Research news: Tourettes Action funding more research

Posted on 1 May 2015

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Researchers from Nottingham University studying alterations in brain structure & function that occur in TS

Tourettes Action are pleased to report they are funding more research into Tourettes Syndrome by researchers from Nottingham University. Below is an overview of the research being carried out by the researchers:

Key aims:
The overall aims of our research programme are centred around two key objectives as follows:
1. One key objective is to understand more about the pattern of subtle alterations in brain structure and function that occur in Tourette syndrome (TS). In particular, we want to understand and identify those alterations in brain structure and function, measured using brain imaging techniques, that will help use develop better and more accurate clinical diagnoses, and more importantly, allow us to accurately and reliably predict future clinical and behavioural outcomes (prognosis).
2. A second key objective is to develop novel and effective engineering-based therapeutic interventions that offer an alternative to drug therapies, are suitable for widespread use within the clinic, and are inexpensive and potentially suitable for safe and effective home administration.

Scientific background to the TA funded project:
While the neurobiological basis for TS remains poorly understood it likely involves a complex interaction between genetic and environmental factors that exert an influence over the developing brain. It is known that in TS there may be many structural and functional alterations from typical patterns of brain development. Some of these alterations may be causes of the clinical symptoms seen in TS while others may be a consequence of the disorder and associated with the control of tics.
Communication in the brain is carried out by a particular kind of brain cell called a neuron and is based upon a combination of electrical and chemical signals. When a neuron is not communicating its electrical activity is in a ‘resting state’; however when it is communicating information it becomes electrically active or ‘excited’ and this electrical activity leads to the release of a brain chemical, called a neurotransmitter, which influences the activation of other neurons that it is in contact with. This chemical contact between neurons occurs at a special part of the cell called a synapse.
The structure of the brain’s communication pathways is established early in development. Milestones include: the growth and migration of neurons; the formation of synapses; and experience-dependent consolidation of synaptic connections. These events typically produce brain networks with balanced excitatory and inhibitory influences and disruption to this balance is proposed as a common basis for many common neurodevelopmental disorders including autism, ADHD, and TS.
GABA is an important brain chemical that plays a key role in the way that brain cells communicate with one another. It is the main ‘inhibitory’ neurotransmitter in the brain -- this means that the release of GABA tends to decrease the activity or excitability of neurons that it comes into contact with. GABA is present in 25–50% of synapses and contributes to almost all brain functions. As a consequence dysfunction in GABA signaling is core to many common neurodevelopmental disorders, and has been particularly associated with TS.
In humans GABA functioning can be studied in two main ways. First, it can be studied directly using a type of brain scanning known as magnetic resonance spectroscopy (MRS), which allows us to measure the concentration of brain chemicals, including GABA, found within a brain area. Second, it can be studied indirectly using a brain stimulation technique called transcranial magnetic stimulation (TMS). In this case, the effects of GABA neurons can be inferred from alterations in brain excitability that are triggered by magnetic stimulation of the brain.
A major theoretical and practical question currently exists however with respect to these two approaches. This question revolves around whether these two different techniques are each measuring the same or different pools of GABA. This question is particularly important with regard to our understanding of TS as these two techniques have produced inconsistent findings in individuals with TS.
Our current study aims to answer this question by measuring GABA using both techniques in the same group of individuals before and after a drug called Gabapentin (a drug that has the effect of altering GABA concentrations) is given and examining whether both techniques show the same change in GABA after the drug has been given. Importantly, responses to the drug Gabapentin will be compared against a group of individuals who, unknown to them, were not given the drug, (a so-called placebo condition).

The results of this study will appear on the Tourettes Action website in January 2016.

If you would like to know more about this study and any other research please contact research manager Seonaid Anderson

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