Centre for Discovery Brain Sciences
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Alannah Mole

Alannah Mole's biography and research focus.

Miss Alannah Mole

PhD Student - Murray Lab

  • Hugh Robson Building
  • 15 George Square
  • Edinburgh, EH8 9XD

Contact details

Personal profile

Representative confocal micrograph showing die-back pathology in an immunohistochemically-labelled external oblique muscle preparation from a late-symptomatic Smn2B/- mouse model
Representative confocal micrograph showing die-back pathology in an immunohistochemically-labelled external oblique muscle preparation from a late-symptomatic Smn2B/- mouse model
  • 2012-2017 MSci Neuroscience, University of Glasgow

Research

Nerve axons degenerate during development, following injury and across a range of neurodegenerative conditions, including motor neurone diseases. Degeneration can proceed as a retraction (die-back) away from the muscle (Fig. 1), or as a fragmentation of the axon, in a process known as Wallerian degeneration. Evidence suggests that these two mechanisms operate discretely. For example, Wallerian degeneration is delayed following a nerve injury during die-back conditions both in disease and during normal development in mice. It is therefore tempting to hypothesise that die-back mechanisms somehow oppose Wallerian degeneration pathways, however, evidence of this is limited. Mitochondrial defects have been reported in a number of die-back neuropathies. An increase in mitochondrial proteins has also been associated with an acceleration in Wallerian degeneration. We hypothesise that changes in mitochondrial dynamics contribute to determining the rate of Wallerian degeneration.

My project aims to develop and utilise an ex vivo model of peripheral nerve injury to investigate the role that mitochondria play in protecting axons from injury during neonatal development, and explore whether similar changes are also responsible for the delay in Wallerian degeneration observed during die-back neuropathies. Overall, this will help us to better understand the mechanisms that are involved in governing the rate of axonal degeneration, which is key if we are to target neurodegeneration.