![Gaynor Smith](https://profiles-cardiff.imgix.net/attachments/2602?w=200&h=200&auto=format&crop=faces&fit=crop&q=90")
Dr Gaynor Smith
(hi/ei)
- Ar gael fel goruchwyliwr ôl-raddedig
Timau a rolau for Gaynor Smith
Uwch Ddarlithydd, Sefydliad Ymchwil Dementia
Trosolwyg
Mecanweithiau moleciwlaidd niwrobioleg a chlefyd niwroddirywiol
Mae anhwylderau niwroddirywiol fel clefydau Alzheimer, Parkinson a Huntington yn gyflyrau anwelladwy a gwanychol sy'n arwain at ddirywiad cynyddol gwahanol boblogaethau niwronau. Mae camweithrediad mitochondrial, agregu protein ac ymatebion glial wedi'u haddasu yn nodweddion unedig ar draws y clefydau hyn a hyd yn oed yn amlwg mewn camau prodromal. Mae gan fy labordy ddiddordeb mewn deall y mecanweithiau moleciwlaidd a chellog cadwredig sy'n sail i'r prosesau niwrobiolegol sylfaenol hyn, o Drosophila i bobl.
Nodau Ymchwil:
- Darganfod genynnau newydd sy'n rheoli cynnal mitocondria mewn niwronau gan ddefnyddio dull genetig diduedd in vivo .
- Ymchwilio i sut mae genynnau newydd a ddarganfuwyd o ddulliau GWAS yn cyfrannu at fecanweithiau patholegol clefyd Alzheimer.
Cysylltiadau:
Sefydliad Ymchwil Dementia y DU (UK DRI)
Is-adran Meddygaeth Seicolegol a Niwrowyddorau Clinigol (DPMCN)
https://www.cardiff.ac.uk/medicines-discovery/about-us
Sefydliad Darganfod Meddyginiaethau (MDI)
https://www.medicinesdiscoveryinstitute.com/
Cyhoeddiad
2026
- Storer, F. et al. 2026. Phosphoinositide turnover through PLCγ regulates Draper-dependent engulfment in glia [Pre-print]. bioRxiv (10.64898/2026.06.04.729572)
2025
- Lucas-Clarke, H. J. et al. 2025. Alzheimer’s disease risk gene Wwox protects against amyloid pathology through metabolic reprogramming [Pre-print]. bioRxiv (10.1101/2025.05.01.651195)
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
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
2021
- 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)
- 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)
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
- 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)
- 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)
2015
- 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. 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)
- 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)
- 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)
- 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)
2014
- 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)
- 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)
- 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)
- 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)
2013
- 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)
- 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)
- 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)
- 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
- 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)
- 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. 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. 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. 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
- 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)
- 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. 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.
- Smith, G. 2011. Optimisation and mechanistic insights of dyskinesia in rodent models of Parkinson’s disease. PhD Thesis , Cardiff University.
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
- Storer, F. et al. 2026. Phosphoinositide turnover through PLCγ regulates Draper-dependent engulfment in glia [Pre-print]. bioRxiv (10.64898/2026.06.04.729572)
- Lucas-Clarke, H. J. et al. 2025. Alzheimer’s disease risk gene Wwox protects against amyloid pathology through metabolic reprogramming [Pre-print]. bioRxiv (10.1101/2025.05.01.651195)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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. 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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)
- 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. 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. 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. 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)
- 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)
- 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. 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.
- Lane, E. L. and Smith, G. A. 2010. Understanding graft-induced dyskinesia. Regenerative Medicine 5 (5), pp.787-797. (10.2217/rme.10.42)
Thesis
- Smith, G. 2011. Optimisation and mechanistic insights of dyskinesia in rodent models of Parkinson’s disease. PhD Thesis , Cardiff University.
Ymchwil
1. Darganfod Rheoleiddwyr Newydd Mitocondria Axonal
Ein nod yw nodi genynnau sy'n rheoli cynnal a chadw mitochondrial mewn axons niwronau gan ddefnyddio dulliau genetig diduedd, in vivo. Er gwaethaf rôl ganolog mitocondria mewn iechyd niwronau, cymharol ychydig sy'n hysbys am eu biogenesis, trafnidiaeth, deinameg, neu swyddogaeth mewn axons in vivo. Eto, mae camweithrediad mitochondrial mewn terfynellau yn gysylltiedig yn gryf ag anhwylderau niwroddirywiol.
Mae iechyd niwronau yn dibynnu ar gydbwysedd rhwng diraddiad mitocondrial trwy mitophagy a biogenesis, llwybrau sydd wedi'u cadw'n fawr o bobl i infertebratau. Mae chwaraewyr allweddol fel PINK1 a Parkin, a nodweddwyd gyntaf yn Drosophila, yn dangos pŵer dulliau genetig i ddatgelu mecanweithiau sylfaenol. Nododd gwaith mewn pryfed hefyd fod Miro a Milton yn hanfodol ar gyfer cludo mitocondrial a datgysylltiad rheoledig o'r cytosgerbwd mewn rhanbarthau uchel-Ca²⁺.
Mae mitocondria yn ddeinamig, yn cael eu cyfuno a'u hollti'n gyson i reoleiddio rhannu protein a mtDNA. Mae rheoleiddwyr fel OPA1, Marf, Drp1, a Fis1 yn rheoli'r cydbwysedd hwn. Mae fy labordy yn defnyddio sgrinio genetig diduedd yn Drosophila i ddarganfod rheoleiddwyr newydd o mitocondria axonal, archwilio eu rolau swyddogaethol, a deall sut mae mitocondria yn cyfathrebu ag organellau eraill, gan gynnwys peroxisomes a'r reticulum endoplasmig, i drefnu metaboledd niwronau.
2. Deall Cyfraniadau Genetig i Glefyd Alzheimer
Rydym hefyd yn anelu at ymchwilio i sut mae genynnau a nodwyd trwy Astudiaethau Cymdeithas Genome-Wide (GWAS) yn cyfrannu at fecanweithiau patholegol clefyd Alzheimer. Rhagwelir y bydd nifer y bobl sy'n byw gyda dementia yn y DU yn fwy na 2 filiwn erbyn 2050, ac ar hyn o bryd nid oes unrhyw driniaeth sy'n arafu dilyniant y clefyd.
Mae nodweddion patholegol allweddol yn cynnwys rhyngweithiadau niwroimiwnedd wedi'u camreoleiddio, newidiadau metabolig a thrawsgrifio, a chronni plac amyloid. Mae Prifysgol Caerdydd, dan arweiniad yr Athro Julie Williams, wedi bod ar flaen y gad o ran ymdrechion GWAS mewn clefyd Alzheimer. Mae fy labordy, mewn cydweithrediad ag eraill yn Sefydliad Ymchwil Dementia y DU (UK DRI), yn canolbwyntio ar gysylltu genynnau a nodwyd gan GWAS â'r prosesau biolegol sy'n gyrru clefydau, gan ddefnyddio Drosophila fel model i ddatgelu mecanweithiau sy'n sail i niwroddirywiad.
Addysgu
|
Rwy'n cyfrannu at addysgu dan arweiniad ymchwil ar draws rhaglenni israddedig ac ôl-raddedig yn yr Ysgol Feddygaeth. Mae fy addysgu yn pwysleisio ymgysylltiad beirniadol â llenyddiaeth gynradd, integreiddio safbwyntiau clinigol a gwyddonol, a datblygu sgiliau dysgu annibynnol. Rwyf hefyd yn Gymrawd o'r Academi Addysg Uwch (FHEA). Cyrsiau: MBBCh - Tiwtor - Aseswr SSC "Sail mitocondrial clefyd Parkinson" ME3048 Ffarmacoleg feddygol – Goruchwyliwr – Aseswr BI3001 Prosiect blwyddyn olaf – Goruchwyliwr – Aseswr BI4001 Prosiect ymchwil uwch – Goruchwyliwr – Aseswr MBBCh - Tiwtor Personol – Cymorth a chyfeirio Allanol a BIOSI PTY - Goruchwyliwr - Aseswr MRes - Goruchwyliwr – Aseswr Rhaglen Radd Rhyngweithiol a BSc mewn Ffarmacoleg Feddygol (ME3037, ME3093, ME3092) Goruchwyliwr – Aseswr Lleoliadau Myfyrwyr CSC - Goruchwyliwr – Mentor Myfyrwyr ymchwil haf drwy'r cynllun CUROP - Goruchwyliwr – Mentor MSc mewn uwch dîm datblygu Niwrowyddoniaeth. Cyd-arweinydd ar gyfer y modiwl a Darlithydd sy'n cael ei redeg gan y Meddyg. |
Bywgraffiad
Enillais fy BSc mewn Ffisioleg o Brifysgol Caerdydd ac arhosais yno i gwblhau fy PhD yn labordy yr Athro Stephan Dunnett lle canolbwyntiais ar ddeall sut yr effeithiodd strategaethau triniaeth fel trawsblannu celloedd a therapi L-DOPA ganlyniad ffenoteipig modelau Parkinson.
Dechreuais fy hyfforddiant ôl-ddoethurol yn Ysgol Feddygol Harvard yn labordy yr Athro Ole Isacson lle nodweddais y diffygion histopatholegol ac ymddygiadol ym model llygoden Q175 o glefyd Huntington, a defnyddio stratagïau therapi genynnau a gweinyddu moleciwlau bach i liniaru ffenoteipiau mewn modelau cnofilod clefyd Parkinson. Astudiais sawl ffenoteip mitochondrial ymhellach yng nghlaf Parkinson a samplau meinwe rheoli a oedd yn agored i docsinau penodol mitochondrial. Gyrrodd hyn newidiadau gwahaniaethol mewn morffoleg mitochondrial, ffosfforeiddiad LRRK2, cynhyrchu rhywogaethau ocsigen adweithiol, potensial bilen mitochondrial a lefelau mitophagy .
Yn ystod fy ail swydd ôl-ddoethurol yn labordy yr Athro Marc Freeman, a leolir gyntaf ym Mhrifysgol Massachusetts yna symud i Brifysgol Iechyd a Gwyddoniaeth Oregon, parheais i astudio mitocondria yn Drosophila a sgrinio ar gyfer addaswyr newydd deinameg mitocondrial mewn niwronau.
Bydd fy ngrŵp ymchwil fy hun ym Mhrifysgol Caerdydd yn parhau i astudio deinameg mitochondrial mewn niwronau ac yn ymchwilio i addaswyr genetig clefyd Alzheimer a chlefyd Huntington.
Meysydd goruchwyliaeth
Rwy'n goruchwylio myfyrwyr PhD, prosiectau ymchwil MSc, myfyrwyr Blwyddyn Hyfforddiant Proffesiynol, a lleoliadau ymchwil israddedig.
Mae fy ymagwedd oruchwylio yn pwysleisio dylunio arbrofol cryf, meddwl beirniadol, ac annibyniaeth flaengar, ochr yn ochr â mentora mewn cyfathrebu, cyhoeddi a datblygiad gyrfa. Rwyf wedi goruchwylio nifer o fyfyrwyr doethuriaeth i'w cwblhau ac yn cefnogi ymchwilwyr gyrfa gynnar yn rheolaidd sy'n symud ymlaen i gymrodoriaethau a swyddi annibynnol.
Mae croeso i ddarpar fyfyrwyr PhD ac MSc sydd â diddordeb mewn bioleg mitocondrial, niwroddirywiad, neu ddelweddu in vivo gysylltu â ni.
Ymgysylltu
I am a trained as a STEM ambassador. I am involved with ‘Brain Games’ events held at Cardiff Museum and also contribute to patient and career events run by local charities both within the University and externally. I also contribute to Pint of Science, with my lastest lecture centered on how we use fruit flies in research “Me, Myself and Fly”. I also also take part in the In2 Science mentor scheme, which offers small group sessions and a placement day for Year 12 high school students from disadvantaged backgrounds.
Contact Details
Themâu ymchwil
Arbenigeddau
- Mitocondria
- Drosophila
- Clefyd Alzheimer
- niwron