Mice again...they apparently function as a good model of a brain with ASD. This study has found that a neuropeptide, called oxytocin, can restore social behavior in mice. It has a long way to go before getting to humans but I can just imagine the benefits something like this could have on the ASD community. So many of our kids struggle with social behavior deficits over many other issues and it can be the single most limiting factor for them in terms of having a job or joining in community events
Treatment restores sociability in autism mouse model
Date: January 22, 2015
Source: University of California, Los
Angeles (UCLA), Health Science
Summary:
Researchers
have treated mice that mimic human autism with a neuropeptide called oxytocin,
and have found that it restores normal social behavior. In addition, the
findings suggest that giving oxytocin as early as possible in the animal's life
leads to more lasting effects in adults and
adolescents.
Among
the problems people with Autism spectrum disorders (ASD) struggle with are
difficulties
with social behavior and communication. That can translate to an
inability to make friends, engage in routine conversations, or pick up on the
social cues that are second nature to most people. Similarly, in a mouse model
of ASD, the animals, like humans, show little interest in interacting or
socializing with other mice.
One
drug, risperidone, works in both humans and mice with ASD to treat other
symptoms of the disorder -- including repetitive behaviors--but no medication
has been found to help socialization.
Now
researchers at UCLA have treated ASD mice with a neuropeptide--molecules used
by neurons to communicate with each other--called oxytocin, and have found that
it restores normal social behavior. In addition, the findings suggest that
giving oxytocin as early as possible in the animal's life leads to more lasting
effects in adults and adolescents. This suggests there may be critical times
for treatment that are better than others.
The
study appears in the January 21 online edition of the journal Science
Translational Medicine.
Mouse
models of neuropsychiatric diseases provide a platform for understanding the
mechanisms behind disorders and development of new therapies, noted Daniel
Geschwind, a UCLA professor of psychiatry, neurology and human genetics, and
senior author of the study. In 2011, Geschwind and his colleagues developed a
mouse model for ASD by knocking out a gene called CNTNAP2 (contactin-associated
protein-like 2), which scientists believe plays an important role in the brain
circuits responsible for language and speech. Previous research has linked
common CNTNAP2 variants to heightened autism risk in the general population,
while rare variants can lead to an inherited form of autism called cortical
dysplasia-focal epilepsy syndrome (CDFE).
It's
known that the oxytocin is involved in regulating various aspects of social
behavior. Among its other roles, oxytocin neurons in the brain's hypothalamus
interact with several other brain regions, including the amygdala, hippocampus,
and frontal cortex, where they influence such behaviors as fear, memory, and
social behavior.
"The
oxytocin system is a key mediator of social behavior in mammals, including
humans, for maternal behavior, mother-infant bonding, and social memory,"
said Geschwind, who holds UCLA's Gordon and Virginia MacDonald Distinguished
Chair in Human Genetics and is the director of the Center for Autism Research
and Treatment at the Semel Institute for Neuroscience and Human Behavior at
UCLA. "So it seemed like a natural target for us to go after."
In
the ASD mice, the researchers found a decrease in the number of oxytocin
neurons in the hypothalamus and, overall, a decrease in oxytocin levels
throughout the brain. But when they administered oxytocin to the ASD mice,
sociability, defined as time spent interacting normally with other mice, was
restored. Then, using a second strategy, the researchers also found that by
giving the mice melanocortin, an agonist (which binds to specific receptors on
a cell to activate it) caused a natural release of oxytocin from brain cells,
which also improved social deficits.
"The
study shows that a primary deficit in oxytocin may cause the social problems in
these mice, and that correcting this deficit can correct social behavior,"
said Geschwind. "We were surprised as well to discover a relationship
between the cntnap2 protein and oxytocin--the absence of cntnap2 effected
oxytocin neurons in the hypothalamus."
The
biggest surprise, though, said Geschwind, was finding that early postnatal
administration of the oxytocin led to longer positive effects upon social
behavior when measured several weeks later. "This suggests that there may
be critical windows of time for treatment that are better than others."
Because
the autistic mice share similar symptoms and behaviors with people on the
autism spectrum, the model offered a promising way to test new therapies that
may one day help people with autism. The next stage, said Geschwind, is
determining how limited a treatment can be given during early development of
the animal, refining the window of maximum therapeutic effect with the hope
this therapy may someday be applicable to humans.
The
study was funded by the National Institute of Mental Health (R01 MH081754-02R,
NIH/NS50220); the NIH Autism Centers of Excellence (HD055784-01;
5R01-MH081754-04); Simons Foundation Autism Research Initiative; Autism Speaks
(7657); NIH/National Institute of Neurological Disorders and Stroke (R01
NS049501 and R01 NS074312), and the Brain Disorder Award from McKnight
Foundation.
Story Source:
The
above story is based on materials provided by University of California,
Los Angeles (UCLA), Health Sciences. Note: Materials may be
edited for content and length.
Journal Reference:
- O. Penagarikano, M. T. Lazaro, X.-H.
Lu, A. Gordon, H. Dong, H. A. Lam, E. Peles, N. T. Maidment, N. P. Murphy,
X. W. Yang, P. Golshani, D. H. Geschwind.Exogenous and evoked oxytocin
restores social behavior in the Cntnap2 mouse model of autism. Science
Translational Medicine, 2015; 7 (271): 271ra8 DOI: 10.1126/scitranslmed.3010257
Cite This Page:
University
of California, Los Angeles (UCLA), Health Sciences. "Treatment restores
sociability in autism mouse model." ScienceDaily. ScienceDaily, 22 January
2015. <www.sciencedaily.com/releases/2015/01/150122154818.htm>
No comments:
Post a Comment