Scientists watch neurons with Rett's syndrome develop|
SAN DIEGO, USA: Scientists have studied autism in a laboratory dish, obtaining new information that raises hope the condition can one day be treatable.
In the journal Cell, scientists at the University of California, San Diego described how they were able to re-programme skin cells from patients with a mutation in the MeCP2 gene which has been implicated in one of the autism spectrum disorders, Rett's syndrome.
Rett's syndrome affects primarily girls. Early symptoms appear just after a child has learned to walk and say a few words. Normal development slows down and children lose speech and motor skills.
By re-programming cells from patients, the scientists were able to watch neurons with Rett's syndrome develop. They found that the neurons developed fewer functional connections.
"Mental disease and particularly autism still carry the stigma of bad parenting," said an author of the study, Dr Alysson Muotri, an assistant professor at UC-San Diego's department of molecular and cellular medicine. "We show very clearly that autism is a biological disease that is caused by a developmental defect directly affecting brain cells."
Previously, scientists have had to study the autistic brain by imaging the brains of patients or examining the brain tissue of people who have died. However, a new avenue of research has opened in the last few years as scientists have learned to reprogram skin cells back to the embryonic state, then forward to all kind of roles including brain, blood and heart tissue. This allowed researchers to create brain cells from people with Rett syndrome and track their development.
"It is quite amazing that we can recapitulate a psychiatric disease in a Petri dish," said another of the study's authors, Dr Fred Gage, a professor at the Salk Laboratory of Genetics. "Being able to study Rett's neurons in a dish allows us to identify subtle alterations in the functionality of the neuronal circuitry that we never had access to before."
(Source: Journal Sentinel, November 12, 2010)