Kicking in Womb Helps Babies Develop Sense of Their Own Body

MedicalResearch.com Interview with:
"38 week fetus" by Zappys Technology Solutions is licensed under CC BY 2.0Kimberley Whitehead

Neuroscience, Physiology & Pharmacology
University College London

MedicalResearch.com: What is the background for this study?

Response: Fetuses move a lot! Very similar movement patterns are seen in both pre-term and full-term newborn infants, but their function is unclear. In animals such as rats, spontaneous movement and consequent feedback from the environment during the early developmental period trigger specific patterns of electrical activity in the brain that are necessary for proper brain mapping.

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Specific Brain Circuit Permanently Switched On In Patients With Anxiety Disorders

MedicalResearch.com Interview with:
Dr Oliver J Robinson Ph.D.
Section on Neurobiology of Fear and Anxiety,
National Institute of Mental Health, NIH, Bethesda, MD,
Institute of Cognitive Neuroscience
University College London, London, UK

Medical Research: What are the main findings of the study?

Dr. Robinson: This study is looking at a symptom of anxiety disorders known as “negative affective bias”. This describes the tendency of people with anxiety disorders to focus on negative or threatening information at the expense of positive information.

We completed a number of previous studies looking at so called “adaptive” anxiety in healthy individuals – this is the normal, everyday anxiety that everyone experiences; walking home in the dark, for instance (in these prior studies we used unpredictable electrical shocks to make people anxious and stressed). When we made healthy people transiently anxious in this way we showed that this was also associated with negative affective bias and driven by a specific brain circuit: the dorsal medial prefrontal (anterior cingulate) cortex—amygdala aversive amplification circuit.

In this study we showed that the same circuit that was engaged by transient anxiety in our healthy sample was actually engaged ‘at baseline’ (i.e. without stress) in our patient group. This suggests that this mechanism which can be temporarily activated in healthy controls becomes permanently ‘switched on’ in our patient group. This might explain why people with anxiety disorders show persistent ‘negative affective biases’.

Furthermore, the extent to which this circuit was turned on correlated with self-reported anxiety. That is to say the more anxious an individual said they were, the greater the activity in this circuit. Therefore, there seems to be more of a dimension or scale of anxiety, rather than a simple well/unwell diagnosis.
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Brain Mapping May Allow Earlier Detection of Brain Abnormalities

MedicalResearch.com Interview with:

dr_Aalex_d_leowAlex Leow, MD PhD
Psychiatric Institute
Chicago, IL 60612 and

 

Tony J. Simon, PhD University of California, Davis MIND Institute Sacramento, CA 95817Tony J. Simon, PhD
University of California,
Davis MIND Institute Sacramento,
CA 95817

MedicalResearch.com: What are the main findings of the study?

Answer: Fragile X syndrome (FXS) is the most common inherited cause of intellectual disabilities and the most prevalent known single-gene cause of autism in males. The fragile X mental retardation 1 gene (FMR1) can be mutated with expanded numbers of CGG trinucleotide repeats in the 5’ untranslated region on the Xq27.3 site of the X chromosome. Normally, unaffected individuals have fewer than 45 CGG repeats in FMR1. When the size of the CGG repeat exceeds 200 FMR1 is silenced and the mutation is categorized as full, generating the FXS phenotype. If the expansion is between 55–200 repeats, then the individual is generally classified as a fragile X premutation carrier (fXPC). An estimated 40% of male and 8-16% of female premutation carriers later develop Fragile X-Associated Tremor/Ataxia Syndrome (FXTAS), which is a late-onset (usually 50-70 years old) neurodegenerative disorder.

We recruited 46 neurologically symptomless young to middle aged carriers of the FMR1 gene mutation. They were age and gender matched with 42 unaffected control individuals without the gene mutation. Both groups were evaluated by cognitive testing as well as novel neuroimaging techniques termed “brain connectomics,” based on diffusion tensor imaging (DTI) whole-brain tractography.  A connectome is a comprehensive map, like a wiring diagram, of neural connections in the brain. Our study is the first-ever connectome study to compare fXPCs and controls.

In short, brain connectomics enable scientists for the first time to study the global organizational properties of the human brain by applying cutting edge computational techniques, based on graph theory, to these comprehensive maps of neural connections (i.e., the brain graphs). Our main finding was that, in neurologically symptomless male carriers  we detected a correlation between brain graphs’ efficiency in processing information and the number of CGG repeats in the mutated region of FMR1 (we estimated that each additional CGG repeat that in these males represents an effective increase of ~1.5 years  of “brain aging”). The correlation may prove to be an effective marker of early brain aging in otherwise neurologically symptomless premutation carriers. The study also further confirmed previous findings of smaller brain stem volumes in male fXPCS than in male controls.

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