This review highlights the role of microglia in neuro-inflammation and their impact on neuroplasticity following ischemic stroke.
Stroke is a medical emergency that causes damage to the brain by interfering with the blood supply to the brain, a lack of blood flow to the brain leads to depletion of oxygen and nutrients to the brain/ part of which can eventually cause permanent damage, resulting death of an individual. Stroke initiates a powerful inflammatory cascade in the brain and also causes immunosuppression, which is addressed as stroke-induced immunosuppression. The immune cells, such as dendritic cells, lymphocytes, neutrophils, microglia cells, and the residing macrophages in the innate immune system in the central nervous system. Microglial cells are a type of resident glial cells present in the brain and spinal cord, which are accountable for the development of the brain and proper function of the neuronal system. The resident immune cells also play a crucial role in injury response as well as injury repair. Microglial cells serve as a “double-edged sword “due to their nature of being beneficiary coupled with detrimental effects in the central nervous system (CNS). The beneficial aspects are- immune defense in CNS, shapes and regulates neural connections (neuroplasticity), and also aids in repairing and rejuvenating the damaged brain tissues. The detrimental aspects include neuro-inflammation, synaptic pruning, and alterations implicated in neurodegeneration. This article reviews the role of microglial cells in inducing neuroinflammation, as the activation of microglial cells has a huge impact on neuroinflammation accompanied by neuroplasticity. Thereby, alterations in microglial cells in such a way to enhance the neuronal-plasticity after the occurrence of ischemic stroke. This remodeling can pave a novel approach in decreasing the damage in ischemic stroke.
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Are et al. (2025) studied this question.
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