Deans' stroke musings: Phagocytic microglia and macrophages in brain injury and repair

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, June 30, 2022

Phagocytic microglia and macrophages in brain injury and repair

In stroke do we even know if the dead neurons are being cleaned up properly? Or do we need to send maggots in there to do the job? Ask your doctor this simple question.

Phagocytic microglia and macrophages in brain injury and repair

Fang Yu1,2| Yangfan Wang1,2| Anne R. Stetler1,2| Rehana K. Leak3|Xiaoming Hu1,2| Jun Chen1,2This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.© 2022 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.1Geriatric Research, Education and Clinical Center, Veterans Affairs Pittsburgh Health Care System, Pittsburgh, Pennsylvania, USA2Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA3Graduate School of Pharmaceutical Sciences, School of Pharmacy, Duquesne University, Pittsburgh, Pennsylvania, USACorrespondenceJun Chen, Geriatric Research, Education and Clinical Center, Veterans Affairs Pittsburgh Health Care System, University Drive, Pittsburgh, PA 15261, USA.Email: chenj2@upmc.eduFunding informationNIH, Grant/Award Number: NS0105430; VA, Grant/Award Number: 821-RC- NB- 30556, I01BX003377, I01BX003651, I01BX005290 and I01BX005589

Abstract

Aims:

Phagocytosis is the cellular digestion of extracellular particles, such as patho-gens and dying cells, and is a key element in the evolution of central nervous system (CNS) disorders. Microglia and macrophages are the professional phagocytes of the CNS. By clearing toxic cellular debris and reshaping the extracellular matrix, microglia/macrophages help pilot the brain repair and functional recovery process. However, CNS resident and invading immune cells can also magnify tissue damage by igniting runaway inflammation and phagocytosing stressed—but viable—neurons.

Discussion:

Microglia/macrophages help mediate intercellular communication and react quickly to the “find- me” signals expressed by dead/dying neurons. The acti-vated microglia/macrophages then migrate to the injury site to initiate the phago-cytic process upon encountering “eat- me” signals on the surfaces of endangered cells. Thus, healthy cells attempt to avoid inappropriate engulfment by expressing “do not- eat- me” signals. Microglia/macrophages also have the capacity to phagocytose immune cells that invade the injured brain (e.g., neutrophils) and to regulate their pro- inflammatory properties. During brain recovery, microglia/macrophages engulf myelin debris, initiate synaptogenesis and neurogenesis, and sculpt a favorable extracellular matrix to support network rewiring, among other favorable roles. Here, we review the multilayered nature of phagocytotic microglia/macrophages, including the molecular and cellular mechanisms that govern microglia/macrophage-induced phagocytosis in acute brain injury, and discuss strategies that tap into the therapeutic potential of this engulfment process.

Conclusion:

Identification of biological targets that can temper neuroinflammation after brain injury without hindering the essential phagocytic functions of microglia/macrophages will expedite better medical management of the stroke recovery stage.

KEYWORDS

acute brain injury, brain repair, microglia/macrophage, phagocytosis