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Antibiotics weaken Alzheimer's disease progression through changes in the gut
microbiome
Long-term antibiotic treatment in mice decreases levels of disease-causing
plaques and enhances neuroinflammatory activity of microglial cells
Date:
July 21, 2016
Source:
University of Chicago Medical Center
Summary:
Long-term treatment with broad spectrum antibiotics decreased levels of
amyloid plaques, a hallmark of Alzheimer's disease, and activated inflammatory
microglial cells in the brains of mice in a new study by neuroscientists.
FULL STORY
Alzheimer's disease.
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Long-term treatment with broad spectrum antibiotics decreased levels of
amyloid plaques, a hallmark of Alzheimer's disease, and activated inflammatory
microglial cells in the brains of mice in a new study by neuroscientists from
the University of Chicago.
The study, published July 21, 2016, in Scientific Reports, also showed
significant changes in the gut microbiome after antibiotic treatment,
suggesting the composition and diversity of bacteria in the gut play an
important role in regulating immune
system activity that impacts progression of Alzheimer's disease.
"We're exploring very new territory in how the gut influences brain health,"
said Sangram Sisodia, PhD, Thomas Reynolds Sr. Family Professor of
Neurosciences at the University of Chicago and senior author of the study.
"This is an area that people who
work with neurodegenerative diseases are going to be increasingly interested
in, because it could have an influence down the road on treatments."
Two of the key features of Alzheimer's disease are the development of
amyloidosis, accumulation of amyloid-ß (Aß) peptides in the brain, and
inflammation of the microglia, brain cells that perform immune system
functions in the central nervous system.
Buildup of Aß into plaques plays a central role in the onset of Alzheimer's,
while the severity of neuro-inflammation is believed to influence the rate of
cognitive decline from the disease.
For this study, Sisodia and his team administered high doses of broad-spectrum
antibiotics to mice over five to six months. At the end of this period,
genetic analysis of gut bacteria from the antibiotic-treated mice showed that
while the total mass of
microbes present was roughly the same as in controls, the diversity of the
community changed dramatically. The antibiotic-treated mice also showed more
than a two-fold decrease in Aß plaques compared to controls, and a
significant elevation in the
inflammatory state of microglia in the brain. Levels of important signaling
chemicals circulating in the blood were also elevated in the treated mice.
While the mechanisms linking these changes is unclear, the study points to the
potential in further research on the gut microbiome's influence on the brain
and nervous system.
"We don't propose that a long-term course of antibiotics is going to be a
treatment -- that's just absurd for a whole number of reasons," said Myles
Minter, PhD, a postdoctoral scholar in the Department of Neurobiology at
UChicago and lead author of the
study. "But what this study does is allow us to explore further, now that
we're clearly changing the gut microbial population and have new bugs that are
more prevalent in mice with altered amyloid deposition after antibiotics."
The study is the result of one the first collaborations from the Microbiome
Center, a joint effort by the University of Chicago, the Marine Biological
Laboratory and Argonne National Laboratory to support scientists at all three
institutions who are
developing new applications and tools to understand and harness the
capabilities of microbial systems across different fields. Sisodia, Minter and
their team worked with Eugene B. Chang, Martin Boyer Professor of Medicine at
UChicago, and Vanessa Leone,
PhD, a postdoctoral scholar in Chang's lab, to analyze the gut microbes of the
mice in this study.
Minter said the collaboration was enabling, and highlighted the
ross-disciplinary thinking necessary to tackle a seemingly intractable disease
like Alzheimer's. "Once you put ideas together from different fields that have
largely long been believed to
be segregated from one another, the possibilities are really amazing," he said.
Sisodia cautioned that while the current study opens new possibilities for
understanding the role of the gut microbiome in Alzheimer's disease, it's just
a beginning step.
"There's probably not going to be a cure for Alzheimer's disease for several
generations, because we know there are changes occurring in the brain and
central nervous system 15 to 20 years before clinical onset," he said. "We
have to find ways to
intervene when a patient starts showing clinical signs, and if we learn how
changes in gut bacteria affect onset or progression, or how the molecules they
produce interact with the nervous system, we could use that to create a new
kind of personalized
medicine."
Story Source:
The above post is reprinted from materials provided by University of Chicago
Medical Center. Note: Materials may be edited for content and length.
Journal Reference:
Myles R. Minter, Can Zhang, Vanessa Leone, Daina L. Ringus, Xiaoqiong Zhang,
Paul Oyler-Castrillo, Mark W. Musch, Fan Liao, Joseph F. Ward, David M.
Holtzman, Eugene B. Chang, Rudolph E. Tanzi, Sangram S. Sisodia.
Antibiotic-induced perturbations in gut
microbial diversity influences neuro-inflammation and amyloidosis in a murine
model of Alzheimer’s disease. Scientific Reports, 2016; 6: 30028 DOI:
10.1038/srep30028
Cite This Page:
MLA
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Chicago
University of Chicago Medical Center. "Antibiotics weaken Alzheimer's disease
progression through changes in the gut microbiome: Long-term antibiotic
treatment in mice decreases levels of disease-causing plaques and enhances
neuroinflammatory activity of
microglial cells." ScienceDaily. ScienceDaily, 21 July 2016. .
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