Neuroinflammation: friend and foe for ischemic stroke

So it is more difficult to solve that you expected. WHAT THE FUCK IS YOUR STRATEGY TO SOLVE IT? I'm guessing burying your head in the sand because

you are waiting for SOMEONE ELSE TO SOLVE THE PROBLEM. That behavior would get you fired in my book.

Neuroinflammation: friend and foe for ischemic stroke

• Richard L. Jayaraj,
• Sheikh Azimullah,
• Rami Beiram,
• Fakhreya Y. Jalal &
• Gary A. Rosenberg 

Journal of Neuroinflammation volume 16, Article number: 142 (2019) Cite this article

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Abstract

Stroke, the third leading cause of death and disability worldwide, is undergoing a change in perspective with the emergence of new ideas on neurodegeneration. The concept that stroke is a disorder solely of blood vessels has been expanded to include the effects of a detrimental interaction between glia, neurons, vascular cells, and matrix components, which is collectively referred to as the neurovascular unit. Following the acute stroke, the majority of which are ischemic, there is secondary neuroinflammation that both promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. The proinflammatory signals from immune mediators rapidly activate resident cells and influence infiltration of a wide range of inflammatory cells (neutrophils, monocytes/macrophages, different subtypes of T cells, and other inflammatory cells) into the ischemic region exacerbating brain damage. In this review, we discuss how neuroinflammation has both beneficial as well as detrimental roles and recent therapeutic strategies to combat pathological responses. Here, we also focus on time-dependent entry of immune cells to the ischemic area and the impact of other pathological mediators, including oxidative stress, excitotoxicity, matrix metalloproteinases (MMPs), high-mobility group box 1 (HMGB1), arachidonic acid metabolites, mitogen-activated protein kinase (MAPK), and post-translational modifications that could potentially perpetuate ischemic brain damage after the acute injury. Understanding the time-dependent role of inflammatory factors could help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.(What is your strategy for creating these solutions?)