![Gaynor Smith](https://profiles-cardiff.imgix.net/attachments/2602?w=200&h=200&auto=format&crop=faces&fit=crop&q=90")
Dr Gaynor Smith
(she/her)
- Available for postgraduate supervision
Teams and roles for Gaynor Smith
Senior Lecturer, Dementia Research Institute
Overview
Molecular mechanisms of neurobiology, mitochondrial biology and neurodegenerative disease
Neurodegenerative disorders such as Alzheimer’s, Parkinson’s and Huntington’s diseases are incurable and debilitating conditions that result in the progressive degeneration of different neuronal populations. Mitochondrial dysfunction, protein aggregation and altered glial responses are unifying features across these diseases and even manifest in prodromal stages. My laboratory is interested in understanding the conserved molecular and cellular mechanisms underpinning these basic neurobiological processes, from Drosophila to humans.
Research Goals:
- To discover new genes which control mitochondria maintenance in neurons using an unbiased in vivo genetic approach.
- To investigate how new genes discovered from GWAS approaches contribute to the pathological mechanisms of Alzheimer’s disease.
Affiliations:
UK Dementia Research Institute (UK DRI)
Division of Psychological Medicine and Clinical Neurosciences (DPMCN)
https://www.cardiff.ac.uk/medicines-discovery/about-us
Medicines Discovery Institute (MDI)
https://www.medicinesdiscoveryinstitute.com/
Publication
2024
- Kors, S. et al., 2024. New insights into the functions of ACBD4/5-like proteins using a combined phylogenetic and experimental approach across model organisms. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1871 119843. (10.1016/j.bbamcr.2024.119843)
2023
- Maddison, D. et al. 2023. Analysis of mitochondrial dynamics in adult drosophila axons. Cold Spring Harbor Protocol 2023 (2) 107819. (10.1101/pdb.top107819)
- Maddison, D. et al. 2023. Clonal imaging of mitochondria in the dissected fly wing. Cold Spring Harbor Protocol 2023 (2) 108051. (10.1101/pdb.prot108051)
- Maddison, D. C. et al. 2023. COPI-regulated mitochondria-ER contact site formation maintains axonal integrity. Cell Reports 42 (8) 112883. (10.1016/j.celrep.2023.112883)
- Mattedi, F. et al., 2023. Live imaging of mitochondria in the intact fly wing. Cold Spring Harbor Protocol 2023 (2) 108052. (10.1101/pdb.prot108052)
- Rees, D. et al., 2023. Acyl-ghrelin attenuates neurochemical and motor deficits in the 6-OHDA model of Parkinson’s Disease. Cellular and Molecular Neurobiology 43 , pp.2377-2384. (10.1007/s10571-022-01282-9)
- Smith, G. et al. 2023. How neurons maintain their axons long-term: an integrated view of axon biology and pathology. Frontiers in Neuroscience 17 1236815. (10.3389/fnins.2023.1236815)
- Townsend, L. N. et al., 2023. Cdk12 maintains the integrity of adult axons by suppressing actin remodeling. Cell Death Discovery 9 (1) 348. (10.1038/s41420-023-01642-4)
2021
- Lin, T. et al., 2021. TSG101 negatively regulates mitochondrial biogenesis in axons. Proceedings of the National Academy of Sciences 118 (20) e2018770118. (10.1073/pnas.2018770118)
- Peters, O. M. et al. 2021. Genetic diversity of axon degenerative mechanisms in models of Parkinson's disease. Neurobiology of Disease 155 105368. (10.1016/j.nbd.2021.105368)
2020
- Precious, S. V. et al. 2020. Dopaminergic progenitors derived from epiblast stem cells function similarly to primary VM-derived progenitors when transplanted into a Parkinson’s disease model. Frontiers in Neuroscience 14 312. (10.3389/fnins.2020.00312)
2019
- Malik, B. R. et al. 2019. Autophagic and endo-lysosomal dysfunction in neurodegenerative disease. Molecular Brain 12 (1) 100. (10.1186/s13041-019-0504-x)
- Smith, G. A. et al. 2019. Glutathione-S-transferase regulates mitochondrial populations in axons through increased glutathione oxidation. Neuron 103 (1), pp.52-65.e6. (10.1016/j.neuron.2019.04.017)
2017
- Breger, L. S. et al. 2017. Influence of chronic L-DOPA treatment on immune response following allogeneic and xenogeneic graft in a rat model of Parkinson's disease. Brain, Behavior, and Immunity 61 , pp.155-164. (10.1016/j.bbi.2016.11.014)
2016
- Lewis, E. A. and Smith, G. A. 2016. Using Drosophila models of Huntington's disease as a translatable tool. Journal of Neuroscience Methods 265 , pp.89-98. (10.1016/j.jneumeth.2015.07.026)
- Smith, G. A. et al. 2016. Fibroblast biomarkers of sporadic Parkinson's Disease and LRRK2 kinase inhibition. Molecular Neurobiology 53 (8), pp.5161-5177. (10.1007/s12035-015-9435-4)
2015
- Hallett, P. et al., 2015. Successful function of Autologous iPSC-derived dopamine neurons following transplantation in a non-human primate model of Parkinson's disease. Cell Stem Cell 16 (3), pp.269-274. (10.1016/j.stem.2015.01.018)
- Rocha, E. M. et al., 2015. Glucocerebrosidase gene therapy prevents α-synucleinopathy of midbrain dopamine neurons. Neurobiology of Disease 82 , pp.495-503. (10.1016/j.nbd.2015.09.009)
- Rocha, E. M. et al., 2015. Progressive decline of glucocerebrosidase in aging and Parkinson's disease. Annals of Clinical and Translational Neurology 2 (4), pp.433-438. (10.1002/acn3.177)
- Rocha, E. M. et al., 2015. Sustained systemic glucocerebrosidase inhibition induces brain α-Synuclein aggregation, microglia and complement C1q activation in mice. Antioxidants and Redox Signaling 23 (6), pp.550-564. (10.1089/ars.2015.6307)
- Smith, G. A. et al. 2015. A nurr1 agonist causes neuroprotection in a Parkinson's Disease lesion model primed with the toll-like receptor 3 dsRNA inflammatory stimulant poly(I:C). PLoS ONE 10 (3) e0121072. (10.1371/journal.pone.0121072)
2014
- Davies, S. E. et al., 2014. Enhanced ubiquitin-dependent degradation by Nedd4 protects against α-synuclein accumulation and toxicity in animal models of Parkinson's disease. Neurobiology of Disease 64 , pp.79-87. (10.1016/j.nbd.2013.12.011)
- McLean, J. R. et al., 2014. ALS-associated peripherin spliced transcripts form distinct protein inclusions that are neuroprotective against oxidative stress. Experimental Neurology 261 , pp.217-229. (10.1016/j.expneurol.2014.05.024)
- McLean, J. R. et al., 2014. Widespread neuron-specific transgene expression in brain and spinal cord following synapsin promoter-driven AAV9 neonatal intracerebroventricular injection. Neuroscience Letters. 576 , pp.73-78. (10.1016/j.neulet.2014.05.044)
- Smith, G. A. et al. 2014. Progressive axonal transport and synaptic protein changes correlate with behavioral and neuropathological abnormalities in the heterozygous Q175 KI mouse model of Huntington's disease. Human Molecular Genetics 23 (17), pp.4510-4527. (10.1093/hmg/ddu166)
2013
- Heuer, A. , Smith, G. A. and Dunnett, S. B. 2013. Comparison of 6-hydroxydopamine lesions of the substantia nigra and the medial forebrain bundle on a lateralised choice reaction time task in mice. European Journal of Neuroscience 37 (2), pp.294-302. (10.1111/ejn.12036)
- Peters, O. M. et al. 2013. Chronic administration of dimebon does not ameliorate amyloid-β pathology in 5xFAD transgenic mice. Journal of Alzheimer's Disease 36 (3), pp.589-596. (10.3233/JAD-130071)
- Smith, G. A. and Snyder, E. Y. 2013. Two cells are better than one: optimizing stem cell survival by co-grafting “helper” cells that offer regulated trophic support. Experimental Neurology 247 , pp.751-754. (10.1016/j.expneurol.2013.07.003)
- Sundberg, M. et al., 2013. Improved cell therapy protocols for Parkinson's disease based on differentiation efficiency and safety of hESC-, hiPSC-, and non-human primate iPSC-derived dopaminergic neurons. Stem Cells 31 (8), pp.1548-152. (10.1002/stem.1415)
2012
- Heuer, A. et al. 2012. Unilateral nigrostriatal 6-hydroxydopamine lesions in mice I: Motor impairments identify extent of dopamine depletion at three different lesion sites. Behavioural Brain Research 228 (1), pp.30-43. (10.1016/j.bbr.2011.11.027)
- Smith, G. A. et al. 2012. Pharmacological modulation of amphetamine-induced dyskinesia in transplanted hemi-parkinsonian rats. Neuropharmacology 63 (5), pp.818-828. (10.1016/j.neuropharm.2012.06.011)
- Smith, G. A. , Dunnett, S. B. and Lane, E. L. 2012. Amphetamine-induced rotation in the transplanted hemi-parkinsonian rat - Response to pharmacological modulation. Behavioural Brain Research 232 (2), pp.411-415. (10.1016/j.bbr.2012.04.003)
- Smith, G. A. et al. 2012. Unilateral nigrostriatal 6-hydroxydopamine lesions in mice II: Predicting L-DOPA-induced dyskinesia. Behavioural Brain Research 226 (1), pp.281-292. (10.1016/j.bbr.2011.09.025)
- Smith, G. A. et al. 2012. L-dopa and graft-induced dyskinesia in the 6-OHDA-lesioned mouse [Abstract]. Cell Transplantation 21 (4), pp.792-792.
- Smith, G. A. , Isacson, O. and Dunnett, S. B. 2012. The search for genetic mouse models of prodromal Parkinson's disease. Experimental Neurology 237 (2), pp.267-273. (10.1016/j.expneurol.2012.06.035)
- Smith, G. A. et al. 2012. Amphetamine-induced dyskinesia in the transplanted hemi-Parkinsonian mouse. Journal of Parkinson's Disease 2 , pp.107-113. (10.3233/JPD-2012-12102)
2011
- Lane, E. L. et al. 2011. Context-driven changes in 1-DOPA-induced behaviours in the 6-OHDA lesioned rat. Neurobiology of Disease 42 (1), pp.99-107. (10.1016/j.nbd.2011.01.010)
- Smith, G. 2011. Optimisation and mechanistic insights of dyskinesia in rodent models of Parkinson’s disease. PhD Thesis , Cardiff University.
- Smith, G. A. et al. 2011. Developments in Graft-Induced Dyskinesia [Abstract]. Cell Transplantation 20 (4), pp.584-585.
- Smith, G. A. , Lane, E. L. and Dunnett, S. B. 2011. Graft-Induced Dyskinesia in Transplanted Hemiparkinsonian Mice and Rats: A Pharmacological Manipulation [Abstract]. Cell Transplantation 20 (4), pp.585-585.
- Torres, E. M. et al. 2011. Increased efficacy of the 6-hydroxydopamine lesion of the median forebrain bundle in small rats, by modification of the stereotaxic coordinates. Journal of Neuroscience Methods 200 (1), pp.29-35. (10.1016/j.jneumeth.2011.06.012)
2010
- Lane, E. L. and Smith, G. A. 2010. Understanding graft-induced dyskinesia. Regenerative Medicine 5 (5), pp.787-797. (10.2217/rme.10.42)
Articles
- Breger, L. S. et al. 2017. Influence of chronic L-DOPA treatment on immune response following allogeneic and xenogeneic graft in a rat model of Parkinson's disease. Brain, Behavior, and Immunity 61 , pp.155-164. (10.1016/j.bbi.2016.11.014)
- Davies, S. E. et al., 2014. Enhanced ubiquitin-dependent degradation by Nedd4 protects against α-synuclein accumulation and toxicity in animal models of Parkinson's disease. Neurobiology of Disease 64 , pp.79-87. (10.1016/j.nbd.2013.12.011)
- Hallett, P. et al., 2015. Successful function of Autologous iPSC-derived dopamine neurons following transplantation in a non-human primate model of Parkinson's disease. Cell Stem Cell 16 (3), pp.269-274. (10.1016/j.stem.2015.01.018)
- Heuer, A. , Smith, G. A. and Dunnett, S. B. 2013. Comparison of 6-hydroxydopamine lesions of the substantia nigra and the medial forebrain bundle on a lateralised choice reaction time task in mice. European Journal of Neuroscience 37 (2), pp.294-302. (10.1111/ejn.12036)
- Heuer, A. et al. 2012. Unilateral nigrostriatal 6-hydroxydopamine lesions in mice I: Motor impairments identify extent of dopamine depletion at three different lesion sites. Behavioural Brain Research 228 (1), pp.30-43. (10.1016/j.bbr.2011.11.027)
- Kors, S. et al., 2024. New insights into the functions of ACBD4/5-like proteins using a combined phylogenetic and experimental approach across model organisms. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1871 119843. (10.1016/j.bbamcr.2024.119843)
- Lane, E. L. et al. 2011. Context-driven changes in 1-DOPA-induced behaviours in the 6-OHDA lesioned rat. Neurobiology of Disease 42 (1), pp.99-107. (10.1016/j.nbd.2011.01.010)
- Lane, E. L. and Smith, G. A. 2010. Understanding graft-induced dyskinesia. Regenerative Medicine 5 (5), pp.787-797. (10.2217/rme.10.42)
- Lewis, E. A. and Smith, G. A. 2016. Using Drosophila models of Huntington's disease as a translatable tool. Journal of Neuroscience Methods 265 , pp.89-98. (10.1016/j.jneumeth.2015.07.026)
- Lin, T. et al., 2021. TSG101 negatively regulates mitochondrial biogenesis in axons. Proceedings of the National Academy of Sciences 118 (20) e2018770118. (10.1073/pnas.2018770118)
- Maddison, D. et al. 2023. Analysis of mitochondrial dynamics in adult drosophila axons. Cold Spring Harbor Protocol 2023 (2) 107819. (10.1101/pdb.top107819)
- Maddison, D. et al. 2023. Clonal imaging of mitochondria in the dissected fly wing. Cold Spring Harbor Protocol 2023 (2) 108051. (10.1101/pdb.prot108051)
- Maddison, D. C. et al. 2023. COPI-regulated mitochondria-ER contact site formation maintains axonal integrity. Cell Reports 42 (8) 112883. (10.1016/j.celrep.2023.112883)
- Malik, B. R. et al. 2019. Autophagic and endo-lysosomal dysfunction in neurodegenerative disease. Molecular Brain 12 (1) 100. (10.1186/s13041-019-0504-x)
- Mattedi, F. et al., 2023. Live imaging of mitochondria in the intact fly wing. Cold Spring Harbor Protocol 2023 (2) 108052. (10.1101/pdb.prot108052)
- McLean, J. R. et al., 2014. ALS-associated peripherin spliced transcripts form distinct protein inclusions that are neuroprotective against oxidative stress. Experimental Neurology 261 , pp.217-229. (10.1016/j.expneurol.2014.05.024)
- McLean, J. R. et al., 2014. Widespread neuron-specific transgene expression in brain and spinal cord following synapsin promoter-driven AAV9 neonatal intracerebroventricular injection. Neuroscience Letters. 576 , pp.73-78. (10.1016/j.neulet.2014.05.044)
- Peters, O. M. et al. 2021. Genetic diversity of axon degenerative mechanisms in models of Parkinson's disease. Neurobiology of Disease 155 105368. (10.1016/j.nbd.2021.105368)
- Peters, O. M. et al. 2013. Chronic administration of dimebon does not ameliorate amyloid-β pathology in 5xFAD transgenic mice. Journal of Alzheimer's Disease 36 (3), pp.589-596. (10.3233/JAD-130071)
- Precious, S. V. et al. 2020. Dopaminergic progenitors derived from epiblast stem cells function similarly to primary VM-derived progenitors when transplanted into a Parkinson’s disease model. Frontiers in Neuroscience 14 312. (10.3389/fnins.2020.00312)
- Rees, D. et al., 2023. Acyl-ghrelin attenuates neurochemical and motor deficits in the 6-OHDA model of Parkinson’s Disease. Cellular and Molecular Neurobiology 43 , pp.2377-2384. (10.1007/s10571-022-01282-9)
- Rocha, E. M. et al., 2015. Glucocerebrosidase gene therapy prevents α-synucleinopathy of midbrain dopamine neurons. Neurobiology of Disease 82 , pp.495-503. (10.1016/j.nbd.2015.09.009)
- Rocha, E. M. et al., 2015. Progressive decline of glucocerebrosidase in aging and Parkinson's disease. Annals of Clinical and Translational Neurology 2 (4), pp.433-438. (10.1002/acn3.177)
- Rocha, E. M. et al., 2015. Sustained systemic glucocerebrosidase inhibition induces brain α-Synuclein aggregation, microglia and complement C1q activation in mice. Antioxidants and Redox Signaling 23 (6), pp.550-564. (10.1089/ars.2015.6307)
- Smith, G. A. et al. 2016. Fibroblast biomarkers of sporadic Parkinson's Disease and LRRK2 kinase inhibition. Molecular Neurobiology 53 (8), pp.5161-5177. (10.1007/s12035-015-9435-4)
- Smith, G. A. et al. 2014. Progressive axonal transport and synaptic protein changes correlate with behavioral and neuropathological abnormalities in the heterozygous Q175 KI mouse model of Huntington's disease. Human Molecular Genetics 23 (17), pp.4510-4527. (10.1093/hmg/ddu166)
- Smith, G. et al. 2023. How neurons maintain their axons long-term: an integrated view of axon biology and pathology. Frontiers in Neuroscience 17 1236815. (10.3389/fnins.2023.1236815)
- Smith, G. A. et al. 2011. Developments in Graft-Induced Dyskinesia [Abstract]. Cell Transplantation 20 (4), pp.584-585.
- Smith, G. A. et al. 2012. Pharmacological modulation of amphetamine-induced dyskinesia in transplanted hemi-parkinsonian rats. Neuropharmacology 63 (5), pp.818-828. (10.1016/j.neuropharm.2012.06.011)
- Smith, G. A. , Dunnett, S. B. and Lane, E. L. 2012. Amphetamine-induced rotation in the transplanted hemi-parkinsonian rat - Response to pharmacological modulation. Behavioural Brain Research 232 (2), pp.411-415. (10.1016/j.bbr.2012.04.003)
- Smith, G. A. et al. 2012. Unilateral nigrostriatal 6-hydroxydopamine lesions in mice II: Predicting L-DOPA-induced dyskinesia. Behavioural Brain Research 226 (1), pp.281-292. (10.1016/j.bbr.2011.09.025)
- Smith, G. A. et al. 2012. L-dopa and graft-induced dyskinesia in the 6-OHDA-lesioned mouse [Abstract]. Cell Transplantation 21 (4), pp.792-792.
- Smith, G. A. , Isacson, O. and Dunnett, S. B. 2012. The search for genetic mouse models of prodromal Parkinson's disease. Experimental Neurology 237 (2), pp.267-273. (10.1016/j.expneurol.2012.06.035)
- Smith, G. A. , Lane, E. L. and Dunnett, S. B. 2011. Graft-Induced Dyskinesia in Transplanted Hemiparkinsonian Mice and Rats: A Pharmacological Manipulation [Abstract]. Cell Transplantation 20 (4), pp.585-585.
- Smith, G. A. et al. 2019. Glutathione-S-transferase regulates mitochondrial populations in axons through increased glutathione oxidation. Neuron 103 (1), pp.52-65.e6. (10.1016/j.neuron.2019.04.017)
- Smith, G. A. et al. 2015. A nurr1 agonist causes neuroprotection in a Parkinson's Disease lesion model primed with the toll-like receptor 3 dsRNA inflammatory stimulant poly(I:C). PLoS ONE 10 (3) e0121072. (10.1371/journal.pone.0121072)
- Smith, G. A. and Snyder, E. Y. 2013. Two cells are better than one: optimizing stem cell survival by co-grafting “helper” cells that offer regulated trophic support. Experimental Neurology 247 , pp.751-754. (10.1016/j.expneurol.2013.07.003)
- Smith, G. A. et al. 2012. Amphetamine-induced dyskinesia in the transplanted hemi-Parkinsonian mouse. Journal of Parkinson's Disease 2 , pp.107-113. (10.3233/JPD-2012-12102)
- Sundberg, M. et al., 2013. Improved cell therapy protocols for Parkinson's disease based on differentiation efficiency and safety of hESC-, hiPSC-, and non-human primate iPSC-derived dopaminergic neurons. Stem Cells 31 (8), pp.1548-152. (10.1002/stem.1415)
- Torres, E. M. et al. 2011. Increased efficacy of the 6-hydroxydopamine lesion of the median forebrain bundle in small rats, by modification of the stereotaxic coordinates. Journal of Neuroscience Methods 200 (1), pp.29-35. (10.1016/j.jneumeth.2011.06.012)
- Townsend, L. N. et al., 2023. Cdk12 maintains the integrity of adult axons by suppressing actin remodeling. Cell Death Discovery 9 (1) 348. (10.1038/s41420-023-01642-4)
Thesis
- Smith, G. 2011. Optimisation and mechanistic insights of dyskinesia in rodent models of Parkinson’s disease. PhD Thesis , Cardiff University.
Research
1. Discovering New Regulators of Axonal Mitochondria
We aim to identify genes that control mitochondrial maintenance in neuronal axons using unbiased, in vivo genetic approaches. Despite the central role of mitochondria in neuronal health, relatively little is known about their biogenesis, transport, dynamics, or function in axons in vivo. Yet, mitochondrial dysfunction in terminals is strongly linked to neurodegenerative disorders.
Neuronal health depends on a balance between mitochondrial degradation via mitophagy and biogenesis, pathways highly conserved from humans to invertebrates. Key players such as PINK1 and Parkin, first characterized in Drosophila, illustrate the power of genetic approaches to reveal fundamental mechanisms. Work in flies also identified Miro and Milton as critical for mitochondrial transport and regulated detachment from the cytoskeleton in high-Ca²⁺ regions.
Mitochondria are dynamic, constantly undergoing fusion and fission to regulate protein and mtDNA sharing. Regulators such as OPA1, Marf, Drp1, and Fis1 control this balance. My lab employs unbiased genetic screening in Drosophila to discover new regulators of axonal mitochondria, explore their functional roles, and understand how mitochondria communicate with other organelles, including peroxisomes and the endoplasmic reticulum, to orchestrate neuronal metabolism.
2. Understanding Genetic Contributions to Alzheimer’s Disease
We also aim to investigate how genes identified through Genome-Wide Association Studies (GWAS) contribute to the pathological mechanisms of Alzheimer’s disease. The number of people living with dementia in the UK is projected to exceed 2 million by 2050, and currently there is no treatment that slows disease progression.
Key pathological features include dysregulated neuroimmune interactions, metabolic and transcriptional changes, and amyloid plaque accumulation. Cardiff University, led by Prof. Julie Williams, has been at the forefront of GWAS efforts in Alzheimer’s disease. My lab, in collaboration with others at the UK Dementia Research Institute (UK DRI), focuses on linking GWAS-identified genes to the biological processes that drive disease, using Drosophila as a model to uncover mechanisms underlying neurodegeneration.
Teaching
|
I contribute to research-led teaching across undergraduate and postgraduate programmes within the School of Medicine. My teaching emphasises critical engagement with primary literature, integration of clinical and scientific perspectives, and the development of independent learning skills. I am also a Fellow of the Higher Education Academy (FHEA). Courses: MBBCh - Tutor - Assessor SSC “The mitochondrial basis of Parkinson’s disease” ME3048 Medical pharmacology – Supervisor – Assessor BI3001 Final year project – Supervisor – Assessor BI4001 Advanced research project – Supervisor – Assessor MBBCh - Personal Tutor – Support and signposting External and BIOSI PTY - Supervisor – Assessor MRes - Supervisor – Assessor Intercalated Degree Programme & BSc in Medical Pharmacology (ME3037, ME3093, ME3092) Supervisor – Assessor CSC Student Placements - Supervisor – Mentor Summer research students through the CUROP scheme - Supervisor – Mentor MSc in Neuroscience senior development team. Co-lead for the Medic run module and Lecturer. |
Biography
I obtained my BSc in Physiology from Cardiff University and remained there to completed my PhD in the laboratory of Prof. Stephan Dunnett where I focused on understanding how treatment strategies such as cell transplantation and L-DOPA therapy effected the phenotypic outcome of Parkinson’s models.
I began my post-doctoral training at Harvard Medical School in the laboratory of Prof. Ole Isacson where I characterized the histopathological and behavioural deficits in the Q175 mouse model of Huntington’s disease, and used gene therapy stratagies and small molecule administration to mitigate phenotypes in rodent models of Parkinson’s disease. I further studied several mitochondrial phenotypes in Parkinson’s patient and control tissue samples that were exposed to mitochondrial specific toxins. This drove differential changes in mitochondrial morphology, LRRK2 phosphorylation, reactive oxygen species generation, mitochondrial membrane potential and mitophagy levels.
During my second post-doctoral position in the laboratory of Prof. Marc Freeman, first based at the University of Massachusetts then moving to Oregon Health and Science University I continued to study mitochondria in Drosophila and screened for new modifiers of mitochondrial dynamics in neurons.
My own research group at Cardiff University will continue to study mitochondrial dynamics in neurons and investigate genetic modifiers of Alzheimer’s disease and Huntington’s disease.
Supervisions
I supervise PhD students, MSc research projects, Professional Training Year students, and undergraduate research placements.
My supervisory approach emphasises strong experimental design, critical thinking, and progressive independence, alongside mentoring in communication, publication, and career development. I have supervised multiple doctoral students to completion and regularly support early-career researchers progressing to fellowships and independent positions.
Prospective PhD and MSc students interested in mitochondrial biology, neurodegeneration, or in vivo imaging are welcome to get in touch.
Engagement
Our lab supports several outreach programes:
In2Science outreach programme for high school students from disadvantaged backgrounds
Science in Health (SIH) placements and SIH-live for 6th form students across Wales
Pint of Science/ Science with a Pint
UK DRI Patient Open days
Wellcome Trust INSPIRE scheme
Neuroscience in the Valleys – School outreach programme
Conference organizer for:
UK-Japan Neuroscience Symposium series
Contact Details
Research themes
Specialisms
- Mitochondria
- Drosophila
- Alzheimer's disease
- neuron