Department of Clinical Neurosciences
Cambridge Institute for Medical Research (CIMR)
The chronic presence of cell injury and damage in Alzheimer’s disease (AD) leads to glial activation and increased production of inflammatory cytokines, which in turn lead to further neuronal damage (Morales I. et al., 2014). Recent Genome wide-association studies (GWAS) have identified several disease-associated genetic variants among AD patients, including a missense mutation in ABI3 (Sims R. et al., 2017). ABI3 is an adaptor protein involved in actin cytoskeleton organisation by participating in the WAVE2 complex (Hirao N. et al., 2006) and has been shown to inhibit tumor metastasis in vitro (Latini F. et al., 2011). In the brain, ABI3 is highly expressed in microglia however, its role in microglial cellular functions is poorly understood. I am currently investigating the changes in ABI3 expression and cellular function in microglia in the context of AD. The further aim of my PhD project is to investigate the functional link between AD-associated mutant ABI3 and microglial function.
Recombinant protein expression
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