University of Nebraska suggests cure for some Autisms
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Woo-Yang Kim, Ph.D., associate professor, developmental neuroscience, led a team of researchers from UNMC and Creighton University into a deeper exploration of a genetic mutation that reduces the function of certain neurons in the brain.
Dr. Kim’s findings were published in this week’s online issue of Nature Neuroscience.
“This is an exciting development because we have identified the pathological mechanism for a certain type of autism and intellectual disability,” Dr. Kim said.
Recent studies have shown that the disorder occurs when a first-time mutation causes only one copy of the human AT-rich interactive domain 1B (ARID1B) gene to remain functional, but it was unknown how it led to abnormal cognitive and social behaviors.
The team created and analyzed a genetically modified mouse and found that a mutated Arid1b gene impairs GABA neurons, the 'downer' neurotransmitter, leading to an imbalance of communication in the brain.
GABA blocks impulses between nerve cells in the brain. Low levels of GABA may be linked to anxiety or mood disorders, epilepsy and chronic pain. It counters glutamate (the upper neurotransmitter), as the two mediate brain activation in a Yin and Yang manner. People take GABA supplements for anxiety.
“In normal behavior, the brain is balanced between excitation and inhibition,” Dr. Kim said. “But when the inhibition is decreased, the balance is broken and the brain becomes more excited causing abnormal behavior.
“We showed that cognitive and social deficits induced by an Arid1b mutation in mice are reversed by pharmacological treatment with a GABA receptor modulating drug. And, now we have a designer mouse that can be used for future studies.”
Next steps for Dr. Kim and his team are to even further refine the specific mechanism for autism and intellectual disability and to identify which of the many GABA neurons are specifically involved.
Dr. Kim’s research was supported by a $1.7 million grant from the National Institute of Neurological Disorders and Stroke and a $400,000 Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health
Bolding in first sentence mine.
It should be noted the scientists' never said fix the writers of the press release did. But as an official press release, it represents the University
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Professionally Identified and joined WP August 26, 2013
DSM 5: Autism Spectrum Disorder, DSM IV: Aspergers Moderate Severity
“My autism is not a superpower. It also isn’t some kind of god-forsaken, endless fountain of suffering inflicted on my family. It’s just part of who I am as a person”. - Sara Luterman
There is substantial research prior to this indicating that innately low (too low) levels of GABA increases adverse symptoms for some on the spectrum, while increasing GABA for them can improve executive function, anxiety, clarity of thinking.
Suddenly we are seeing various announcements as if this is new knowledge. It isn't new, but the evidence is growing.
I fear it will be promoted in future as the latest "cure" - it isn't - and the dollar signs will start to go bing bing bing. Not everyone on the spectrum seems to have the GABA deficiency (more work on this is needed) so raising their GABA levels would slow them down to lower levels of functions possibly.
I have known for a few years now that I am in the low GABA segment of the spectrum, and for me low dose Clonazepam (subclinical dose level) attentuates the troublesome symptoms mentioned above. It doesn't "cure" my neural wiring ASD hardware, nor affect it, - I still have the positives of my AS (pattern spotting etc). It was a terrific breakthrough for me personally to find what normalising my GABA levels could do for my daily life. I hope more will find benefit from this in the future. It didn't help my hypersensitivity to noise, and some other factors. But what it did help, it helped a lot.
I have never heard (in relation to the above article) that GABA levels is related to IHC, and I wonder if that is some kind of mistake in translation at some stage of the write up. There was some research done 10 years ago which found that there were abnormalities in GABA neural transmission related to Fragile X Syndrome, and FXS people may have IHC, but most people with IHC don't have FXS, and FXS is often misdiagnosed as Autism, though the research rarely factors in this potential sampling error.
To date despite years of indications, there has been no large scale study on the GABA levels of ASD people and whether raising them for those who have low levels improves function. GABA seems particularly a factor for that part of the spectrum affected by seizures, as some researchers have noticed over the years. Their work didn't make headlines. I had seizures, but not epilepsy. I have not had a seizure since my own GABA breakthrough a few years ago, and while that may be coincidental, my view is that is it probably not coincidental.
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