Inflammation is important in the body’s defense against foreign invaders, like bacteria, as well as trauma to tissue and internal organs. However, when inflammation gets out of control and becomes chronic, it can cause damage to the body. This is true in the body’s general immune responses and in the case of the brain and Alzheimer’s Disease.
When we think of inflammation, we often think of the hot, red, and itchy reaction of the skin to a bug bite. The chemokines and cytokines that cause these inflammatory responses are present throughout all parts of the body. In the brain, misfolded tau protein activates a release of inflammatory markers, leading to neuroinflammation. Tau protein has been identified as one of the main proteins involved in Alzheimer’s Disease pathology and it is important to know which factors might cause its levels to increase. Markers of inflammation, most commonly TNF-a, IL-6, YKL, soluble trk2, and CRP, can be measured in the cerebrospinal fluid to monitor the amount of inflammation in the brain. When levels of neuroinflammation get too high, they can help tau spread throughout the brain, which in turn causes more inflammation, starting an ongoing cycle. The impact of neuroinflammation on tau is especially important because levels of tau are closely tied to clinical symptoms
If inflammation can increase the spread of tau in the brain, therefore progressing cognitive decline, it follows that discovering how to decrease the neuroinflammation will lead to possibilities for decreasing the progression of Alzheimer’s Disease. Currently, a lot of energy within Alzheimer’s Disease research is being dedicated to investigating “modifiable risk factors” so that people can protect their brains against cognitive decline. One of the biggest modifiable risk factors for Alzheimer's Disease is physical activity, which has been shown to decrease neuroinflammation and therefore may be one way to help fight against the disease. What is your favorite way to stay active and protect your brain?
References:
Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., & Zhao, L. (2017). Inflammatory responses and inflammation-associated diseases in organs. Oncotarget, 9(6), 7204–7218. https://doi.org/10.18632/oncotarget.23208
Eikelenboom, P., van Exel, E., Hoozemans, J. J. M., Veerhuis, R., Rozemuller, A. J. M., & van Gool, W. A. (2010). Neuroinflammation – An Early Event in Both the History and Pathogenesis of Alzheimer’s Disease. Neurodegenerative Diseases, 7(1–3), 38–41. https://doi.org/10.1159/000283480
Laurent, C., Buée, L., & Blum, D. (2018). Tau and neuroinflammation: What impact for Alzheimer’s Disease and Tauopathies? Biomedical Journal, 41(1), 21–33. https://doi.org/10.1016/j.bj.2018.01.003
Ryan, S. M., & Kelly, Á. M. (2016). Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease. Ageing Research Reviews, 27, 77–92. https://doi.org/10.1016/j.arr.2016.03.007
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