Don’t Give your Inflammasomes any Matches


Anyone found to be unaware of the tight connection between inflammation and dementias like Alzheimer’s and Fronto-Temporal Dementia needs remedial neurology classes if they intend to practice medicine in the 21st century. Countless studies underscore the correlations between higher inflammatory states and dementia, but we need more studies like today’s spot-light on the role of inflammasomes in amyloid beta and tau pathology to explain how it works. Functional MD’s like myself feel a little flutter inside when research like this proves what we have been preaching. Helping patients live healthier more abundant lives unhindered by these debilitating diseases requires open-mindedness and willingness to use all the tools available for our patients.

Medical research long ago uncovered connections between Alzheimer’s and collections of proteins called amyloid beta outside brain cells as well as with tau protein collections inside the cells. Understanding how it happens will hopefully lead to both treatment therapies and prevention strategies. Although functional MD’s already discern the role of a low inflammatory diet in treating dementia, we are open to as deep an understanding as possible to optimize our patient’s health and recovery.

German researchers recently published their findings in the prestigious journal, Nature, describing how the inflammasomes inside brain microglia appear to play a key role in these proteins sticking together and causing harm. Microglia cells reside in the brain as part of the immune system regulating the environment of brain cells which do our thinking, etc. They and other cells possess organelles, or intracellular structures, called inflammasomes which modulate inflammation responses within that cell and also influence other cell’s inflammation thermostat.

By hyperphosphorylating the tau protein, they cause the protein to let go of the cellular inner structure where they normally reside. They then start clumping together. Eventually this can trigger cell death and ultimately to the dementia symptoms we see in patients.

While the researchers and other scientists search for drug or antibodies to turn off this process once it starts, in functional medicine, we aim to apply discernment in regards to what we do now and what we do if that super drug never arrives. Obviously, helping our patients lower dietary inflammation, removing toxins, and addressing chronic infections are starting points towards a healthier, more abundant lives. Without their own understanding and discernment, our patients and readers will veer off the road to good health. Hopefully they will then never need the super expensive, super drug if it does materialize 5, 10, or 20 years in the future.

Original Article
Christina Ising, Carmen Venegas, Shuangshuang Zhang, Hannah Scheiblich, Susanne V. Schmidt, Ana Vieira-Saecker, Stephanie Schwartz, Shadi Albasset, Róisín M. McManus, Dario Tejera, Angelika Griep, Francesco Santarelli, Frederic Brosseron, Sabine Opitz, James Stunden, Maximilian Merten, Rakez Kayed, Douglas T. Golenbock, David Blum, Eicke Latz, Luc Buée, Michael T. Heneka. NLRP3 inflammasome activation drives tau pathology. Nature, 2019; DOI: 10.1038/s41586-019-1769-z
Thanks to Science Daily:
DZNE – German Center for Neurodegenerative Diseases. “Inflammatory processes drive progression of Alzheimer’s and other brain diseases: New insights into disease mechanisms, report in Nature.” ScienceDaily. ScienceDaily, 20 November 2019. <www.sciencedaily.com/releases/2019/11/191120131318.htm>.


Sanctuary Functional Medicine, under the direction of Dr Eric Potter, IFMCP MD, provides functional medicine services to Nashville, Middle Tennessee and beyond. We frequently treat patients from Kentucky, Alabama, Mississippi, Georgia, Ohio, Indiana, and more... offering the hope of healthier more abundant lives to those with chronic illness.

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