Centre for Brain Research seminar: Nrf2/ARE signalling as a novel target for amyotrophic lateral sclerosis Event as iCalendar

Dr. Kiaei is a graduate of Otago University in Biochemistry. Currently he is an Assistant Professor and director of a leading research laboratory at the University of Arkansas for Medical Sciences (UAMS) in Little Rock, Arkansas, USA. His research focuses on investigating the mechanism(s) of neurodegeneration and developing therapeutic strategies for ALS. Dr. Kiaei has conducted several preclinical therapeutic studies using mouse model of ALS. He has published multiple studies on the pathogenesis of ALS and testing drugs that block neuroinflammation, oxidative damage in ALS mice.

Dr. Kiaei has recently moved his laboratory to the University of Arkansas for Medical Sciences in the Department of Neurobiology and Developmental Sciences. He uses transgenic mouse models of ALS as well as primary astrocytes and motor neurons to study the pathogenesis of motor neuron degeneration. Current projects in his laboratory include Nrf2/ARE signaling, its mechanism and involvement in neurodegeneration and implication as an endogenous neuroprotective pathway to block neurodegeneration. Dr. Kiaei’s lab is also interested to study the latest genetic linkage and discoveries for ALS, such as TDP-43 mutation and TDP-43 proteinopathy, Ubiqulin2 mutation, and hexanucleotide repeat expansion (C9ORF72) that cause familial ALS.

Dr. Kiaei’s seminar will be a discussion on his new discoveries on Nrf2/ARE (NF-E2 related factor 2/antioxidant response element) signaling program as a promising target for the treatment of ALS and other neurodegenerative diseases. Nrf2 is a key regulatory factor in the coordinated induction of the ARE-driven “battery” of neuroprotective genes, including, antioxidant, anti-inflammatory and mitochondrial protective genes. Oxidative damage, neuroinflammation and mitochondrial dysfunction are all implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases. These pathophysiological pathways play pivotal role in neuronal death. Nrf2/ARE signaling has the capability to control these pathways and thus, exploration of the Nrf2/ARE pathway as a target for neurotherapeutics in neurodegenerative diseases is of high importance and very promising.