According to the Alzheimer's Association,
an estimated 5.3 million Americans are currently diagnosed with Alzheimer's
disease (AD) in the year of 2015. Needless to say, research regarding the
causes and treatments of such a disease is of extreme importance to scientists.
ScienceDaily's article, Researchers discover role of microglia during early progression of
Alzheimer's disease, accredited to the Boston University Medical Center on
October 5, 2015 offers vital information on the spread of Alzheimer's disease.
As learned in class; beyond neurons, the brain consists of a second type of
mass: glial cells. There are three kinds of glial cells at work in the brain,
one of which being microglia. Essentially, microglia works as the brain's
personal maintenance man. An important aspect of microglia's job is to
effectively devour and rid the brain of damaged or threatening cells. Boston
University Medical Center explains that once microglia devour and remove
dangerous cells, exosomes are released. Exosomes are communicators that initiate an immune response by
being taken up by other cells in the brain.
According to the Boston University Medical
Center, symptoms of Alzheimer's tend to follow a build up a dangerous protein,
by the name of tau, in the brain. The buildup of tau is seen in parts of the
brain that play large roles in learning and memory. What was previously
unclear, is how this tau is spread throughout the brain. The researchers of
this study predicted that tau fibrils are actually spread by the release of the tau-containing exosomes. This study was manipulated by lowering microglia levels, as well as
inhibiting the release of exosomes by microglia. Sure enough, as researchers
lowered the concentration of microglia, they observed less active spreading of
tau across brain regions and restored levels of neural excitation. Specifically
inhibiting exosome release demonstrated a slowed spread of tau as well.
The results of this study suggests that tau-containing exosomes play a large part in spreading tau throughout the brain during the
early stages of AD. Caution needs to be taken here, as communication between
microglia and other cells in the brain is vital for brain health; however,
creating a drug that could inhibit the release of strictly tau-infected
exosomes could be one step towards slowing, and ultimately preventing the
spread of Alzheimer’s Disease.
References:
ScienceDaily Article:
http://www.sciencedaily.com/releases/2015/10/151005132725.htm
Alzheimer's Association Statistic:
http://www.alz.org/facts/
This blog post interested me a great deal because we covered parts of the brain a couple weeks ago in our class. I had always considered microglia as a beneficial part of the brain. It is, as you said, “the brain's personal maintenance man." It interested me how just by lowering the levels of microglia, the spread of the protein tau throughout the brain was reduced. However, it made me wonder if the decreased levels of microglia would have a detrimental effect on the brain as it gets rid of dead cells, unhealthy and inactive synapses. Scientists would have to deal with an extremely delicate balance while trying to reduce Alzheimer’s through this new perspective.
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