Preventive Approaches for Post-Stroke Depression: Where Do We Stand? A Systematic Review

Woranush, Warunya; Moskopp, Mats Leif; Sedghi, Annahita; Stuckart, Isabella; Noll, Thomas; Barlinn, Kristian; Siepmann, Timo

doi:10.2147/ndt.s337865

Cited by 19 publications

(9 citation statements)

References 81 publications

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“…52-54 Patients might even be less prone to post-stroke depression, representing a severe burden to recovery after stroke. 55 The application of tDCS as an adjunctive treatment in rehabilitation regimes after stroke could thus effectively improve recovery of function. Consistently, the recent literature shows that in humans, tDCS improved long-term motor recovery when applied in addition to established rehabilitation regimes but not alone.…”

Section: Discussionmentioning

confidence: 99%

Transcranial-Direct-Current-Stimulation Accelerates Motor Recovery After Cortical Infarction in Mice: The Interplay of Structural Cellular Responses and Functional Recovery

Walter

Pikhovych

Endepols

et al. 2022

Neurorehabil Neural Repair

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Background Transcranial direct current stimulation (tDCS) promotes recovery after stroke in humans. The underlying mechanisms, however, remain to be elucidated. Animal models suggest tDCS effects on neuroinflammation, stem cell proliferation, neurogenesis, and neural plasticity. Objective In a longitudinal study, we employed tDCS in the subacute and chronic phase after experimental focal cerebral ischemia in mice to explore the relationship between functional recovery and cellular processes. Methods Mice received photothrombosis in the right motor cortex, verified by Magnetic Resonance Imaging. A composite neuroscore quantified subsequent functional deficits. Mice received tDCS daily: either 5 sessions from day 5 to 9, or 10 sessions with days 12 to 16 in addition. TDCS with anodal or cathodal polarity was compared to sham stimulation. Further imaging to assess proliferation and neuroinflammation was performed by immunohistochemistry at different time points and Positron Emission Tomography at the end of the observation time of 3 weeks. Results Cathodal tDCS at 198 kC/m2 (220 A/m2) between days 5 and 9 accelerated functional recovery, increased neurogenesis, decreased microglial activation, and mitigated CD16/32-expression associated with M1-phenotype. Anodal tDCS exerted similar effects on neurogenesis and microglial polarization but not on recovery of function or microglial activation. TDCS on days 12 to 16 after stroke did not induce any further effects, suggesting that the therapeutic time window was closed by then. Conclusion Overall, data suggest that non-invasive neuromodulation by tDCS impacts neurogenesis and microglial activation as critical cellular processes influencing functional recovery during the early phase of regeneration from focal cerebral ischemia.

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Section: Discussionmentioning

confidence: 99%

Transcranial-Direct-Current-Stimulation Accelerates Motor Recovery After Cortical Infarction in Mice: The Interplay of Structural Cellular Responses and Functional Recovery

Walter

Pikhovych

Endepols

et al. 2022

Neurorehabil Neural Repair

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“…Rehabilitation of the affected individuals takes significant time, and substantial financial resources incurred in prolonged treatment can take a toll on the finances of the family involved. Woranush et al [ 205 ] established that the efficacy of post-stroke depression increases with the duration of preventive treatment. Therefore, improved outcomes will be realized if the medications used provide rapid and robust responses.…”

Section: Future Research In Drug Therapy Of Psdmentioning

confidence: 99%

Pathophysiology and Current Drug Treatments for Post-Stroke Depression: A Review

Frank

Gruenbaum

Zlotnik

et al. 2022

IJMS

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Post-stroke depression (PSD) is a biopsychosocial disorder that affects individuals who have suffered a stroke at any point. PSD has a 20 to 60 percent reported prevalence among stroke survivors. Its effects are usually adverse, can lead to disability, and may increase mortality if not managed or treated early. PSD is linked to several other medical conditions, including anxiety, hyper-locomotor activity, and poor functional recovery. Despite significant awareness of its adverse impacts, understanding the pathogenesis of PSD has proved challenging. The exact pathophysiology of PSD is unknown, yet its complexity has been definitively shown, involving mechanisms such as dysfunction of monoamine, the glutamatergic systems, the gut-brain axis, and neuroinflammation. The current effectiveness of PSD treatment is about 30–40 percent of all cases. In this review, we examined different pathophysiological mechanisms and current pharmacological and non-pharmacological approaches for the treatment of PSD.

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“…The pathogenesis of PSD is complex, and any single mechanism cannot fully elucidate the occurrence and development of PSD (3)(4)(5). Based on the increased expression of inflammatory factors and the activation of inflammation-related pathways in PSD patients and animal models, a study has demonstrated that inflammatory mechanisms play an important role in the development of PSD (6).…”

Section: Introductionmentioning

confidence: 99%

Aerobic exercise reverses the NF-κB/NLRP3 inflammasome/5-HT pathway by upregulating irisin to alleviate post-stroke depression

Tang¹,

Liao²,

Liu³

et al. 2022

Ann Transl Med

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Background: Post-stroke depression (PSD) is one of the most common and serious sequelae of stroke.The pathogenesis of PSD involves both psychosocial and biological mechanisms, and aerobic exercise is a potential therapeutic target. We conducted an in-depth exploration of the protective mechanisms of aerobic exercise in a PSD mouse model. Methods:In this study, C57BL/6 mice were used as the research objects, and a PSD mouse model was established by combining middle cerebral artery occlusion and chronic unpredictable mild stimulation.Real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assays, adeno-associated virus microinjection technology, co-immunoprecipitation, fluorescence in-situ hybridization, and western blotting were performed. A moderate-load treadmill exercise was used for aerobic exercise intervention. The moderate-intensity aerobic exercise training method adopted 0 slopes and treadmill adaptation training for 5 days. We verified the effects of aerobic exercise on the nuclear factor kappa B (NF-κB)/nucleotide-binding oligomerization domain--like receptor protein 3 (NLRP3) inflammasome/5-hydroxytryptamine (5-HT) pathway.Results: Aerobic exercise effectively alleviated the neurological damage caused by PSD (P<0.01). The results from the PSD mouse model in vivo were consistent with those of the cell experiments. Moreover, overexpression of irisin improves depression-like behavior in PSD mice. We confirmed that aerobic exercise is involved in PSD through 5-HT, which inhibits NF-κB/NLRP3 inflammasome initiation through irisin and alleviates mitochondrial damage under stress by reducing calcium overload, thereby inhibiting NLRP3 inflammasome activation.Conclusions: Aerobic exercise reversed the NF-κB/NLRP3 inflammasome/5-HT pathway by upregulating irisin expression to alleviate PSD.

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Preventive Approaches for Post-Stroke Depression: Where Do We Stand? A Systematic Review

Cited by 19 publications

References 81 publications

Transcranial-Direct-Current-Stimulation Accelerates Motor Recovery After Cortical Infarction in Mice: The Interplay of Structural Cellular Responses and Functional Recovery

Transcranial-Direct-Current-Stimulation Accelerates Motor Recovery After Cortical Infarction in Mice: The Interplay of Structural Cellular Responses and Functional Recovery

Pathophysiology and Current Drug Treatments for Post-Stroke Depression: A Review

Aerobic exercise reverses the NF-κB/NLRP3 inflammasome/5-HT pathway by upregulating irisin to alleviate post-stroke depression

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