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Dr Dayne Beccano-Kelly
(he/him)
Teams and roles for Dayne Beccano-Kelly
Research Fellow, Dementia Research Institute
Overview
Parkinson’s is the fastest growing neurological condition, affecting around 145,000 people in the UK alone. While current treatments can ease symptoms, they do not slow or stop the disease, highlighting an urgent need for new approaches.
My lab focuses on how brain cells communicate and what goes wrong in the earliest stages of Parkinson’s (PD). We believe that subtle “miscommunication” between neurons sets the stage for the wider loss of brain cells later in PD that leads to the onset of symptoms. By studying these processes in research models, we aim to uncover the mechanisms that drive disease progression and identify opportunities to intervene before irreversible damage occurs.
Ultimately, my goal is to shift how we approach Parkinson’s — from managing symptoms to slowing or even preventing disease — and to ensure that our discoveries translate into meaningful benefits for people living with the condition.
Publication
2024
- Ng, B. et al. 2024. Tau depletion in human neurons mitigates Aβ-driven toxicity. Molecular Psychiatry 29, pp. 2009-2020. (10.1038/s41380-024-02463-2)
2023
- Beccano-Kelly, D. A. et al. 2023. Calcium dysregulation combined with mitochondrial failure and electrophysiological maturity converge in Parkinson’s iPSC-dopamine neurons. iScience 26(7), article number: 107044. (10.1016/j.isci.2023.107044)
2022
- Burley, S., Beccano-Kelly, D. A., Talbot, K., Llana, O. C. and Wade-Martins, R. 2022. Hyperexcitability in young iPSC-derived C9ORF72 mutant motor neurons is associated with increased intracellular calcium release. Scientific Reports 12(1), article number: 7378. (10.1038/s41598-022-09751-3)
2020
- Mancini, A. et al. 2020. From synaptic dysfunction to neuroprotective strategies in genetic Parkinson’s disease: lessons from LRRK2. Frontiers in Cellular Neuroscience 14 (10.3389/fncel.2020.00158)
2019
- Überbacher, C. et al. 2019. Application of CRISPR/Cas9 editing and digital droplet PCR in human iPSCs to generate novel knock-in reporter lines to visualize dopaminergic neurons. Stem Cell Research 41 (10.1016/j.scr.2019.101656)
- Benkert, J. et al. 2019. Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease. Nature Communications 10(1) (10.1038/s41467-019-12834-x)
2015
- Volta, M. et al. 2015. Chronic and acute LRRK2 silencing has no long-term behavioral effects, whereas wild-type and mutant LRRK2 overexpression induce motor and cognitive deficits and altered regulation of dopamine release.. Parkinsonism & Related Disorders 21(10), pp. 1156-1163. (10.1016/j.parkreldis.2015.07.025)
2014
- Munsie, L. N. et al. 2014. Retromer-dependent neurotransmitter receptor trafficking to synapses is altered by the Parkinson's disease VPS35 mutation p.D620N.. Human Molecular Genetics 24(6), pp. 1691-1703. (10.1093/hmg/ddu582)
- Beccano-Kelly, D. A. et al. 2014. LRRK2 overexpression alters glutamatergic presynaptic plasticity, striatal dopamine tone, postsynaptic signal transduction, motor activity and memory.. Human Molecular Genetics 24(5), pp. 1336-1349. (10.1093/hmg/ddu543)
- Beccano-Kelly, D. A. et al. 2014. Synaptic function is modulated by LRRK2 and glutamate release is increased in cortical neurons of G2019S LRRK2 knock-in mice.. Frontiers in Cellular Neuroscience (10.3389/fncel.2014.00301)
- Vilarino-Guell, C. et al. 2014. DNAJC13 mutations in Parkinson disease.. Human Molecular Genetics 23(7), pp. 1794-1801. (10.1093/hmg/ddt570)
- Brigidi, G. S. et al. 2014. Palmitoylation of δ-catenin by DHHC5 mediates activity-induced synapse plasticity.. Nature Neuroscience 17(4), pp. 522-532. (10.1038/nn.3657)
- Walker, M. D. et al. 2014. Behavioral deficits and striatal DA signaling in LRRK2 p.G2019S transgenic rats: a multimodal investigation including PET neuroimaging. Journal of Parkinson{'}s disease 4(3), pp. 483-498. (10.3233/JPD-140344)
2012
- Doherty, G. H., Beccano-Kelly, D., Yan, S. D., Gunn-Moore, F. J. and Harvey, J. 2012. Leptin prevents hippocampal synaptic disruption and neuronal cell death induced by amyloid β.. Neurobiology of Aging 34(1), pp. 226-237. (10.1016/j.neurobiolaging.2012.08.003)
- Beccano-Kelly, D. and Harvey, J. 2012. Leptin: a novel therapeutic target in Alzheimer's disease?. International Journal of Alzheimer’s Disease 2012, article number: 594137. (10.1155/2012/594137)
2009
- Milligan, C. J. et al. 2009. Robotic multiwell planar patch-clamp for native and primary mammalian cells.. Nature Protocols 4, pp. 244-255. (10.1038/nprot.2008.230)
2006
- Josephs, K. A. et al. 2006. Atypical progressive supranuclear palsy with corticospinal tract degeneration.. Journal of Neuropathology and Experimental Neurology 65(4), pp. 396-405. (10.1097/01.jnen.0000218446.38158.61)
Articles
- Ng, B. et al. 2024. Tau depletion in human neurons mitigates Aβ-driven toxicity. Molecular Psychiatry 29, pp. 2009-2020. (10.1038/s41380-024-02463-2)
- Beccano-Kelly, D. A. et al. 2023. Calcium dysregulation combined with mitochondrial failure and electrophysiological maturity converge in Parkinson’s iPSC-dopamine neurons. iScience 26(7), article number: 107044. (10.1016/j.isci.2023.107044)
- Burley, S., Beccano-Kelly, D. A., Talbot, K., Llana, O. C. and Wade-Martins, R. 2022. Hyperexcitability in young iPSC-derived C9ORF72 mutant motor neurons is associated with increased intracellular calcium release. Scientific Reports 12(1), article number: 7378. (10.1038/s41598-022-09751-3)
- Mancini, A. et al. 2020. From synaptic dysfunction to neuroprotective strategies in genetic Parkinson’s disease: lessons from LRRK2. Frontiers in Cellular Neuroscience 14 (10.3389/fncel.2020.00158)
- Überbacher, C. et al. 2019. Application of CRISPR/Cas9 editing and digital droplet PCR in human iPSCs to generate novel knock-in reporter lines to visualize dopaminergic neurons. Stem Cell Research 41 (10.1016/j.scr.2019.101656)
- Benkert, J. et al. 2019. Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease. Nature Communications 10(1) (10.1038/s41467-019-12834-x)
- Volta, M. et al. 2015. Chronic and acute LRRK2 silencing has no long-term behavioral effects, whereas wild-type and mutant LRRK2 overexpression induce motor and cognitive deficits and altered regulation of dopamine release.. Parkinsonism & Related Disorders 21(10), pp. 1156-1163. (10.1016/j.parkreldis.2015.07.025)
- Munsie, L. N. et al. 2014. Retromer-dependent neurotransmitter receptor trafficking to synapses is altered by the Parkinson's disease VPS35 mutation p.D620N.. Human Molecular Genetics 24(6), pp. 1691-1703. (10.1093/hmg/ddu582)
- Beccano-Kelly, D. A. et al. 2014. LRRK2 overexpression alters glutamatergic presynaptic plasticity, striatal dopamine tone, postsynaptic signal transduction, motor activity and memory.. Human Molecular Genetics 24(5), pp. 1336-1349. (10.1093/hmg/ddu543)
- Beccano-Kelly, D. A. et al. 2014. Synaptic function is modulated by LRRK2 and glutamate release is increased in cortical neurons of G2019S LRRK2 knock-in mice.. Frontiers in Cellular Neuroscience (10.3389/fncel.2014.00301)
- Vilarino-Guell, C. et al. 2014. DNAJC13 mutations in Parkinson disease.. Human Molecular Genetics 23(7), pp. 1794-1801. (10.1093/hmg/ddt570)
- Brigidi, G. S. et al. 2014. Palmitoylation of δ-catenin by DHHC5 mediates activity-induced synapse plasticity.. Nature Neuroscience 17(4), pp. 522-532. (10.1038/nn.3657)
- Walker, M. D. et al. 2014. Behavioral deficits and striatal DA signaling in LRRK2 p.G2019S transgenic rats: a multimodal investigation including PET neuroimaging. Journal of Parkinson{'}s disease 4(3), pp. 483-498. (10.3233/JPD-140344)
- Doherty, G. H., Beccano-Kelly, D., Yan, S. D., Gunn-Moore, F. J. and Harvey, J. 2012. Leptin prevents hippocampal synaptic disruption and neuronal cell death induced by amyloid β.. Neurobiology of Aging 34(1), pp. 226-237. (10.1016/j.neurobiolaging.2012.08.003)
- Beccano-Kelly, D. and Harvey, J. 2012. Leptin: a novel therapeutic target in Alzheimer's disease?. International Journal of Alzheimer’s Disease 2012, article number: 594137. (10.1155/2012/594137)
- Milligan, C. J. et al. 2009. Robotic multiwell planar patch-clamp for native and primary mammalian cells.. Nature Protocols 4, pp. 244-255. (10.1038/nprot.2008.230)
- Josephs, K. A. et al. 2006. Atypical progressive supranuclear palsy with corticospinal tract degeneration.. Journal of Neuropathology and Experimental Neurology 65(4), pp. 396-405. (10.1097/01.jnen.0000218446.38158.61)
Research
Research
Our work focuses on understanding the mechanisms that drive the progression of Parkinson’s and related disorders, with the aim of identifying opportunities for early intervention and translation to patient benefit. By combining patient-derived stem cells, animal models and neuroimaging, we seek to uncover the earliest dysfunctions that precede neuronal degeneration and to define critical windows for therapeutic intervention.
Models of disease
We use both human induced pluripotent stem cells (iPSCs) carrying late-onset Parkinson’s mutations (LRRK2, GBA, VPS35, DNAJC13) and genetically modified rodent models. These approaches allow us to recapitulate the temporal progression of disease and to investigate how specific mutations perturb neuronal physiology.
Synaptic dysfunction
Specialised neuronal functions such as neurotransmission and network activity underpin brain physiology and everything we do from walking and talking to thinking and moving; however it can also confer specific vulnerabilities. Using whole-cell patch clamp electrophysiology, we characterise early synaptic disturbances that precede degeneration, providing insight into the mechanisms that trigger disease onset.
Therapeutic timing
Through a UKRI Future Leaders Fellowship, we are mapping the temporal sequence of Parkinson’s to identify when interventions will be most effective. This approach aims to reveal new therapeutic targets and maximise the efficacy of their modulation by intervening at defined windows of vulnerability.
Translation and patient impact
A key strand of our research integrates neuroimaging and cognitive testing in models, creating a bridge between in vitro and in vivo findings and allowing for translation to application in the clinic. Translation and patient well-being remain central to our programme, with the goal of ensuring that fundamental discoveries provide tangible benefits to people living with Parkinson’s disease.
Biography
Dayne Beccano-Kelly began his scientific career with an integrated Biochemistry with Industry BSc at the University of Leeds and Mayo Clinic Jacksonville under the tutalege of Dr. Dennis Dickson. Upon completion in 2006, he went on to do a PhD in Synaptic Neuroscience in 2010 under the supervision of Dr. Hugh Pearson at University of Leeds. He then undertook postdoctoral training at the University of Dundee, where he investigated synaptic biology in models of Alzheimer’s disease.
In 2012, he moved to the University of British Columbia as a senior postdoctoral fellow in the laboratory of Matthew J. Farrer, expanding his research into translational neuroscience and the genetics of Parkinson’s disease. In 2015, he was awarded a Parkinson’s UK Career Development Fellowship at the University of Oxford, where he incorporated stem cell technologies into his work on neurodegeneration.
In 2021, Dr Beccano-Kelly received a prestigious UKRI Future Leaders Fellowship and joined the UK Dementia Research Institute at Cardiff University as a Group Leader. His laboratory now focuses on how synaptic changes drive the earliest stages of neurodegeneration, with the goal of identifying therapeutic strategies to prevent or delay the progression of Parkinson’s disease
Professional memberships
Trustee and Director of the British Neuroscience Association: 2025 – Present
MRC Black in biomedical Research Advisory Group: 2023 - Present
MRC Council Infrastructure and Capital Strategic Advisory Group (ICSAG): 2021 – 2025
British Neuroscience Association Council member - Joint Meetings Secretary: 2020 – 2025
World Parkinson Coalition Science Ambassador: 2020 – 2023
Committees and reviewing
French National Research Agency grant reviewer: 2025
Royal society panel reviewer for Career Development Fellowships: 2023 – Present
Telethon Science grant reviewer: 2022
MRC Capital/Mid-range Equipment Funding Panel: 2021 – Present