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Thursday, October 29, 2009
Genetic mutation ups schizophrenia risk
COLD SPRING HARBOR, N.Y. - A U.S.-led team of geneticists
says it has identified a mutation on human chromosome 16 that
substantially increases the risk of developing schizophrenia.
Cold Spring Harbor Laboratory geneticist Jonathan Sebat, who
led the study, said the mutation is a copy number variant --
an area of the genome where the number of copies of genes
differs between individuals. The newly discovered copy number
variant is located in a region referred to by scientists as
16p11.2. By studying the genomes of 4,551 patients and 6,391
healthy individuals, Sebat's team determined having one extra
copy of that region is associated with schizophrenia. "In the
general population this duplication is quite rare, occurring
in roughly one in 5,000 persons," Sebat said. "But for people
that carry the extra copy, the risk of developing schizo-
phrenia is increased by more than eight-fold." Studies by
other groups have shown losing one copy of 16p11.2 confers
high risk of autism and other developmental disorders in
children. Taken together, the researchers said the studies
suggest some genes are shared between schizophrenia and aut-
ism. The findings are detailed in the early online edition of
the journal Nature Genetics and will appear in the journal's
November print issue.
FDA OK's new leukemia treatment
WASHINGTON - The U.S. Food and Drug Administration says it
has approved the use of the drug Arzerra for chronic lympho-
cytic leukemia. The FDA said it approved Arzerra (ofatumumab)
for patients with the slowly progressing cancer of the blood
and bone marrow when the cancer is no longer being controlled
by other forms of chemotherapy. Chronic lymphocytic leukemia
primarily affects people older than 50 and arises from a
group of white blood cells known as B-cells that are part of
the body's immune system, officials said. The drug was
approved under the FDA's accelerated approval process, which
allows earlier approval of drugs that satisfy unmet medical
needs and are reasonably likely to allow patients to live
longer or with fewer side effects of a disease. Arzerra is
manufactured by London-based GlaxoSmithKline.
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Enzyme found essential for nerve growth
BOSTON - U.S. medical researchers say they've determined an
enzyme known as Mst3b is essential for regenerating damaged
axons, or nerve fibers, in an animal model. The scientists
at Children's Hospital Boston said their discovery could lead
to new treatments for human brain and spinal cord injuries in
both the peripheral and central nervous systems. Led by Nina
Irwin and Larry Benowitz, the scientists discovered Mst3b
appears to be a master regulator of a cell-signaling pathway
controlling axon growth. Mst3b, a protein kinase, in turn
activates signals that switch on the genes necessary for
axons to grow. Working with live rats whose optic nerve was
damaged -- a common model of central-nervous-system injury
-- the researchers said they showed that in the absence of
Mst3b, axons show very little regeneration, even in the
presence of factors known to enhance axon growth. "All the
growth factors we've tested -- oncomodulin, inosine, brain-
derived neurotropic factor, nerve growth factor -- act
through Mst3b," Benowitz said. "In fact, activating Mst3b by
itself is enough to cause growth even if there are no growth
factors around. In terms of basic understanding of nerve
cells, this is a very exciting finding." The research appears
in the early online edition of the journal Nature Neuro-
science.
Testicular tumors linked to childhood ills
OXFORD, England - British and Danish scientists say they've
determined testicular tumors can explain why some diseases
are more common in children of older fathers. Researchers at
Britain's Oxford University and Denmark's Copenhagen Univer-
sity Hospital say they've discovered a link between some
severe childhood genetic disorders and rare testicular tum-
ors that occur in older men. Specifically, the scientists
said the germ cells that make mutant gene-carrying sperm seem
to be the same cells that produce the tumor. "We think most
men develop these tiny clumps of mutant cells in their test-
icles as they age," said Oxford University Professor Andrew
Wilkie, who led the research. "They are rather like moles in
the skin, usually harmless in themselves. But by being lo-
cated in the testicle, they also make sperm -- causing chil-
dren to be born with a variety of serious conditions. We call
them 'selfish' because the mutations benefit the germ cell,
but are harmful to offspring." He said the findings help
explain the origins of several serious conditions that affect
childhood growth and development, as well as some conditions
causing stillbirth. The study is detailed in the journal
Nature Genetics.
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Antipsychotic meds cause kids' weight gain
MANHASSET, N.Y. - U.S. medical scientists say they've deter-
mined newer anti-psychotic medications that cause weight
gain in adults can also have a similar effect on children.
A study by the Feinstein Institute for Medical Research and
the Zucker Hillside Hospital followed children and adolesc-
ents who had been prescribed anti-psychotic medicines for
the first time and observed the impact the medications had
on weight gain and metabolic changes. The researchers said
they identified a "worrisome" degree of weight gain and
changes in blood glucose and lipid metabolism that can be
precursors of diabetes, hypertension, metabolic syndrome,
stroke and heart attack. The 272 children tested were 4-19
years old. "The data sheds further light on the frequency and
severity of weight gain associated with these newer anti-
psychotics," said Dr. Christoph Correll. "Our findings sug-
gest increased caution in prescribing them to pediatric
patients." The study is reported in the Journal of the
American Medical Association.
Epilepsy drugs might help treat other ills
ST. LOUIS - U.S. scientists say they've found anti-epileptic
drugs may be effective in treating neurodegenerative dis-
orders such as Alzheimer's and Parkinson's diseases. The
researchers said they determined neurons in the brain were
protected after treatment with T-type calcium-channel
blockers, which are commonly used to treat epilepsy. Assis-
tant Professor Jianxin Bao and colleagues from the Washington
University School of Medicine in St. Louis said they were one
of the first teams to explore the possible protective effects
of blockers for T-type calcium channels. The mechanisms for
neuroprotection by anti-epileptic drugs were previously un-
known. Bao's team established cell culture models to directly
test whether the drugs could preserve neurons in long- and
short-term cultures in vitro. They said they found neurons
showed an increase in viability after treatment with either
L-type or T-type calcium channel inhibitors. Furthermore,
they said their research suggests more than one calcium-sig-
naling mechanism exists to regulate long- and short-term
neuron survival. "Our data provides implications for the use
of this family of anti-epileptic drugs in developing new
treatments for neuronal injury, and for the need of further
studies of the use of such drugs in age-related neurodegen-
erative disorders," said Bao. The research appears in the
BMC journal Molecular Neurodegeneration.
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