MIT Researchers Recreate Autism In Mice

[Guest guest]

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have produced mice with two of the most common traits of autism - compulsive, repetitive behavior and avoidance of social interaction. They further showed that this gene, which is also implicated in many cases of human autism, appears to produce autistic behavior by interfering with communication between brain cells. The finding, reported in the March 20 online edition of Nature, could help researchers find new pathways for developing drugs to treat autism, says senior author Guoping Feng, professor of brain and cognitive sciences and member of the McGovern Institute for Brain Research at MIT. About one in 110 children in the United States has an autism spectrum disorder, which can range in severity and symptoms but usually includes difficulties with language in addition to social avoidance and repetitive behavior. There are currently no effective drugs to treat autism, but the new finding could help uncover new drug targets, Feng says. "We now have a very robust model with a known cause for autistic-like behaviors. We can figure out the neural circuits responsible for these behaviors, which could lead to novel targets for treatment," he says. The new mouse model also gives researchers a new way to test potential autism drugs before trying them in human patients. In the past 10 years, large-scale genetic studies have identified hundreds of gene mutations that occur more frequently in autistic patients than in the general population. However, each patient has only one or a handful of those mutations, making it difficult to develop drugs against the disease. In this study, the researchers focused on one of the most common of those genes, known as shank3. Shank3 is found in synapses - the junctions between brain cells that allow them to communicate with each other. Feng, who joined MIT and the McGovern Institute last year, began studying shank3 a few years ago because he thought that synaptic proteins might contribute to autism and similar brain disorders, such as obsessive compulsive disorder. At a synapse, one cell sends messages by releasing chemicals called neurotransmitters, which interact with the cell receiving the signal (known as the postsynaptic cell). This signal provokes the postsynaptic cell to alter its activity in some way - for example, turning a gene on or off. Shank3 is a "scaffold" protein, meaning that it helps to organize the hundreds of other proteins clustered on the postsynaptic cell membrane, which are necessary to coordinate the cell's response to synaptic signals. Feng targeted shank3 because it is found primarily in a part of the brain called the striatum, which is involved in motor activity, decision-making and the emotional aspects of behavior. Malfunctions in the striatum are associated with several brain disorders, including autism and OCD. Feng theorized that those disorders might be caused by faulty synapses. In a 2007 study, Feng showed that another postsynaptic protein found in the striatum, SAPAP3, can cause OCD-like behavior in mice when mutated. In the new Nature study, Feng and his colleagues found that shank3 mutant mice showed compulsive behavior (specifically, excessive grooming) and avoidance of social interaction. "They're just not interested in interacting with other mice," he says. The study, funded in part by the Simons Foundation Autism Research Initiative, offers the first direct evidence that mutations in shank3 produce autistic-like behavior. Even though only a small percentage of autistic patients have mutations in shank3, Feng believes that many other cases may be caused by disruptions of other synaptic proteins. He is now doing a study, with researchers from the Broad Institute, to determine whether mutations in a group of other synaptic genes are associated with autism in human patients. If that turns out to be the case, it should be possible to develop treatments that restore synaptic function, regardless of which particular synaptic protein is defective in the individual patient, Feng says. Feng performed some of the research while at Duke, and several of his former Duke colleagues are authors on the Nature paper, including lead author Joao Peca and Professor Lascola. Funding: Simons Foundation Autism Research Initiative (SFARI), National Institute of Mental Health, The Hartwell Foundation, NARSAD, and the Portuguese Foundation for Science and TechnologySourceMIT

[Guest guest]

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have produced mice with two of the most common traits of autism - compulsive, repetitive behavior and avoidance of social interaction. They further showed that this gene, which is also implicated in many cases of human autism, appears to produce autistic behavior by interfering with communication between brain cells. The finding, reported in the March 20 online edition of Nature, could help researchers find new pathways for developing drugs to treat autism, says senior author Guoping Feng, professor of brain and cognitive sciences and member of the McGovern Institute for Brain Research at MIT. About one in 110 children in the United States has an autism spectrum disorder, which can range in severity and symptoms but usually includes difficulties with language in addition to social avoidance and repetitive behavior. There are currently no effective drugs to treat autism, but the new finding could help uncover new drug targets, Feng says. "We now have a very robust model with a known cause for autistic-like behaviors. We can figure out the neural circuits responsible for these behaviors, which could lead to novel targets for treatment," he says. The new mouse model also gives researchers a new way to test potential autism drugs before trying them in human patients. In the past 10 years, large-scale genetic studies have identified hundreds of gene mutations that occur more frequently in autistic patients than in the general population. However, each patient has only one or a handful of those mutations, making it difficult to develop drugs against the disease. In this study, the researchers focused on one of the most common of those genes, known as shank3. Shank3 is found in synapses - the junctions between brain cells that allow them to communicate with each other. Feng, who joined MIT and the McGovern Institute last year, began studying shank3 a few years ago because he thought that synaptic proteins might contribute to autism and similar brain disorders, such as obsessive compulsive disorder. At a synapse, one cell sends messages by releasing chemicals called neurotransmitters, which interact with the cell receiving the signal (known as the postsynaptic cell). This signal provokes the postsynaptic cell to alter its activity in some way - for example, turning a gene on or off. Shank3 is a "scaffold" protein, meaning that it helps to organize the hundreds of other proteins clustered on the postsynaptic cell membrane, which are necessary to coordinate the cell's response to synaptic signals. Feng targeted shank3 because it is found primarily in a part of the brain called the striatum, which is involved in motor activity, decision-making and the emotional aspects of behavior. Malfunctions in the striatum are associated with several brain disorders, including autism and OCD. Feng theorized that those disorders might be caused by faulty synapses. In a 2007 study, Feng showed that another postsynaptic protein found in the striatum, SAPAP3, can cause OCD-like behavior in mice when mutated. In the new Nature study, Feng and his colleagues found that shank3 mutant mice showed compulsive behavior (specifically, excessive grooming) and avoidance of social interaction. "They're just not interested in interacting with other mice," he says. The study, funded in part by the Simons Foundation Autism Research Initiative, offers the first direct evidence that mutations in shank3 produce autistic-like behavior. Even though only a small percentage of autistic patients have mutations in shank3, Feng believes that many other cases may be caused by disruptions of other synaptic proteins. He is now doing a study, with researchers from the Broad Institute, to determine whether mutations in a group of other synaptic genes are associated with autism in human patients. If that turns out to be the case, it should be possible to develop treatments that restore synaptic function, regardless of which particular synaptic protein is defective in the individual patient, Feng says. Feng performed some of the research while at Duke, and several of his former Duke colleagues are authors on the Nature paper, including lead author Joao Peca and Professor Lascola. Funding: Simons Foundation Autism Research Initiative (SFARI), National Institute of Mental Health, The Hartwell Foundation, NARSAD, and the Portuguese Foundation for Science and TechnologySourceMIT

[Guest guest]

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have produced mice with two of the most common traits of autism - compulsive, repetitive behavior and avoidance of social interaction. They further showed that this gene, which is also implicated in many cases of human autism, appears to produce autistic behavior by interfering with communication between brain cells. The finding, reported in the March 20 online edition of Nature, could help researchers find new pathways for developing drugs to treat autism, says senior author Guoping Feng, professor of brain and cognitive sciences and member of the McGovern Institute for Brain Research at MIT. About one in 110 children in the United States has an autism spectrum disorder, which can range in severity and symptoms but usually includes difficulties with language in addition to social avoidance and repetitive behavior. There are currently no effective drugs to treat autism, but the new finding could help uncover new drug targets, Feng says. "We now have a very robust model with a known cause for autistic-like behaviors. We can figure out the neural circuits responsible for these behaviors, which could lead to novel targets for treatment," he says. The new mouse model also gives researchers a new way to test potential autism drugs before trying them in human patients. In the past 10 years, large-scale genetic studies have identified hundreds of gene mutations that occur more frequently in autistic patients than in the general population. However, each patient has only one or a handful of those mutations, making it difficult to develop drugs against the disease. In this study, the researchers focused on one of the most common of those genes, known as shank3. Shank3 is found in synapses - the junctions between brain cells that allow them to communicate with each other. Feng, who joined MIT and the McGovern Institute last year, began studying shank3 a few years ago because he thought that synaptic proteins might contribute to autism and similar brain disorders, such as obsessive compulsive disorder. At a synapse, one cell sends messages by releasing chemicals called neurotransmitters, which interact with the cell receiving the signal (known as the postsynaptic cell). This signal provokes the postsynaptic cell to alter its activity in some way - for example, turning a gene on or off. Shank3 is a "scaffold" protein, meaning that it helps to organize the hundreds of other proteins clustered on the postsynaptic cell membrane, which are necessary to coordinate the cell's response to synaptic signals. Feng targeted shank3 because it is found primarily in a part of the brain called the striatum, which is involved in motor activity, decision-making and the emotional aspects of behavior. Malfunctions in the striatum are associated with several brain disorders, including autism and OCD. Feng theorized that those disorders might be caused by faulty synapses. In a 2007 study, Feng showed that another postsynaptic protein found in the striatum, SAPAP3, can cause OCD-like behavior in mice when mutated. In the new Nature study, Feng and his colleagues found that shank3 mutant mice showed compulsive behavior (specifically, excessive grooming) and avoidance of social interaction. "They're just not interested in interacting with other mice," he says. The study, funded in part by the Simons Foundation Autism Research Initiative, offers the first direct evidence that mutations in shank3 produce autistic-like behavior. Even though only a small percentage of autistic patients have mutations in shank3, Feng believes that many other cases may be caused by disruptions of other synaptic proteins. He is now doing a study, with researchers from the Broad Institute, to determine whether mutations in a group of other synaptic genes are associated with autism in human patients. If that turns out to be the case, it should be possible to develop treatments that restore synaptic function, regardless of which particular synaptic protein is defective in the individual patient, Feng says. Feng performed some of the research while at Duke, and several of his former Duke colleagues are authors on the Nature paper, including lead author Joao Peca and Professor Lascola. Funding: Simons Foundation Autism Research Initiative (SFARI), National Institute of Mental Health, The Hartwell Foundation, NARSAD, and the Portuguese Foundation for Science and TechnologySourceMIT

[Guest guest]

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have produced mice with two of the most common traits of autism - compulsive, repetitive behavior and avoidance of social interaction. They further showed that this gene, which is also implicated in many cases of human autism, appears to produce autistic behavior by interfering with communication between brain cells. The finding, reported in the March 20 online edition of Nature, could help researchers find new pathways for developing drugs to treat autism, says senior author Guoping Feng, professor of brain and cognitive sciences and member of the McGovern Institute for Brain Research at MIT. About one in 110 children in the United States has an autism spectrum disorder, which can range in severity and symptoms but usually includes difficulties with language in addition to social avoidance and repetitive behavior. There are currently no effective drugs to treat autism, but the new finding could help uncover new drug targets, Feng says. "We now have a very robust model with a known cause for autistic-like behaviors. We can figure out the neural circuits responsible for these behaviors, which could lead to novel targets for treatment," he says. The new mouse model also gives researchers a new way to test potential autism drugs before trying them in human patients. In the past 10 years, large-scale genetic studies have identified hundreds of gene mutations that occur more frequently in autistic patients than in the general population. However, each patient has only one or a handful of those mutations, making it difficult to develop drugs against the disease. In this study, the researchers focused on one of the most common of those genes, known as shank3. Shank3 is found in synapses - the junctions between brain cells that allow them to communicate with each other. Feng, who joined MIT and the McGovern Institute last year, began studying shank3 a few years ago because he thought that synaptic proteins might contribute to autism and similar brain disorders, such as obsessive compulsive disorder. At a synapse, one cell sends messages by releasing chemicals called neurotransmitters, which interact with the cell receiving the signal (known as the postsynaptic cell). This signal provokes the postsynaptic cell to alter its activity in some way - for example, turning a gene on or off. Shank3 is a "scaffold" protein, meaning that it helps to organize the hundreds of other proteins clustered on the postsynaptic cell membrane, which are necessary to coordinate the cell's response to synaptic signals. Feng targeted shank3 because it is found primarily in a part of the brain called the striatum, which is involved in motor activity, decision-making and the emotional aspects of behavior. Malfunctions in the striatum are associated with several brain disorders, including autism and OCD. Feng theorized that those disorders might be caused by faulty synapses. In a 2007 study, Feng showed that another postsynaptic protein found in the striatum, SAPAP3, can cause OCD-like behavior in mice when mutated. In the new Nature study, Feng and his colleagues found that shank3 mutant mice showed compulsive behavior (specifically, excessive grooming) and avoidance of social interaction. "They're just not interested in interacting with other mice," he says. The study, funded in part by the Simons Foundation Autism Research Initiative, offers the first direct evidence that mutations in shank3 produce autistic-like behavior. Even though only a small percentage of autistic patients have mutations in shank3, Feng believes that many other cases may be caused by disruptions of other synaptic proteins. He is now doing a study, with researchers from the Broad Institute, to determine whether mutations in a group of other synaptic genes are associated with autism in human patients. If that turns out to be the case, it should be possible to develop treatments that restore synaptic function, regardless of which particular synaptic protein is defective in the individual patient, Feng says. Feng performed some of the research while at Duke, and several of his former Duke colleagues are authors on the Nature paper, including lead author Joao Peca and Professor Lascola. Funding: Simons Foundation Autism Research Initiative (SFARI), National Institute of Mental Health, The Hartwell Foundation, NARSAD, and the Portuguese Foundation for Science and TechnologySourceMIT

[Guest guest]

So the huge increase of autism is genetic? Complete

balderdash, or posh as says. Oh wait, they can make

drugs/profits and appear to be helping desperate people, investors

line up!!

On 3/20/2011 6:04 PM, jeremy9282 wrote:

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have

produced mice with two of the most common traits of autism

- compulsive, repetitive behavior and avoidance of social

interaction.

They further showed that this gene, which is also implicated in

many cases of human autism, appears to produce autistic behavior

by interfering with communication between brain cells. The

finding, reported in the March 20 online edition of Nature,

could help researchers find new pathways for developing drugs to

treat autism, says senior author Guoping Feng, professor of

brain and cognitive sciences and member of the McGovern

Institute for Brain Research at MIT.

About one in 110 children in the United States has an autism

spectrum disorder, which can range in severity and symptoms but

usually includes difficulties with language in addition to

social avoidance and repetitive behavior. There are currently no

effective drugs to treat autism, but the new finding could help

uncover new drug targets, Feng says.

"We now have a very robust model with a known cause for

autistic-like behaviors. We can figure out the neural circuits

responsible for these behaviors, which could lead to novel

targets for treatment," he says.

The new mouse model also gives researchers a new way to test

potential autism drugs before trying them in human patients.

In the past 10 years, large-scale genetic studies have

identified hundreds of gene mutations that occur more frequently

in autistic patients than in the general population. However,

each patient has only one or a handful of those mutations,

making it difficult to develop drugs against the disease.

In this study, the researchers focused on one of the most common

of those genes, known as shank3. Shank3 is found in synapses -

the junctions between brain cells that allow them to communicate

with each other. Feng, who joined MIT and the McGovern Institute

la! st year, began studying shank3 a few years ago because he

thought that synaptic proteins might contribute to autism and

similar brain disorders, such as obsessive

compulsive disorder.

At a synapse, one cell sends messages by releasing chemicals

called neurotransmitters, which interact with the cell receiving

the signal (known as the postsynaptic cell). This signal

provokes the postsynaptic cell to alter its activity in some way

- for example, turning a gene on or off. Shank3 is a "scaffold"

protein, meaning that it helps to organize the hundreds of other

proteins clustered on the postsynaptic cell membrane, which are

necessary to coordinate the cell's response to synaptic signals.

Feng targeted shank3 because it is found primarily in a part of

the brain called the striatum, which is involved in motor

activity, decision-making and the emotional aspects of behavior.

Malfunctions in the striatum are associated with several brain

disorders, including autism and OCD. Feng theorized that those

disorders might be caused by faulty synapses.

In a 2007 study, Feng showed that another postsynaptic protein

found in the striatum, SAPAP3, can cause OCD-like behavior in

mice when mutated.

In the new Nature study, Feng and his colleagues found that

shank3 mutant mice showed compulsive behavior (specifically,

excessive grooming) and avoidance of social interaction.

"They're just not interested in interacting with other mice," he

says.

The study, funded in part by the Simons Foundation Autism

Research Initiative, offers the first direct evidence that

mutations in shank3 produce autistic-like behavior.

Even though only a small percentage of autistic patients have

mutations in shank3, Feng believes that many other cases may be

caused by disruptions of other synaptic proteins. He is now

doing a study, with researchers from the Broad Institute, to

determine whether mutations i! n a group of other synaptic genes

are associated with autism in human patients.

If that turns out to be the case, it should be possible to

develop treatments that restore synaptic function, regardless of

which particular synaptic protein is defective in the individual

patient, Feng says.

Feng performed some of the research while at Duke, and several

of his former Duke colleagues are authors on the Nature paper,

including lead author Joao Peca and Professor

Lascola.

Funding: Simons Foundation Autism Research Initiative

(SFARI), National Institute of Mental Health, The Hartwell

Foundation, NARSAD, and the Portuguese Foundation for Science

and Technology

Source

MIT

[Guest guest]

So the huge increase of autism is genetic? Complete

balderdash, or posh as says. Oh wait, they can make

drugs/profits and appear to be helping desperate people, investors

line up!!

On 3/20/2011 6:04 PM, jeremy9282 wrote:

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have

produced mice with two of the most common traits of autism

- compulsive, repetitive behavior and avoidance of social

interaction.

They further showed that this gene, which is also implicated in

many cases of human autism, appears to produce autistic behavior

by interfering with communication between brain cells. The

finding, reported in the March 20 online edition of Nature,

could help researchers find new pathways for developing drugs to

treat autism, says senior author Guoping Feng, professor of

brain and cognitive sciences and member of the McGovern

Institute for Brain Research at MIT.

About one in 110 children in the United States has an autism

spectrum disorder, which can range in severity and symptoms but

usually includes difficulties with language in addition to

social avoidance and repetitive behavior. There are currently no

effective drugs to treat autism, but the new finding could help

uncover new drug targets, Feng says.

"We now have a very robust model with a known cause for

autistic-like behaviors. We can figure out the neural circuits

responsible for these behaviors, which could lead to novel

targets for treatment," he says.

The new mouse model also gives researchers a new way to test

potential autism drugs before trying them in human patients.

In the past 10 years, large-scale genetic studies have

identified hundreds of gene mutations that occur more frequently

in autistic patients than in the general population. However,

each patient has only one or a handful of those mutations,

making it difficult to develop drugs against the disease.

In this study, the researchers focused on one of the most common

of those genes, known as shank3. Shank3 is found in synapses -

the junctions between brain cells that allow them to communicate

with each other. Feng, who joined MIT and the McGovern Institute

la! st year, began studying shank3 a few years ago because he

thought that synaptic proteins might contribute to autism and

similar brain disorders, such as obsessive

compulsive disorder.

At a synapse, one cell sends messages by releasing chemicals

called neurotransmitters, which interact with the cell receiving

the signal (known as the postsynaptic cell). This signal

provokes the postsynaptic cell to alter its activity in some way

- for example, turning a gene on or off. Shank3 is a "scaffold"

protein, meaning that it helps to organize the hundreds of other

proteins clustered on the postsynaptic cell membrane, which are

necessary to coordinate the cell's response to synaptic signals.

Feng targeted shank3 because it is found primarily in a part of

the brain called the striatum, which is involved in motor

activity, decision-making and the emotional aspects of behavior.

Malfunctions in the striatum are associated with several brain

disorders, including autism and OCD. Feng theorized that those

disorders might be caused by faulty synapses.

In a 2007 study, Feng showed that another postsynaptic protein

found in the striatum, SAPAP3, can cause OCD-like behavior in

mice when mutated.

In the new Nature study, Feng and his colleagues found that

shank3 mutant mice showed compulsive behavior (specifically,

excessive grooming) and avoidance of social interaction.

"They're just not interested in interacting with other mice," he

says.

The study, funded in part by the Simons Foundation Autism

Research Initiative, offers the first direct evidence that

mutations in shank3 produce autistic-like behavior.

Even though only a small percentage of autistic patients have

mutations in shank3, Feng believes that many other cases may be

caused by disruptions of other synaptic proteins. He is now

doing a study, with researchers from the Broad Institute, to

determine whether mutations i! n a group of other synaptic genes

are associated with autism in human patients.

If that turns out to be the case, it should be possible to

develop treatments that restore synaptic function, regardless of

which particular synaptic protein is defective in the individual

patient, Feng says.

Feng performed some of the research while at Duke, and several

of his former Duke colleagues are authors on the Nature paper,

including lead author Joao Peca and Professor

Lascola.

Funding: Simons Foundation Autism Research Initiative

(SFARI), National Institute of Mental Health, The Hartwell

Foundation, NARSAD, and the Portuguese Foundation for Science

and Technology

Source

MIT

[Guest guest]

So the huge increase of autism is genetic? Complete

balderdash, or posh as says. Oh wait, they can make

drugs/profits and appear to be helping desperate people, investors

line up!!

On 3/20/2011 6:04 PM, jeremy9282 wrote:

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have

produced mice with two of the most common traits of autism

- compulsive, repetitive behavior and avoidance of social

interaction.

They further showed that this gene, which is also implicated in

many cases of human autism, appears to produce autistic behavior

by interfering with communication between brain cells. The

finding, reported in the March 20 online edition of Nature,

could help researchers find new pathways for developing drugs to

treat autism, says senior author Guoping Feng, professor of

brain and cognitive sciences and member of the McGovern

Institute for Brain Research at MIT.

About one in 110 children in the United States has an autism

spectrum disorder, which can range in severity and symptoms but

usually includes difficulties with language in addition to

social avoidance and repetitive behavior. There are currently no

effective drugs to treat autism, but the new finding could help

uncover new drug targets, Feng says.

"We now have a very robust model with a known cause for

autistic-like behaviors. We can figure out the neural circuits

responsible for these behaviors, which could lead to novel

targets for treatment," he says.

The new mouse model also gives researchers a new way to test

potential autism drugs before trying them in human patients.

In the past 10 years, large-scale genetic studies have

identified hundreds of gene mutations that occur more frequently

in autistic patients than in the general population. However,

each patient has only one or a handful of those mutations,

making it difficult to develop drugs against the disease.

In this study, the researchers focused on one of the most common

of those genes, known as shank3. Shank3 is found in synapses -

the junctions between brain cells that allow them to communicate

with each other. Feng, who joined MIT and the McGovern Institute

la! st year, began studying shank3 a few years ago because he

thought that synaptic proteins might contribute to autism and

similar brain disorders, such as obsessive

compulsive disorder.

At a synapse, one cell sends messages by releasing chemicals

called neurotransmitters, which interact with the cell receiving

the signal (known as the postsynaptic cell). This signal

provokes the postsynaptic cell to alter its activity in some way

- for example, turning a gene on or off. Shank3 is a "scaffold"

protein, meaning that it helps to organize the hundreds of other

proteins clustered on the postsynaptic cell membrane, which are

necessary to coordinate the cell's response to synaptic signals.

Feng targeted shank3 because it is found primarily in a part of

the brain called the striatum, which is involved in motor

activity, decision-making and the emotional aspects of behavior.

Malfunctions in the striatum are associated with several brain

disorders, including autism and OCD. Feng theorized that those

disorders might be caused by faulty synapses.

In a 2007 study, Feng showed that another postsynaptic protein

found in the striatum, SAPAP3, can cause OCD-like behavior in

mice when mutated.

In the new Nature study, Feng and his colleagues found that

shank3 mutant mice showed compulsive behavior (specifically,

excessive grooming) and avoidance of social interaction.

"They're just not interested in interacting with other mice," he

says.

The study, funded in part by the Simons Foundation Autism

Research Initiative, offers the first direct evidence that

mutations in shank3 produce autistic-like behavior.

Even though only a small percentage of autistic patients have

mutations in shank3, Feng believes that many other cases may be

caused by disruptions of other synaptic proteins. He is now

doing a study, with researchers from the Broad Institute, to

determine whether mutations i! n a group of other synaptic genes

are associated with autism in human patients.

If that turns out to be the case, it should be possible to

develop treatments that restore synaptic function, regardless of

which particular synaptic protein is defective in the individual

patient, Feng says.

Feng performed some of the research while at Duke, and several

of his former Duke colleagues are authors on the Nature paper,

including lead author Joao Peca and Professor

Lascola.

Funding: Simons Foundation Autism Research Initiative

(SFARI), National Institute of Mental Health, The Hartwell

Foundation, NARSAD, and the Portuguese Foundation for Science

and Technology

Source

MIT

[Guest guest]

So the huge increase of autism is genetic? Complete

balderdash, or posh as says. Oh wait, they can make

drugs/profits and appear to be helping desperate people, investors

line up!!

On 3/20/2011 6:04 PM, jeremy9282 wrote:

MIT Researchers Recreate Autism In Mice

http://www.medicalnewstoday.com/articles/219485.php

By mutating a single gene, researchers at MIT and Duke have

produced mice with two of the most common traits of autism

- compulsive, repetitive behavior and avoidance of social

interaction.

They further showed that this gene, which is also implicated in

many cases of human autism, appears to produce autistic behavior

by interfering with communication between brain cells. The

finding, reported in the March 20 online edition of Nature,

could help researchers find new pathways for developing drugs to

treat autism, says senior author Guoping Feng, professor of

brain and cognitive sciences and member of the McGovern

Institute for Brain Research at MIT.

About one in 110 children in the United States has an autism

spectrum disorder, which can range in severity and symptoms but

usually includes difficulties with language in addition to

social avoidance and repetitive behavior. There are currently no

effective drugs to treat autism, but the new finding could help

uncover new drug targets, Feng says.

"We now have a very robust model with a known cause for

autistic-like behaviors. We can figure out the neural circuits

responsible for these behaviors, which could lead to novel

targets for treatment," he says.

The new mouse model also gives researchers a new way to test

potential autism drugs before trying them in human patients.

In the past 10 years, large-scale genetic studies have

identified hundreds of gene mutations that occur more frequently

in autistic patients than in the general population. However,

each patient has only one or a handful of those mutations,

making it difficult to develop drugs against the disease.

In this study, the researchers focused on one of the most common

of those genes, known as shank3. Shank3 is found in synapses -

the junctions between brain cells that allow them to communicate

with each other. Feng, who joined MIT and the McGovern Institute

la! st year, began studying shank3 a few years ago because he

thought that synaptic proteins might contribute to autism and

similar brain disorders, such as obsessive

compulsive disorder.

At a synapse, one cell sends messages by releasing chemicals

called neurotransmitters, which interact with the cell receiving

the signal (known as the postsynaptic cell). This signal

provokes the postsynaptic cell to alter its activity in some way

- for example, turning a gene on or off. Shank3 is a "scaffold"

protein, meaning that it helps to organize the hundreds of other

proteins clustered on the postsynaptic cell membrane, which are

necessary to coordinate the cell's response to synaptic signals.

Feng targeted shank3 because it is found primarily in a part of

the brain called the striatum, which is involved in motor

activity, decision-making and the emotional aspects of behavior.

Malfunctions in the striatum are associated with several brain

disorders, including autism and OCD. Feng theorized that those

disorders might be caused by faulty synapses.

In a 2007 study, Feng showed that another postsynaptic protein

found in the striatum, SAPAP3, can cause OCD-like behavior in

mice when mutated.

In the new Nature study, Feng and his colleagues found that

shank3 mutant mice showed compulsive behavior (specifically,

excessive grooming) and avoidance of social interaction.

"They're just not interested in interacting with other mice," he

says.

The study, funded in part by the Simons Foundation Autism

Research Initiative, offers the first direct evidence that

mutations in shank3 produce autistic-like behavior.

Even though only a small percentage of autistic patients have

mutations in shank3, Feng believes that many other cases may be

caused by disruptions of other synaptic proteins. He is now

doing a study, with researchers from the Broad Institute, to

determine whether mutations i! n a group of other synaptic genes

are associated with autism in human patients.

If that turns out to be the case, it should be possible to

develop treatments that restore synaptic function, regardless of

which particular synaptic protein is defective in the individual

patient, Feng says.

Feng performed some of the research while at Duke, and several

of his former Duke colleagues are authors on the Nature paper,

including lead author Joao Peca and Professor

Lascola.

Funding: Simons Foundation Autism Research Initiative

(SFARI), National Institute of Mental Health, The Hartwell

Foundation, NARSAD, and the Portuguese Foundation for Science

and Technology

Source

MIT