Several neurological diseases have been associated with the activation of multiple immune signalling pathways as the classical complement pathway. Such overactivated immune signalling, which is proposed to contribute to the disease progression, is linked to an increase in expression of pro-inflammatory cytokines, aberrant activation of glial cells and dysregulated glial-neuronal interactions. My research project therefore seeks to investigate the underlying mechanisms and consequences of chronic complement pathway activation in neurodegeneration and genome instability disorders such as Ataxia Telangiectasia.
