We will present data obtained
with mouse models of autism, that demonstrate the utility of the system.
Not exact matches
«The successful restoration
of normal function demonstrated in the
mouse models suggests that if we can develop therapies to address the loss
of Mecp2,» Baylor's Zoghbi says, «we may be able to reverse neurological damage in children and adults
with Rett,
autism and related neuropsychiatric disorders.»
A new
mouse model of a genetically - linked type
of autism reveals more about the role
of genes in the disorder and the underlying brain changes associated
with autism's social and learning problems.
Scientists at Duke Health who developed the new
model also discovered that targeting a brain receptor in
mice with this type
of autism could ease repetitive behaviors and improve learning in some animals.
To study the relationship between
autism and subplate neuron development in
mice, Kanold, Nagode and their collaborators began
with a well - established
mouse model of autism.
In a study published earlier this year, Jiang and other collaborators at Duke described a
mouse model of autism in which they deleted a prominent
autism gene called SHANK3, which is mutated in 1 percent
of people
with the disorder.
The
mouse models of autism on a normal lab diet (
with a medium glycemic index) are already known to generate fewer new neurons, and some
of their existing cells and neuronal connections are abnormal compared
with those
of normal
mice.
By demonstrating that a widely used
mouse model of autism does have gastrointestinal problems, and that these problems are associated
with behavioral symptoms, the new research «shows us something fabulous,» says Betty Diamond, an immunologist at the Feinstein Institute for Medical Research in Manhasset, New York.
Researchers Daniel Nagode and Patrick Kanold, together
with their colleagues, used a well - established
mouse model of autism, which involves injecting valproic acid (VPA) on
mouse embryos during day 12
of their 20 - day gestational period.
This study therefore characterizes the structural and cellular bone phenotype in a
mouse model of autism that can be further utilized to investigate therapeutic avenues to treat bone fractures in children
with autism.