Dr Andrew Furley: Research

Work in our laboratory is focussed on the function of a family of neural cell adhesion molecules related to the human proteins L1CAM and CNTN (L1CNTNs). Humans with mutations in L1CAM suffer a spectrum of neurological disease from mild mental retardation through to severe childhood hydrocephalus (Kenwrick et al., 2000).

We have shown that some aspects of this disease can be explained by defects in the guidance of cortical axons to the spinal cord through the pyramidal decussation during development (Cohen et al., 1998).

However, as large multidomain cell surface molecules, the functions of L1 and its sister molecules (e.g. NrCAM, TAG-1, F3/contactin) are complex and these proteins have been implicated in a wide variety of neural diseases from Multiple Sclerosis to Autism (Katidou et al., 2008), through involvement in processes as different as the proliferation of neural stem cells and progenitors (Dihne et al., 2003; Bizzoca et al., 2003), to the organisation of mature cellular structures such as the Node of Ranvier (Poliak et al., 2003).

To understand this complexity, we are using a combination of cell biological, transgenic and knockout techniques. Current work in the laboratory is focussed on the mechanism of L1CNTN function in sensory neuron axon guidance (Law et al., 2008; Dang et al., 2012), and in the control of neural progenitor and stem cell proliferation and differentiation (Xenaki et al., 2011; Bizzoca et al., 2012).

Additionally, we are interested in these also in the context of diseases of the nervous system, including particularly ataxia, addiction and medulloblastoma.

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