Dr Caroline Herron

Main interest are in alterations in synaptic function and synaptic plasticity in models of Alzheimer's disease. Synaptic plasticity (long-term potentiation ; LTP) linked to memory is known to be reduced in transgenic mice that express FAD mutations. In addition amyloid derived diffusible ligands which are synthetic forms of oligomeric beta amyloid also disrupt LTP in the hippocampus. We have investigated how potential therapeutic agents including Il1beta- receptor antagonist, JNK inhibitors, L-type calcium channel blockers, peroxisome proliferator activated receptor agonists (PPARg), simvastatin and more recently cannabidiol (the non-psychoactive component of cannabis) can attentuate the effects of beta amyloid and also reverse deficits in LTP in transgenic mouse models. Techniques: Brain slice electrophysiology; Western blot quantification of beta amyloid and associated alterations in signalling proteins; cell viability assays; Elisa.