Elizabeth Fisher

BIOGRAPHY

ACADEMIC POSITION:
Professor, Department of Neurodegenerative Disease

AWARDS:
• Faculty Member of the Year winner for Neurological Disorders 2011
• Fellow of the Society of Biology 2010
• Membership of EMBO 2009
• Fellow of the Academy of Medical Sciences 2007

RESEARCH INTERESTS:
We are interested in learning more of the genetic basis of two disorders that involve neurodegeneration in humans: motor neuron diseases and Down syndrome. We work with the mouse as a genetic model of humans. Motor neuron diseases (MNDs) are common and incurable, and arise when the motor neurons that extend from the brain into the spinal cord and out to the muscles, degenerate and die. Spinal muscular atrophy, one form of MND is the biggest single genetic killer of children, and amyotrophic lateral sclerosis (ALS) is an adult form of MND that arises in mid-life. Although single genes are known that cause MNDs, it is not clear how the mutant genes exert their effects or what other genes can modify the pathways involved. Many different cellular systems are affected, including the transport of vesicles, organelles, molecules, in the axon and cell body. We are particularly interested in one transport complex, dynein, which transports many different cargoes from the synapse to the cell body and which moves vesicles around in the cell body. We are looking at the effects of mutant dynein and how this relates to motor neuron cell death. We are also working with mouse models of Down syndrome. Down syndrome is the most common known genetic form of mental retardation. Down syndrome commonly results in the histopathology of Alzheimer's disease in the brain, in the mid-30s (although not necessarily behavioural changes). Some form of neurodegeneration may be taking place, and, interestingly, there are also changes in axonal transport in Down syndrome. We are characterizing our mouse models in order to look specifically at axonal transport, and then to try to work out which genes are responsible for any changes we find, as such genes are likely to be important for neurodegeneration in the general population.

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