Dr Matilda Jackson from the Robinson Research Institute’s Molecular Neurogenetics Research Group attended the Australasian Neuroscience Society Annual Scientific Meeting in Hobart in November 2016.
Matilda presented her research on Arx PA2 mice seize the day: characterizing the phenotype of expanded polyalanine tract mutations.
This is what Matilda had to say about her experience:
What was a highlight of the conference?
The conference dinner was held at MONA (Museum of Old and New Art) with a private viewing also included. The current exhibition is titled ‘On the origin of art’ which asked four biocultural scientists/philosophers how art had a basis in biology. We were given interactive headphones which allowed us to listen to each person’s interpretation of how art and biology were linked, and how each exhibition portrayed this, giving a different insight and perspective into science.
Did you meet any researchers or collaborators of significance? Why are they important to your work?
The Australasian Neuroscience Society annual meeting is attended by both clinicians and researchers that are focused on further understanding the brain and nervous system, a key aspect of my research. Our laboratory focuses on understanding both the molecular mechanisms and phenotypic outcomes that arise due to loss or altered function of ARX and IQSEC2; two frequently mutated genes on the X-chromosome that contribute to X-linked intellectual disability and epilepsy. We are therefore in communication with multiple research groups in regards to additional in vitro analyses (molecular mechanisms) and behavioural tests (phenotypic outcomes) that we can undertake with their assistance/guidance to further our current knowledge and expertise.
How will the experience support you and your research going forward?
Being able to attend and listen to both national and international speakers across a broad scope of neurobiology has expanded my knowledge of current studies and/or technologies and how these could be incorporated into my research. Listening to talks specifically on autism, schizophrenia, epilepsy, axonal development, cytoskeleton organization, cognitive training, injury and repair, and motor function and disease has allowed me to see what research is being undertaken on distinct mechanisms/disorders that overlap and are largely associated with our research into the molecular underpinnings of intellectual disability.
What was the most exciting thing you learned/experienced at the Conference?
I attended plenary lectures from two leading neuroscientists who discussed the use of optical approaches for interrogating neural circuits and the study of axonal development and repair. Both these plenary lectures investigated the growth and development of the nervous system and to how it adapted after mechanical or chemical interference. By investigating how neurons behave during both growth and repair, we can aim to further understand what happens when things go wrong during early prenatal periods, and whether certain aspects can be rescued/treated.
What was the most interesting or unexpected moment of your travel?
One of the symposia sessions was titled ‘Exploring the role of zinc in cognition’, with one of the talks investigating the link between huntingtin over-expression and zinc deficiency. While my main focus was to attend the ANS conference to further my understanding on neural/brain development and function in regards to my research into the underlying molecular pathology of intellectual disability. Huntington research is also another area of interest of mine, as members of my father’s family suffer from Huntington’s.