Acquired epilepsy in Alzheimer’s disease
People with Alzheimer's disease (AD) are 10 times more likely to develop epilepsy compared with age-matched controls. Recurrent seizures and their treatment with conventional antiepileptic drugs may exacerbate cognitive decline, yet the pathological basis for the increased risk of epilepsy is largely unknown, and there are no treatments that prevent epilepsy in AD patients. The relationships between the pathological processes of AD and neuronal hyperexcitability are poorly understood. Elucidating the pathomechanisms of epileptogenesis in AD is critical in identifying effective therapeutic strategies to prevent the development of epilepsy in this high risk and vulnerable population.
The novelty of this project lies in its aims to directly address the mechanisms of epileptogenesis in AD through the study of relevant animal models of AD and acquired epilepsy. It will identify the mechanistic processes of epileptogenesis in AD under a coherent hypothesis. The aims will be achieved by subjecting transgenic AD models reflecting the pathological hallmarks to acquired epileptogenesis and treating them novel compounds. The phenotypic changes (epileptogenesis and cognitive/behavioural outcomes) will be correlated with the molecular and cellular changes in these pathways.
- Dr Jianxiong Chan, Post-doc (molecular biology)
- Ms Juliana Silva, PhD student
- A/Prof Nigel Jones
This research project is available to PhD students to join as part of their thesis.
Please contact the Research Group Leader to discuss your options.
- Chan J, Jones NC, Bush AI, O'brien TJ, Kwan P. A mouse model of Alzheimer's disease displays increased susceptibility to kindling and seizure-associated death. Epilepsia 2015 56 (6), e73-e77.