Dr Thomas Ridler
Postdoctoral Research Associate
Hatherly Hatherly Labs
Hatherly Building, University of Exeter, Prince of Wales Road, Exeter, EX4 4PS, UK
Tom received an undergraduate masters (MSci) in ‘Neuroscience with study in industry’ from the University of Bristol, during which time he spent a year working at Eli Lilly on new drug targets for cognitive impairment in Alzheimer’s and Schizophrenia. He moved to Exeter as a PhD student under the supervision of Dr Jon Brown and Prof Andrew Randall. He continues to work in the Exeter applied Neurophysiology group investigating entorhinal cortex dysfunction in rodent models of dementia.
- MSci Neuroscience with study in industry (University of Bristol)
- PhD Medical Studies (University of Exeter)
Tom is interested in how neurological diseases such as Alzheimer’s disease and frontotemporal dementia produce changes to neuronal networks that ultimately affect cognitive processes. He uses in vivo electrophysiological recordings to measure the activity of neurons from awake-behaving mice, either at the level of single-cells or through large-scale neuronal networks. His current work focuses on the medial entorhinal cortex, one of the first areas to be affected by Alzheimer’s disease pathology, which is essential for processing spatial information.
Ridler, T. , Witton, J. , Phillips, K. G., Randall, A. D. and Brown, J. T. Impaired speed encoding is associated with reduced grid cell periodicity in a mouse model of tauopathy. bioRxiv 595652; doi: https://doi.org/10.1101/595652
Ridler, T. , Matthews, P. , Phillips, K. G., Randall, A. D. and Brown, J. T. (2018), Initiation and slow propagation of epileptiform activity from ventral to dorsal medial entorhinal cortex is constrained by an inhibitory gradient. J Physiol, 596: 2251-2266. doi:10.1113/JP275871
Booth CA*, Ridler T*, Murray TK, Ward MA, de Groot E, Goodfellow M, Phillips KG, Randall AD, Brown JT (2016). Electrical and Network Neuronal Properties Are Preferentially Disrupted in Dorsal, But Not Ventral, Medial Entorhinal Cortex in a Mouse Model of Tauopathy. J Neurosci, 36(2), 312-324; DOI: https://doi.org/10.1523/JNEUROSCI.2845-14.2016 *equal contributions