Graduate Student

Email: ayan8<at>uwo.ca

Education:

M.D./Ph.D. Student in Neuroscience
(2011-Present)

Schulich School of Medicine & Dentistry
University of Western Ontario
London, ON, Canada

B.MSc. (Medical Sciences) (2007-2011)
University of Western Ontario
London, ON, Canada

Research Interests:

The act of reaching out to grasp an object is hardly an effortful process, and it is often taken for granted. Nevertheless, the precise neurological mechanisms underlying this act are not well understood. Reach-to-grasp movements can be subdivided into two systems, the first involving a transport component and the second involving a grip component. The transport component is dependent on extrinsic object properties, including the object's location, and is hypothesized to involve the medial parieto-frontal circuit. On the other hand, the grip component is dependent on intrinsic object properties, including the object's shape and size, and is hypothesized to involve the lateral parieto-frontal circuit. This is further substantiated by evidence from neurophysiological studies involving macaque monkeys, neuro-imaging studies (fMRI) in humans, and studies of patients with optic ataxia.

In order to delineate specific areas involved with reach-to-grasp movements, I will be using transcranial magnetic stimulation (TMS). TMS involves delivering magnetic pulses to perturb various regions in the brain. Unlike neuro-imaging studies, TMS allows for us to make inferences of causality. Moreover, it can be used in the normal population to target brain regions precisely in space and time. Specifically, I am interested in the role of the superior parieto-occipital cortex (SPOC) and the anterior intraparietal sulcus (aIPS) in reach-to-grasp movements. By perturbing these regions with TMS while subjects perform various tasks, I can gain a deeper understanding of how these regions are involved in the different aspects of reach-to-grasp movements.

Publications:

Laliberté, A.M., MacPherson, T.C., Micks, T., Yan, A., & Hill, K.A. (2011). Vision deficits precede structural losses in a mouse model of mitochondrial dysfunction and progressive retinal degeneration. Exp Eye Res; 93(6):833-41. DOI: 10.1016/j.exer.2011.09.017.