Researchers find genetically engineered virus reduces desire to drink ...
www.dailymail.co.uk/.../Is-genetically-engineered-virus-answer-alcoholism...
Oct 25, 2016 - Researchers claim it could reduce desire to drink. Experts found ... That gene then drives the neurons to express a specific protein. After the ...Could a genetically engineered VIRUS cure alcoholism? Researchers claim it could reduce desire to drink
- Experts found alcohol changes the way your brain processes information
- They also identified a way to ease changes and reduce the desire to drink
- The team discovered a genetically engineered virus as the solution
- Virus inhibits the 'go' neurons to reduce alcohol drinking levels
About 17 million adults and more than 850,000 adolescents had some problems with alcohol in the United States in 2012.
Long-term alcohol misuse could harm your liver, stomach, cardiovascular system and bones, as well as your brain.
Chronic
heavy alcohol drinking can lead to a problem that we scientists call
alcohol use disorder, which most people call alcohol abuse or
alcoholism.
Scroll down for videos
Long-term alcohol misuse could harm
your liver, stomach, cardiovascular system and bones, as well as your
brain. Chronic heavy alcohol drinking can lead to a problem that we
scientists call alcohol use disorder, which most people call alcohol
abuse or alcoholism
Whatever
name you use, it is a severe issue that affects millions of people and
their families and causes economic burdens to our society.
Quitting alcohol, like quitting any drug, is hard to do.
One reason may be that heavy drinking can actually change the brain.
Our
research team at Texas A&M University Health Science Center has
found that alcohol changes the way information is processed through
specific types of neurons in the brain, encouraging the brain to crave
more alcohol.
Over time, the more you drink, the more striking the change.
In
recent research we identified a way to mitigate these changes and
reduce the desire to drink using a genetically engineered virus.
Alcohol use disorders include alcohol abuse and alcohol dependence, and can be thought of as an addiction.
Addiction is a chronic brain disease. It causes abnormalities in the connections between neurons.
Heavy alcohol use can cause changes in a region of the brain, called the striatum.
This
part of the brain processes all sensory information (what we see and
what we hear, for instance), and sends out orders to control
motivational or motor behavior.
The striatum, which is located in the forebrain, is a major target for addictive drugs and alcohol.
Drug
and alcohol intake can profoundly increase the level of dopamine, a
neurotransmitter associated with pleasure and motivation, in the
striatum.
Our research team
at Texas A&M University Health Science Center has found that
alcohol changes in how brain neurons process information. The neurons in
the striatum (pictured) have higher densities of dopamine receptors as
compared to neurons in other parts of the brain
The neurons in the striatum have higher densities of dopamine receptors as compared to neurons in other parts of the brain.
As a result, striatal neurons are more susceptible to changes in dopamine levels.
There are two main types of neurons in the striatum: D1 and D2.
While both receive sensory information from other parts of the brain, they have nearly opposite functions.
D1-neurons control 'go' actions, which encourage behavior.
D2-neurons, on the other hand, control 'no-go' actions, which inhibit behavior.
In the study, the team gave mice with
two bottles, one containing water and the other containing 20 percent
alcohol by volume, mixed with drinking water. Then mice were infected
with a genetically engineered virus that delivers a gene into the 'go'
or 'no-go' neurons
Think of D1-neurons like a green traffic light and D2-neurons like a red traffic light.
Dopamine affects these neurons in different ways.
It promotes D1-neuron activity, turning the green light on, and suppresses D2-neuron function, turning the red light off.
As a result, dopamine promotes 'go' and inhibits 'no-go' actions on reward behavior.
Alcohol, especially excessive amounts, can hijack this reward system because it increases dopamine levels in the striatum.
As
a result, your green traffic light is constantly switched on, and the
red traffic light doesn't light up to tell you to stop.
This is why heavy alcohol use pushes you to drink to excess more and more.
These brain changes last a very long time.
But can they be mitigated? That's what we want to find out.
We
started by presenting mice with two bottles, one containing water and
the other containing 20 percent alcohol by volume, mixed with drinking
water.
The bottle containing alcohol was available every other day, and the mice could freely decide which to drink from.
Gradually, most of animals developed a drinking habit.
We
then used a process called viral mediated gene transfer to manipulate
the 'go' or 'no-go' neurons in mice that had developed a drinking habit.
Mice were infected with a genetically engineered virus that delivers a gene into the 'go' or 'no-go' neurons.
That gene then drives the neurons to express a specific protein.
After the protein is expressed,
experts injected the mice with a chemical that recognizes and binds to
it. This binding inhibits or promotes activity in these neurons, letting
us turn the green light off (by inhibiting 'go' neurons) or turn the
red light (by exciting 'no-go' neurons) back on
After the protein is expressed, we injected the mice with a chemical that recognizes and binds to it.
This
binding can inhibit or promote activity in these neurons, letting us
turn the green light off (by inhibiting 'go' neurons) or turn the red
light (by exciting 'no-go' neurons) back on.
Then
we measured how much alcohol the mice were consuming after being
'infected,' and compared it with what they were drinking before.
We
found that either inhibiting the 'go' neurons or turning on the 'no-go'
neurons successfully reduced alcohol drinking levels and preference for
alcohol in the 'alcoholic' mice.
In
another experiment in this study, we found that directly delivering a
drug that excites the 'no-go' neuron into the striatum can also reduce
alcohol consumption.
Conversely,
in a previous experiment we found that directly delivering a drug that
inhibits the 'go' neuron has the same effect.
Both results may help the development of clinical treatment for alcoholism.
Most
people with an alcohol use disorder can benefit from treatment, which
can include a combination of medication, counseling and support groups.
Although
medications, such as Naltrexone, to help people stop drinking can be
effective, none of them can accurately target the specific neurons or
circuits that are responsible for alcohol consumption.
Employing viruses to deliver specific genes into neurons has been for disorders such as Parkinson's disease in humans.
Researchers found that either
inhibiting the 'go' neurons or turning on the 'no-go' neurons
successfully reduced alcohol drinking levels and preference for alcohol
in the 'alcoholic' mice
But
while we've demonstrated that this process can reduce the desire to
drink in mice, we're not yet at the point of using the same method in
humans.
Our
finding provides insight for clinical treatment in humans in the
future, but using a virus to treat alcoholism in humans is probably
still a long way off.
Yifeng Cheng, Ph.D. Candidate, Texas A&M University Health Science Center, Texas A&M University and Jun Wang, Assistant Professor of Neuroscience and Experimental Therapeutics, Texas A&M Health Science Center , Texas A&M University
This article was originally published on The Conversation. Read the original article.
This article was originally published on The Conversation. Read the original article.
No comments:
Post a Comment