Functional and Genomic Characterization of Interneurons in the Fmr1-KO Mouse Brain

The brain’s balance is maintained by two types of neurons: those that excite and those that inhibit activity. Like yin and yang, this balance is essential. This team has found fewer than normal inhibitory cells in the brains of Fragile X mice. They are now working to pinpoint this abnormality and find ways to restore the normal balance and function.

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Brain Imbalance Target of Dr. Erickson’s New Clinical Trial

Craig Erickson lab

According to Dr. Erickson, AZD7325 is a drug that selectively boosts GABA neurotransmission in the brain. GABA is the primary neurochemical in the brain that blocks brain activation. GABA activity is in balance in the brain with Glutamate activity, which is the primary neurochemical that causes brain activation. In Fragile X, GABA activity is insufficient and glutamate activity is excessive, likely causing brain activity to be out of balance. AZD7325 attempts to correct parts of this imbalance by boosting the insufficient GABA activity in the brains of people with Fragile X.

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Clinical Trial of Ganaxolone in Patients with Fragile X Syndrome

Frank Kooy, PhD, at University of Antwerp

With a $90,000 grant from FRAXA Research Foundation funded during 2014-2015, Dr. Frank Kooy and colleagues at the University of Antwerp are conducting a double blind crossover trial of ganaxolone in patients with Fragile X syndrome. Results of this study were mixed (see Marinus: Results from Phase 2 Exploratory Clinical Study Support Continued Development of Ganaxolone in Fragile X Syndrome.)

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Development of a Novel GABA-A Agonist in Fragile X Syndrome

Tori Shaeffer

Of the many genes known to be regulated by FMRP, the gamma-aminobutyric acid receptor A (GABA(A)), is gaining attention as a potential target for the treatment of FXS. Mounting evidence suggests decreased expression and functioning of GABA(A) is involved in the pathophysiology of FXS. Non-selective GABA(A) agonism in animal models of FXS has been associated with normalization of morphological features, GABA(A) expression, and behavior. However, the clinical use of these agents in Fragile X is associated with unwanted side-effects, such as sedation, dulling of cognition, and occasional paradoxical agitation, which limits their use.

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Development of a Novel GABA(A) a2,3 Agonist in Fragile X Syndrome

FRAXA Research Foundation awards $21,000 in 2013 to Dr. Schaeffer to analyze an investigational new compound that targets the GABA-A receptor. This study has led to a clinical trial of the compound, led by Dr. Craig Erickson at Cincinnati Children’s Hospital. Of the many genes known to be regulated by FMRP, the gamma-aminobutyric acid receptor A (GABA(A)), is gaining attention as a potential target for the treatment of FXS. Mounting evidence suggests decreased expression and functioning of GABA(A) is involved in the pathophysiology of FXS.

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What Works, and What Doesn’t

At the start, it’s always hard to know what methods will work best for something as complex as the development of disease-modifying treatments for Fragile X. But, we’ve always tried to let the science lead us down the right path. At this point, the results are unequivocal, and they have shaped how we are looking for the Next Great Thing in Fragile X treatments.

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GABAergic Inhibitory Function in Fragile X Syndrome

With a $100,000 grant from FRAXA Research Foundation, Drs. Joshua Corbin and Molly Huntsman from the Children’s National Medical Center examined the role of a particular class of brain cells (inhibitory interneurons) that dampen excessive activity in the “emotional center of the brain” (the amydala). This inhibition is deficient in Fragile X, and so they are looking for ways to remedy this. This is particularly interesting to parents of children who are overly anxious and emotional. They worked with Dr. Walter Kaufmann, a clinician at Kennedy Krieger Institute in Maryland.

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