New Findings: What is the central question of this study? Can the neuroprotective agent curcumin affect restorative action of neural stem/progenitor cells in the injured rat brain? What is the main finding and its importance? In the presence of curcumin, transplantation of neural stem/progenitor cells in the context of PuraMatrix reduced lesion size and reactive inflammatory responses, and boosted survival rate of grafted neurons. In addition it improved the neurological status of injured animals. This could be beneficial in designing new therapeutic approaches for brain injury based on this combination therapy.
Abstract: Traumatic brain injury (TBI) is catastrophic neurological damage associated with substantial morbidity and mortality. To date, there is no specific treatment for restoring lost brain tissue. In light of the complex pathology of brain injury, the present study evaluated the effects of combination therapy using autologous neural stem/progenitor cells (NS/PCs), PuraMatrix (PM) and curcumin in an animal model of brain injury. After stereotactic biopsy of subventricular zone tissue and culture of NS/PCs, 36 male Wistar rats (150-200 g) were randomly divided into six groups receiving dimethyl sulfoxide (DMSO), curcumin (100 mg kg in DMSO), PM + curcumin (100 mg kg in DMSO), NS/PCs + curcumin (100 mg kg in DMSO), NS/PCs + PM + curcumin (100 mg kg in DMSO) and NS/PCs + PM + curcumin (1 µm) following acute brain injury. The animals were evaluated in term of neurological status for 4 weeks, then decapitated. Nissl and TUNEL staining and immunohistochemistry for bromodeoxyuridine, glial fibrillary acidic protein, doublecortin, Map2, Olig2, Iba1 and CD68 were performed. We found that combination therapy by NS/PCs + PM + curcumin reduced the lesion size, astrogliosis, macrophage and microglial reaction as well as the number of apoptotic cells. Moreover, the transplanted cells were able to survive and differentiate after 4 weeks. Besides these findings, transplantation of NS/PCs in the context of PM and curcumin improved the neurological status of injured animals. In conclusion, our data suggest that this combination therapy can be beneficial in developing future therapeutic approaches for brain injury.
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http://dx.doi.org/10.1113/EP088697 | DOI Listing |
Transl Psychiatry
January 2025
Department of Neurosurgery, General Hospital of Northern Theater Command, Postgraduate Training Base of General Hospital of Northern Theater Command of Jinzhou Medical University, Shenyang, Liaoning, China.
Traumatic brain injury (TBI) is identified as a risk factor for Parkinson's disease (PD), which is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN). However, the precise mechanism by which chronic TBI initiates PD pathogenesis is not yet fully understood. In our present study, we assessed the chronic progression and pathogenesis of PD-like behavior at different intervals in TBI mice.
View Article and Find Full Text PDFJ Prev Alzheimers Dis
February 2025
Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, PR China. Electronic address:
Background: Cognitive decline and the progression to Alzheimer's disease (AD) are traditionally associated with amyloid-beta (Aβ) and tau pathologies. This study aims to evaluate the relationships between microstructural white matter injury, cognitive decline and AD core biomarkers.
Methods: We conducted a longitudinal study of 566 participants using peak width of skeletonized mean diffusivity (PSMD) to quantify microstructural white matter injury.
Am J Pathol
January 2025
Center for the Neural Basis of Cognition; Department of Pathology; Department of Bioengineering; McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address:
The importance of complex systems has become increasingly evident in recent years. The nervous system is one such example with neural networks sitting at the intersection of complex networks and biology. A particularly exciting feature is the resilience of complex systems.
View Article and Find Full Text PDFExp Neurol
January 2025
Brain and Mind Research Institute, Department of Biology, University of Ottawa, Ottawa, Ontario, Canada. Electronic address:
Spasticity is a common comorbidity of spinal cord injury (SCI), disrupting motor function and resulting in significant discomfort. While elements of post-SCI spasticity can be assessed using pre-clinical SCI models, the robust measurement of spasticity severity can be difficult due to its periodic and spontaneous appearance. Electrical stimulation of sensory afferents can elicit spasticity-associated motor responses, such as spasms; however, placing surface electrodes on the hindlimbs of awake animals can induce stress or encumbrance that could influence the expression of behaviour.
View Article and Find Full Text PDFIschemic stroke can cause damage to neurons, resulting in neurological dysfunction. The main treatments in the acute phase include intravenous thrombolysis, endovascular stent-assisted vascular thrombectomy and antiplatelet therapy. Due to the limitations of the time window and the risk of early intracranial hemorrhage, finding active treatment plans is crucial for improving therapy.
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