Eva Pennink ep736@cam.ac.uk
United Kingdom
Cambridge Institute for Medical Research and the Neuroscience Research Centre, Downing College
PhD thesis: TBC
Research interests:
- Dissecting the complex intracellular trafficking mechanisms and cytoskeletal changes that contribute towards maintaining cellular homeostasis.
- Understanding influence of microglia and astrocytes on neuronal health and disease in the central nervous system.
- Modelling neurodegenerative disease in vitro with complex multicellular models.
- Research that informs the development of novel therapeutics that reduce disease pathology and are beneficial for patients.
Neurodegeneration is commonly associated with the accumulation of protein aggregates, which in turn stimulate inflammatory microglia and astrocytes. These glial cells provide neuroprotection through the phagocytosis and degradation of toxic proteins. Myosin motor proteins centrally modulate glial cell functions by regulating intracellular trafficking events and cell morphology.
I will focus my research on myosin VI (MYO6), expressed in astrocytes, and two class I myosins (MYO1F and MYO1G), exclusively found in microglia. By determining the MYO6 interactome within astrocytes and utilising high-resolution localisation experiments I will study its contribution towards endocytosis, autophagy and astrogliosis. To investigate the role of MYO1F and MYO1G in microglial migration, phagocytosis and cytokine secretion I plan to generate gene knockouts, pharmacologically manipulate protein activity and stimulate microglia with pathological insults. Harnessing advanced multicellular organoid models will allow me to study glial cell myosin motor proteins in the context of health or disease.
Who or what inspired you to pursue your research interests?
Seeing the devastating consequences of neurodegeneration first-hand has had led me to commit my research career towards understanding and treating these diseases.
Through my previous work in the discovery and development of therapeutics against Parkinson’s disease and amyloid lateral sclerosis I realised the gaps that remain in our knowledge of the intracellular and intercellular molecular mechanisms that underly disease pathogenesis. Advances in this area of research will enable the identification of novel drug targets and delivery of transformational medicines that are capable of reducing pathological phenotypes to provide patients with long-term benefits.