Caoimhe Goldrick
Academic and Work Experience Prior to Sept 2021 Programme Start
I obtained my bachelor’s degree in Neuroscience from University College Dublin, Ireland. During this time, I undertook a Wellcome Trust-funded project at UCD in the area of Alzheimer’s Disease, as well as an Erasmus placement at Cambridge University modelling Pelizaeus-Merzbacher disease with iPSCs, in the lab of Prof David Rowitch.
Following my studies, I became a research assistant at the National Institute for Cellular Biotechnology at Dublin City University. Here, I developed organotypic models of uveal melanoma from primary patient tumours during a post of 18-months.
Following this, I moved to London where I took up a research assistant position at KCL, exploring the role of molecular chaperones in iPSC-derived astrocytes in the context of Alzheimer's Disease.
PhD Programme- Year 1- MRes and Project Rotations
The MRes year allowed me to gain a wide range of experience through different research projects:
For my first rotation, I joined the lab of Prof Benedikt Berninger. Here, I generated iPSC-derived astrocytes with a view to performing lineage reprogramming of glia into neurons.
During my second rotation, I worked with Dr Ivo Lieberam and Prof Juan Burrone. In this project, I characterised channelrhodopsins and developed iPSC-based elements of neural circuits for integration into a biohybrid robot.
In my final rotation, I worked with Dr Ciro Chiappini and Dr Andrea Serio at the Francis Crick institute. My project focused on investigating mitochondrial dynamics in iPSC-derived astrocytes using nanoneedles
PhD Programme- Years 2 to 4 - Doctoral Studies
My PhD research will take place in the labs of Dr Ivo Lieberam and Prof Juan Burrone. investigating altered cortical excitability in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). FTD and ALS are progressive diseases of the central nervous system that form a neurodegenerative spectrum. Among the most commonly shared genetic alterations in FTD and ALS are TDP-43 pathology and C9orf72 hexanucleotide repeat expansion (C9orf72RE). Increasingly, abnormal cortical and motor neuron excitability is described in FTD and ALS, with such disruptions thought to drive early pre-clinical pathology.
I will investigate pathways driving altered cortical excitability by identifying and examining functional consequences of aberrant splicing events in hiPSC-neuronal circuits models with TDP-43 and C9orf72RE patient genotypes. In our approach, we will collate previously published datasets to bioinformatically identify promising candidate abnormal splicing events, like those impacting neuronal excitability. Furthermore, I will establish the functional consequences of altered splicing by assessing neural activity in hiPSC-neuronal networks with electrophysiology and imaging methods. This research aims to further our understanding of early pathways leading to altered cortical excitability in FTD and ALS.
