Daniel O'Shea headshot

Daniel O’Shea, Ph.D.

Postdoctoral Scholar, Stanford University

SFARI Bridge to Independence Fellow

Daniel J. O’Shea is a postdoctoral scholar at Stanford University. He received his B.S.E. from Princeton University and Ph.D. from Stanford University. He completed his doctorate in the laboratory of Krishna V. Shenoy, where he studied the neural population dynamics that establish robust and flexible feedback control in macaques. In his postdoctoral research with Shenoy and Karl Deisseroth, O’Shea has used electrophysiology, optogenetic and electrical perturbations, two-photon imaging, and computational techniques to dissect the neural computations that support the acquisition, execution and maintenance of a broad repertoire of motor skills.

Deficits in motor cognition are commonly associated with autism. O’Shea plans to interrogate the distributed neural circuits that establish coordinated movement and to understand their dysfunction in autism, focusing on the critical yet poorly understood role of cerebellar-cortical communication.

Project: Precise characterization of computational deficits in motor cognition in autism via corticocerebellar perturbations

Persistent deficits in movement coordination are commonly associated with autism. These diverse motor‐cognitive deficits are correlated with altered cortical dynamics and disrupted cerebellar‐cortical communication. However, we lack a mechanistic understanding of how these circuit alterations mediate behavioral phenotypes, presenting a major obstacle in understanding and treating autism etiopathology. I will employ a dual-species strategy, leveraging targeted viral optogenetic perturbations in the macaque and precision genetic access in the mouse, to investigate the impact of specific alterations in neural population dynamics within complex motor behaviors. This approach will elucidate the neural computational links between circuit derangements and a diverse array of motor‐cognitive phenotypes associated with autism. These impairments are inherently quantifiable and present early in childhood, offering an opportunity for refined diagnosis and robust outcome measures in the development of novel treatments. Moreover, the pervasiveness of autism symptoms across modalities suggests neurodevelopmental abnormalities affecting multiple brain systems. Consequently, precise characterization of the neural underpinnings of motor dysfunction may yield insights into parallel deficits in cortical and cerebellar circuits that control language production, social interaction and cognitive flexibility.

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