Dr Amy Reeve
I first became interested in mitochondrial biology in 2004 when I came to Newcastle to study for my PhD. My PhD project investigated the importance of mitochondrial dysfunction to neurodegeneration, with a particular focus on Parkinson’s.
Since completing my PhD my research has focussed on understanding whether neurons are capable of adapting to mitochondrial dysfunction and whether this is something that we might be able to promote using drugs. My primary interest still lies in investigating these changes in relation to Parkinson’s and this forms the basis of my Parkinson’s UK Fellowship (F-1401).
In order to understand the importance of mitochondrial defects to neuron loss in Parkinson’s, we study a number of different aspects of mitochondrial biology from their structure and dynamics, to their neuronal location and calcium buffering capabilities. Furthermore, I am interested in how astrocytes might be important for the ability of neurons to adapt to mitochondrial dysfunction and how these important glial cells might help support neuronal mitochondrial function.
- Awarded a £136,677 Michael J Fox Foundation Mitochondrial Biomarkers program grant (2018-2020).
- Awarded a £164,000 Senior Fellowship extension by Parkinson’s UK (2017-2019)
- Awarded a £250,000 Career Development Award by Parkinson’s UK (2014-2017)
Recently we found that the distribution of mitochondria to the distal parts of neurons (synapses and axons) was altered in Parkinson’s and we uncovered a population of synapses which were devoid of mitochondrial proteins. We are investigating whether this is evidence of an adaptation to mitochondrial dysfunction and the role which astrocytes play in supporting and modulating neuronal mitochondrial populations.
The movement of mitochondria around dopaminergic neurons is essential to ensure energy provision to support neuronal function. We study the impact of mitochondrial dysfunction and alpha-synuclein on the movements of mitochondria in model systems.
Using Image mass cytometry, a cutting edge technology which enables up to 30 protein targets to be examined in a single neuron we are gathering information about the response of neurons to mitochondrial defects and alpha-synuclein accumulation.
We are working with collaborators within the Centre to design a system in which we can screen for compounds which are capable of improving the survival of dopaminergic neurons with mitochondrial defects.