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Macrophages (Greek: big eaters, from Greek μακρος (makros) = large, φαγειν (phagein) = to eat) are white blood cells that engulf and digest cellular debris, foreign substances, microbes, cancer cells, and anything else that does not have the protein markers specific to healthy body cells on its surface. This process is called phagocytosis.

Macrophages are large phagocytes and are found in all tissues, where they patrol for potential pathogens and cellular waste to dispose of.

Macrophages have a number of tissue-specific variants throughout the body (e.g., microglia, histiocytes, osteoclasts, Kupffer cells, and others), but all of them are part of the mononuclear phagocyte system and perform essentially the same housekeeping role within the body.

Macrophages develop in the bone marrow as monocytes, which circulate in the bloodstream until they settle in the tissues and become one of the many tissue-specific types of macrophage.

Besides phagocytosis, macrophages play a critical role in nonspecific defense (innate immunity) and help initiate specific defense mechanisms (adaptive immunity) by recruiting other immune cells, such as lymphocytes, to help them fight pathogens. In humans, dysfunctional macrophages cause severe diseases, such as chronic granulomatous disease, that result in frequent infections; aging causes macrophages to become increasingly poor at cellular housekeeping and fighting pathogens.

A number of research efforts have focused on trying to return aged, dysfunctional macrophages to more youthful levels of function by modulation of the immune system (in particular microglia – macrophages) using pro-youthful signalling.

One such effort in 2016 sent mesenchymal stem cells to the area of damage and resulted in a reduction of plaques in Alzheimer’s mice, as these stem cells reduce inflammation and encourage pro-youthful function via intracellular signaling [1].

Recently, researchers showed that delivering fresh, functionally young macrophages to the brain results in removal of the plaques (misfolded proteins) associated with Alzheimer’s disease [2].

This means that brain aging is not a one-way process and suggests that we might be able to use our own rejuvenated macrophages to treat this horrific disease and other, similar diseases, including heart disease and Parkinson’s, which also involve plaque accumulation.

Conclusion

Introducing youthful macrophages and boosting their efficiency represents a plausible pathway to treating age-related diseases, and the research world is currently investigating the potential of a number of therapies that do this.

Literature

[1] Naaldijk, Y., Jaeger, C., Fabian, C., Leovsky, C., Blüher, A., Rudolph, L., … & Stolzing, A. (2016). Effect of systemic transplantation of bone marrow‐derived mesenchymal stem cells on neuropathology markers in APP/PS1 Alzheimer’s mice. Neuropathology and applied neurobiology.

[2] Daria, A., Colombo, A., Llobera, G., Hampel, H., Willem, M., Liesz, A., … & Tahirovic, S. (2016). Young microglia restore amyloid plaque clearance of aged microglia. The EMBO Journal, e201694591.

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About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity created by the Aging Analytics Agency. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, and, Keep me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.
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