapy, like problem-solving therapy, is effective.
- Further research is needed to confirm if CVD treatment reduces late-life depression risk.
Abstract:
Both cerebrovascular disease (CVD) and depression are common conditions in the elderly, and there is emerging evidence of a bi-directional relationship: 1) depression can cause CVD and stroke, transient ischemic attack; and 2) subcortical CVD are associated with increased risk for depression. The frequency of poststroke depression is highest during the first month after the stroke, but remains high even after several years. Depression is associated with poorer functional prognosis and higher mortality after stroke. There is good evidence that severity of functional impairment, high neuroticism, low social support as well as genetic factors are associated with an increased risk for post-stroke depression. Deep white matter lesions are the most consistent imaging correlate of depression. Potential mechanisms mediating the association between depression and CVD are neuroinflammation and HPA-axis activation, fronto-subcortical circuit lesions, and serotonergic dysfunction. Antidepressants have demonstrated effect on poststroke depression in meta-analyses, and such drugs as well as vitamin B can reduce the incidence of depression in stroke survivors. In addition, serotonergic drugs may strengthen poststroke motor and cognitive recovery, potentially through restorative mechanisms. Psychotherapeutic strategies such as problem-solving therapy seem to be effective. There is emerging evidence that treatment of cardiovascular disease and risk-factors can reduce the risk for late-life depression, but more studies are needed to test this hypothesis.
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