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Statins reverse learning disabilities caused by genetic disorder

Date: November 10, 2014

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Source: University of California - Los Angeles Health Sciences

Summary: Neuroscientists discovered that statins, a popular class of cholesterol
drugs, reverse the learning deficits caused by a mutation linked to a
common genetic cause of learning disabilities. The findings were
studied in mice genetically engineered to develop the disease, called
Noonan syndrome.

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A mouse ponders a series of maze entrances, trying to recall which one leads to
Credit: UCLA/Silva Lab

[Click to enlarge image]

CLA neuroscientists discovered that statins, a popular class of

cholesterol drugs, reverse the learning deficits caused by a mutation
linked to a common genetic cause of learning disabilities. Published in
the Nov. 10 advance online edition of Nature Neuroscience, the findings were
studied in mice genetically engineered to develop the disease, called Noonan
The disorder can disrupt a child's development in many
ways, often causing unusual facial features, short
stature, heart defects and developmental delays. No
treatment is currently available.

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"Noonan syndrome affects one in 2,000 people, and up

to half of these patients struggle with learning
disabilities," explained principal investigator Alcino
Silva, professor of neurobiology, psychiatry and
psychology at the David Geffen School of Medicine at

Rett syndrome

Down syndrome
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"Our approach identified the mechanism causing the

disease, as well as a treatment that reversed its effects in adult mice. We are excited

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Possible New Drug Targets for the Genetic

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Nov. 1, 2010 Noonan syndrome is a relatively
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about these findings, because they suggest that the treatment we developed may help
the millions of Noonan patients with intellectual disabilities."

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cells level the learning curve by producing a protein
that combats ... full story

While many genes contribute to Noonan syndrome, a single gene causes about half of
all cases. This gene encodes for a protein that regulates another protein called Ras,
which controls how brain cells talk to each other, enabling learning to take place.

more related stories

Working with first author Young-Seok Lee, Silva discovered that the Noonan mutation
creates hyperactive Ras, which disrupts cellular conversations and undermines the
learning process.
"The act of learning creates physical changes in the brain, much like grooves on a
record," said Silva, who is a member of the UCLA Brain Research Institute and UCLA
Integrative Center for Learning and Memory.
"Surplus Ras tips the balance between switching signals on and off in the brain. This
interrupts the delicate cell communication needed by the brain to record learned
"Hyperactive Ras signaling in the brain is to blame for Noonan's neurological and
behavioral symptoms," said Lee, a former UCLA postdoctoral researcher who now runs
his own lab at Chung-Ang University in Seoul, Korea. "An overabundance of Ras
prematurely alters the brain's synapses, leaving no place for the brain to record the
changes necessary for learning."
Drawing upon Silva's previous research with neurofibromatosis 1, another Rasinfluenced disease, the UCLA team treated the mice with lovastatin, an FDA-approved
statin drug currently in wide clinical use.
Here's how it works: statin drugs lower cholesterol by blocking the synthesis of certain
fat molecules that Ras requires to function. The resulting drop in Ras activity allows
brain cells to communicate properly, allowing normal learning to take place.
"Noonan syndrome interferes with the changes in brain cells needed for learning, which
results in learning deficits," Silva said. "Statins act on the root of the problem and
reverse these deficits. This enables the process of learning to physically change the
brain and create memory."
When the UCLA team treated adult Noonan mice with lovastatin, they discovered that
the drop in Ras activity dramatically improved the animals' memory and ability to
remember objects and navigate mazes.
"We were amazed to see that statin treatment restored the adult animals' cognitive
functions to normal. Traditionally, science assumes that therapy needs to start in the
fetal stage to be effective," explained Silva. "Our research suggests that the leading
gene mutation responsible for Noonan syndrome plays critical roles not only in fetal
development, but also in how well the adult brain functions."
According to Silva, UCLA's approach could help the estimated 35 million Americans
who struggle with learning disabilities. The next step will be to bring the drug therapy
into clinical studies for Noonan. For details about trial locations, contact the

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Cite This Page:

Science News



University of California - Los Angeles Health Sciences. "Statins reverse learning

disabilities caused by genetic disorder." ScienceDaily. ScienceDaily, 10 November
2014. <www.sciencedaily.com/releases/2014/11/141110124235.htm>.

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