I received my PhD in Neuroscience from Northwestern University’s Feinberg School of Medicine where I focused on the post-translational modifications of Tau and their role in self-aggregation in Alzheimer’s disease (AD) and other neurogenerative conditions known as non-AD tauopathies.
Given my keen interest in neuroscience and the spreading of hallmark pathology associated with neurodegeneration, I pursued a post-doctoral position at Lund University (Sweden) and then at the Swiss Institute of technology (EPFL), where I focused on the mechanisms of alpha-synuclein transmission in cellular and animal models of Parkinson’s disease (PD) and Multiple System Atrophy (MSA), a related synucleinopathy.
Currently, I am a Senior Research Fellow focusing on the role of cellular connectivity and the spreading of hallmark pathology associated with PD and AD. Our recent work identified a novel molecular mechanism involving the gap junction proteins, the connexins (Cx), in the transmission of alpha-synuclein pathology both in neurons and oligodendrocytes, cell types vulnerable to alpha-synuclein accumulation in PD and MSA, respectively, (Reyes et al., Acta Neuropathologica, 2019).
It is now widely established that aside from the brain, alpha-synuclein accumulation also appears in multiple peripheral tissues in PD. Consistent with these findings, we recently identified alpha-synuclein accumulation in PD and observed a time dependent accumulation of alpha-synuclein pathology in the liver in multiple animal models of PD and MSA, suggesting a potential liver involvement in the clearance of PD associated pathology (Reyes et al., Acta Neuropathologica Comm. 2021).