Saturday, 27 June, 2020
Wolfgang Griswold, MD, PhD, FAAN, Ludvig Boltzmann Institute for Experimental und Clinical Traumatology, Vienna, Austria
Title: Toxic Neuropathies
14.35 - 15.05 (EDT)
Toxic Neuropathies Toxic neuropathies have several causes and the classification goes far beyond the axonal and demyelinating type. In addition to the commonly considered targets for toxicity as the dorsal root ganglia, nerve and axons, also receptors , nerve ending and small fibers need to be considered. Also Ion channels and ionophores are sites of toxicity. The onset of toxicity can be acute, is usually delayed, but can also result in late effects, and is rarely also self propagating.
The frequency of toxic neuropathy is not known, and in addition to commonly used industrial agents, heavy metals, drugs , recreational substances, also rare and nutritional neuropathies occur.
Biography: Prof. Wolfgang Grisold is a specialist for neurology and has a background in neuropathology and neurophysiology. Special interests are general neurology, neurooncology,
|neuromuscular disease in particular in regard to peripheral nerves and the neuromuscular system in cancer He has participated in EU projects on paraneoplastic syndromes. He has experience with autoimmune diseases, in particular myasthenia gravis and inflammatory neuropathies. He is involved in several international neurological societies and has organized several international neurological congresses, among the EANO congress in 2006 in Vienna , the ICNMD 2018, and was involved in the organization of the World Congress of Neurology 2013, in Vienna, as the congress secretary.|
Francesca Bartolini, PhD, Columbia University, New York, NT, USA
Title: Pathogenic Role of Tubulin Post Translational Modifications in Axon Degeneration
15.05 - 15.35 (EDT)
Tubulin, its post-translational modifications, microtubule dynamics and stability play critical roles in neurons, including regulation of long-distance transport, microtubule severing, Ca2+ homeostasis and mitochondria energetics. Each of these functions provides a potential mechanism underlying axon degeneration. Herein, we report that in sensory neurons the CIPN inducing drug bortezomib causes axonopathy and disrupted mitochondria motility by increasing delta 2 tubulin, the only irreversible tubulin modification and marker of hyperstable microtubules. Our data provide a new paradigm for the risk associated with enhanced tubulin longevity in the onset of peripheral neuropathy and offer the unexplored potential for targeting the enzymes involved in this tubulin modification in drug therapies aimed at preventing axonal injury observed in CIPN and possibly other types of related neuropathies.
|Biography: I have a broad knowledge in the field of tubulin biochemistry and microtubule stabilization. When I founded my lab in 2013, I focused my interests to the role of microtubule stability in the onset of neurodegeneration and neuropathic disease. Control of microtubule dynamics and tubulin post-translational modifications is critical to neuronal viability and most of CIPN causing drugs are tubulin poisons. However, virtually nothing is known about whether anomalies in microtubule dynamics and/or tubulin post-translational modifications in sensory neurons can initiate CIPN and whether these changes are primary to disruption of axonal integrity in CIPN and related peripheral neuropathies.|