Dr. Michael Telias

michaelBackground: Dr. Michael Telias is a molecular and cellular neuroscientist. He holds a B.Sc. in Medical Sciences and a M.Sc. in Medical Neurobiology from the Hadassah Medical School & the Faculty of Medicine at the Hebrew University in Jerusalem, Israel. He earned his Ph.D. from the Sackler Faculty of Medicine at Tel Aviv University & the Sourasky Tel Aviv Medical Center. During his Ph.D. he developed human embryonic stem cell (hESC) lines carrying naturally occurring disease-related mutations, diagnosed by pre-implantation genetic diagnosis (Frumkin T, et al., In Vitro Cell Dev Biol, 2010). Using hESC lines carrying the full mutation at the FMR1 locus (Fragile X Syndrome, FXS), Dr. Telias developed neural differentiation protocols and assessed in-vitro neurogenesis of FXS-hESCs as compared to non-mutated counterparts (Telias M, et al., Dev Biol, 2013). Using advanced electrophysiological and molecular techniques, he was able to uncover molecular and cellular phenotypes associated with human FXS neurons that are not observed in animal models for the same disease (Telias M, et al., Stem Cells & Dev. 2015; Telias M, et al., J of Neurosci. 2015; Telias M, et al., Front. Cell. Neurosci. 2016). To date, he has contributed to the publication of 11 PubMed-indexed original scientific papers, 7 of them as first author. For his work, he was awarded with the prestigious Teva National Network of Excellence doctoral scholarship in 2014-2015, among others.

Current Research: As a postdoctoral researcher at the Kramer Lab, Dr. Telias is investigating the molecular and cellular mechanisms underlying electrophysiological remodeling in blind retinas. Upon death of photoreceptors, the surviving retinal layers undergo a dramatic transformation known as “remodeling”. Among other things, remodeling causes retinal ganglion cells (RGCs) to become hyper-excitable, which in turns reduces the fidelity of a super-imposed signal conferred to the retina by vision restoration methodologies, from photo-switches to retinal prosthetics. Therefore, to be able to restore meaningful vision to the blind, we first need to elucidate what is remodeling (i.e., the abnormal intracellular mechanisms and pathways), and what causes it (i.e., what is the signal lost/gained upon photoreceptor death). Dr. Telias is investigating these questions using a combination of electrophysiological, biochemical approaches, including patch-clamp recordings, calcium imaging, immunohistochemistry and qPCR. This work also involves the development of specific mouse strains carrying mutations and reporter genes, as well as the use of viruses to manipulate gene expression in-vivo. He is especially interested in the role played by P2X receptors and HCN channels during retinal degeneration, and how these two components, which are essential for the activity of the photoswitch BENAQ, are related to each other and to the pathophysiology of remodeling.