Monday, June 19, 2017

Can We Delay Dementia? Brain Scavenger Cells May Hold the Key

Can We Delay Dementia? Brain Scavenger Cells May Hold the Key

delay dementia
The body’s clean up crew is made up of scavenger cells called phagocytes. Phagein means “to devour” and -cyte means “cell.” And phagocytes are indeed like billions of little vultures, scarfing down the carcasses of other dead, or dying, cells and consuming foreign materials that shouldn’t be there, like plaque, bacteria, and other infections. In our brain, these scavenger cells are called microglia, and a new study suggests that we may be able to delay dementia via these cells.

Microglial Cells Further Defined

Microglial cells are the primary way our immune system defends our brain and central nervous system. They scavenge by patrolling their specific zones in the brain and scanning for any potential threat. When an injury happens or an invader arrives, molecules are signaled that create an acute inflammatory response (the good inflammation), and like any good immune cells, our microglials jump into action and attempt to neutralize the problem. Since microglial cells are phagocytes, they also devour, or  phagocytose, all cell, bacteria, and other debris. The inflammation that occurs during this process is good because it means those immune cells are on it and are trying to fix the problem.
In addition to their phagocytic properties, microglial cells can also release cytotoxins to destroy damaged or infected neurons, or brain cells. There is concern that this release of cytotoxins can lead to a mass-destruction type of effect, causing more long-term chronic inflammation, the bad inflammation, and a great deal of neural damage. With this chronic inflammation, there has been concern that microglials could actually exacerbate neurological diseases, such as Alzheimer’s and other dementias.

Dementia Pathology

Dementia defines a variety of neurodegenerative diseases that affect the neurons in the brain, and these diseases typically develop slowly and progress over time. Under the umbrella of dementia, we have diseases such as Alzheimer’s disease (the most common dementia), vascular dementia, frontotemporal lobar degeneration (FTD), Huntington’s disease, and even traumatic encephalopathy, which is seen most commonly in pro athletes who played head-contact sports (football, boxing, wrestling, etc.).
We know dementia can be genetic, but studies have shown that there are many things that can damage or destroy our neurons in our brain that may lead to dementia or speed up its development. What can we do to delay dementia? Here are a small handful of studies showing things we can look to avoid to limit potential risk for dementia:

Studying Microglial Cells in the Brain: Can We Delay Dementia?

The new study investigated microglial cell function when gene expression is suppressed in mice. Researchers achieved this by altering the coding of the TREM2 gene. The TREM2 gene is expressed through proteins on the microglial cells and this alteration in the gene intentionally disrupted the gene’s ability to be expressed on the cell.
The result? The lack of the TREM2 gene expression kept the microglial cells from activating and moving to the locations where they were needed to clean up damaged or dead cells and other debris. This not only delayed the ability to resolve inflammation but also reduced blood flow and the metabolism of glucose, a process imperative for energy in the brain. Researchers concluded that activation of these brain phagocytes (the microglial cells) is critical to assuring proper brain functioning and that these findings could lead to new ways to boost the function of microglial cells and delay the onset of dementias, such as Alzheimer’s. More work will need to be done here.
The upshot? While other studies have also made a genetic connection to dementia, the idea that microglial cells are secreting signals that exacerbate inflammation and lead to dementia has also been a theory. However, this new study seems to show that the inability of the microglial cells to respond to the area of damage due to a genetic variant, not a direct effect of the cells themselves, could be the driving force behind the lingering inflammation, and, subsequently, the onset of Alzheimer’s and other dementias. This could be an important piece of the puzzle in the race to discover how we can delay dementia when we as a population are living longer and longer.

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