In a new study performed by researchers from Hiroshima University and the RIKEN Brain Science Institute in Saitama, Japan, specially bred mice with autism were given breast milk dosed with Prozac, generically named fluoxetine, and displayed a significant change in communication patterns, social interactions and other hallmark behaviors of autism.
Additionally, the results revealed that, after 6 daily injections of Prozac, newborn autistic mice had normal voice patterns and a reduction of anxiety all the way through adulthood.
Prozac is an antidepressant of the SSRI or selective serotonin reuptake inhibitor family, one of the most used and most prescribed types of medication. It works by boosting the level of serotonin, a neurotransmitter, in between specific kinds of brain cells in order to stabilize mood and reduce anxiety.
Autism research with human patients has shown that children who develop autism later in life often have low serotonin levels found in essential parts of the brain. Recently published in the journal Science Advances, this separate study suggests that a combination of serotonin shortage and disordered neurotransmitter signaling both are integral parts of developing the variety of diseases on the autism spectrum that presents with inflexible behavior, poor communication and social skills, and a low level for sensory overload.
While Prozac treatment for the mice lasts for the initial three weeks of life, in human children a similar treatment plan lasts from 6 months old to 2 and half years in age. These SSRI treatments are taking place at MIND Institute, part of UC Davis, which specializes in the treatment of neurodevelopment disorders and they’ve already seen results in human patients.
“This study supports what we see clinically,” said Dr. Randi J. Hagerman, medical director of the MIND Institute.
As part of researching causes and treatments of neurodevelopment disorders, Hagerman and fellow researchers have found that in patients between the ages of 2 and 6 with Fragile X, the genetic disorder most frequently at the root of autism, a six-month course of Zoloft, a SSRI antidepressant also called sertraline, made improvements to many cognitive functions, include the use of expressive language.
Additionally, the MIND Institute team have discovered that a treatment of SSRIs seems to stimulate the formation of neural connections and boost new neuron growth in the brains of children with Fragile X autism. Typically autism-type disorders are treated with behavioral therapies only, therefore any improvement with medications that can aid preexisting behavior therapies in being more effective is welcomed, added Hagerman.
“I think it’s making a difference,” she said.
Perhaps not surprisingly, the researchers behind the Prozac study admit it would be “difficult to simply apply the strategy used in this study to humans.” Scientists cannot give SSRIs to human newborns through breast milk before they are actually diagnosed with autism because of research medical ethics. Therefore it is unknown at this time if there could be the same type of reversal effects, rather than treatment effects, as they found in the mice.
At the same time, there have been other research studies which have linked antidepressants, especially Prozac, to an increase in autism rates amongst babies exposed in utero. While this is a challenge, the research results into the link have been inconsistent and have yet taken into consideration that if the mother is taking antidepressants there may be an underlying genetic disposition towards serotonin deficiencies that can manifest as autism in offspring.
Still, only in mice, for the time being, the Japanese scientist of the Prozac study has found that their treatment can normalize certain structures in the brain and thereby better the performance of communication, sensory, and social circuitry when errors in genetic transcription might lead neurodevelopment disorders like autism.
More specifically, the Prozac, when given early in development to a mouse bred to develop autism, created an increase of serotonin that affected the dorsal raphe nucleus section of the midbrain. This key structure is a switching station that has an instrumental part in emotions, learning, and memory. The SSRI treatment can help reestablish the balance between “up” neurons while slowing down other electrical brain signals.
Also, Prozac-treated mice spent more time with unfamiliar peers and exhibited less anxiety in a maze when compared to untreated mice. As newborn pups, their cries showed less fear and stress as well.
“Restoration of normal serotonin levels” in the mice used for research, who had been specially bred, “revealed the reversibility… in the adult” of many of the common and most difficult displays of autism and other neurodevelopment disorders, said the scientists.
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