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Neuropsychiatric disorders and stroke

We seek to make further inroads into understanding the complex interaction between depression and brain ischemia at a mechanistic level.

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Project description

Psychiatric disorders including depression and post-traumatic stress disorder (PTSD) may develop secondary to somatic illness, e.g., after a stroke. However, there is growing evidence of a bidirectional relationship between neuropsychiatric disorders and stroke. Hence, depression can occur both as a cause and as a consequence of stroke. 

The pathomechanisms underlying the development of post-stroke depression (PSD) and PTSD remain poorly understood, not least because of a continued lack of suitable animal models. Recently, we have been able to demonstrate in a well characterized stroke model in mice that animals develop a depression-like phenotype characterized by anhedonia, increased anxiety, and despair following left, transient middle cerebral artery occlusion (MCAO). Moreover, we employ a chronic stress model which results in reproducible biological effects (e.g., reduced weight gain, enlarged adrenal glands, reduced corticosterone levels).  

Serotonin seems to act as an important mediator of post-stroke repair by driving regenerative processes such as neuronal plasticity and by modulating the brain’s inflammatory response to ischemic damage. Therefore, we speculate that antidepressant treatment using 'selective serotonin-reuptake inhibitors or enhancers' (SSRI or SSRE) after stroke may emerge as a novel therapy. We use genetic models (e.g., Tph2 knockout mice lacking brain serotonin, SERT knockout mice) and pharmacological interventions (SSRI, SSRE) to elucidate the effects of serotonergic signaling on acute and chronic stroke outcome.

Chronic psychosocial stress results in increased stroke lesions and worse functional stroke outcome in mice. The effects of stress are mediated by endothelial dysfunction. There are also studies in humans describing a close relationship between psychosocial stress and aging-related molecular pathways. Therefore, we study mechanistically the relationship between psychosocial stress and vascular senescence. We focus on mechanisms of mitochondrial biogenesis and telomere biology.

Furthermore, we recently finished the SATURN study, an exploratory and retrospective cohort study ( Identifier: NCT03496480). Eligible stroke patients were asked to participate in a postal survey to assess traumatization before stroke as a risk factor for neuropsychiatric complications after stroke.

We found that a history of trauma exposure in tandem with endorsing subsequent PTSD symptoms was linked with significantly increased post-stroke PTSD and depressive symptoms together with decreased psychological well-being. Furthermore, younger age, being a woman, and having developed PTSD symptoms in the aftermath of a prior trauma were associated with adverse psychological outcomes after stroke.