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Background: Annually, approximately 7.6 million individuals experience a new ischemic stroke, and roughly 25% of all ischemic strokes are cardiogenic in origin, carrying a high risk of recurrence, death and disability. To prevent future ischemic strokes, especially in younger individuals, it is crucial to detect and treat direct and indirect cardioembolic sources.
View Article and Find Full Text PDFGut Microbiota, Bacterial Translocation, and Stroke: Current Knowledge and Future Directions.
Biomedicines
December 2024
Department of Pharmacology and Toxicology, School of Medicine, University Complutense of Madrid, 28040 Madrid, Spain.
Stroke is one of the most devastating pathologies in terms of mortality, cause of dementia, major adult disability, and socioeconomic burden worldwide. Despite its severity, treatment options remain limited, with no pharmacological therapies available for hemorrhagic stroke (HS) and only fibrinolytic therapy or mechanical thrombectomy for ischemic stroke (IS). In the pathophysiology of stroke, after the acute phase, many patients develop systemic immunosuppression, which, combined with neurological dysfunction and hospital management, leads to the onset of stroke-associated infections (SAIs).
View Article and Find Full Text PDFBioactive Materials Facilitate the Restoration of Neurological Function Post Cerebral Ischemic Stroke.
Int J Nanomedicine
January 2025
Department of Neurology, Neurology Specialist Hospital, The First Hospital of Jilin University, Jilin University, Changchun, People's Republic of China.
The recovery process following ischemic stroke is a complex undertaking involving intricate cellular and molecular interactions. Cellular dysfunction or aberrant pathways can lead to complications such as brain edema, hemorrhagic transformation, and glial scar hyperplasia, hindering angiogenesis and nerve regeneration. These abnormalities may contribute to long-term disability post-stroke, imposing significant burdens on both families and society.
View Article and Find Full Text PDFOrchestrating the frontline: HDAC3-miKO recruits macrophage reinforcements for accelerated myelin debris clearance after stroke.
Theranostics
January 2025
State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and Institutes of Brain Science, Fudan University, Shanghai, China.
Article Synopsis
- White matter is crucial for recovery after ischemic strokes, and recent research suggests microglial HDAC3 may contribute to white matter injury.
- Researchers created knockout mice lacking microglial HDAC3 to study its effects on white matter using various techniques, revealing that these mice showed improved repair and function.
- The study found that HDAC3-deficient microglia enhanced the recruitment of macrophages to clear myelin debris, which plays a significant role in remyelination and recovery post-stroke.
Prediction of Central Post-Stroke Pain by Quantitative Sensory Testing.
Ann Neurol
December 2024
Department of Neurology, Jewish Hospital Berlin, Berlin, Germany.
Objective: Among patients with acute stroke, we aimed to identify those who will later develop central post-stroke pain (CPSP) versus those who will not (non-pain sensory stroke [NPSS]) by assessing potential differences in somatosensory profile patterns and evaluating their potential as predictors of CPSP.
Methods: In a prospective longitudinal study on 75 acute stroke patients with somatosensory symptoms, we performed quantitative somatosensory testing (QST) in the acute/subacute phase (within 10 days) and on follow-up visits for 12 months. Based on previous QST studies, we hypothesized that QST values of cold detection threshold (CDT) and dynamic mechanical allodynia (DMA) would differ between CPSP and NPSS patients before the onset of pain.
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