Profiles
Catherine Blizzard

Catherine Blizzard
Senior Lecturer in Medical Sciences
Medicine
Room 441B (Level 4) , Medical Science 2
+61 3 6226 4623 (phone)
Dr Cathy Blizzard is a senior lecturer and research fellow at the Tasmanian School of Medicine. She leads a lab group focussed upon understanding the pathological changes that lead to motor neuron disease and dementia
Biography
I am a balanced research fellow dedicated to understanding the underlying pathological cause of motor neuron disease (MND) and dementia. My contributions have been deemed the most competitive in my field, as demonstrated by my awarding of my ARC Discovery Early Career Fellowship (DECRA) fellowship, which places me in the top echelon of all early career research fellows in Australia, and the award of most outstanding MND early career researcher in Australia (open to all researchers and clinicians under ten years post PhD, $250,000 prize). Before establishing my research group I was on continuous nationally and internationally competitive fellowship .
Following my PhD, I was recruited to Professor Tracey Dickson's MND team at Menzies Institute for Medical Research and awarded a MND Australia postdoctoral research fellowship (only one that year). Next, I was awarded an early career Alzheimer's Australia (one of seven) fellowship, an IBRO International Training Fellowship (one of only two Australians selected) and then an ARC DECRA. I then established my lab within the Tasmanian School of Medicine.
Memberships
Professional practice
Dr Blizzard has been a member of professional societies including the SfN, ANS and ASMR.
Committee associations
Dr Blizzard has been a member of organising committees for a number of local conferences including:
- Wicking Dementia Research and Education Centre Winter School, 2010
- National Symposium on Neurotrauma, 2010; 2011
Administrative expertise
- Tasmanian State representative for the MND Collective Discovery Research Driving team
- Tasmanian State representative for the Australasian Neuroscience Society
- Journal editor for Scientific Reports
- Organiser of the biannual Tasmanian MND Research Forum
- Member of the organising committee for the 2022 Aus and NZ MND Research Symposium
- Member of the Scientific Advisory Council of the ALS Foundation Netherlands, 2019 onwards
- Reviewer for UK MND Association, 2017 onwards
- Reviewer for MND Research Australia, 2015 onwards
- Reviewer for NHMRC and ARC, 2017 onwards
Teaching
Teaching expertise
- Unit coordinator for CAM203 and CAM208
- Teaching into 53E - Bachelor of Medical Research
- Supervision of PhD, masters and honours students - completed seven PhD students, three as primary supervisor.
Research Invitations
Conference Speaker:
- 12th International Conference of Alzheimer's and Parkinson's diseases, Nice, France, 2015
- 9th FENs Forum of Neuroscience, Milan, Italy, 2014
- Motor Neuron Disease Research Institute of Australia Symposium, Melbourne
- Motor Neuron Disease Research Institute of Australia Symposium, Sydney, 2013
- 23rd International Symposium on ALS/MND, Chicago, USA, 2012
- 32nd Australian Neuroscience Society Meeting, Gold Coast, 2012
- Motor Neuron Disease Research Institute of Australia Symposium, Brisbane, 2012
Public talks:
- Menzies Meet the Researcher – MND Research In Tasmania, 2015
- Guest speaker for Elizabeth College Awards Night, 2014
- Guest speaker for Kingston Ladies Probus – Brain Injury Research in Tasmania, 2014
- Guest speaker for MND Tasmania AGM – Opening of Student Roadshow, 2014
- Guest speaker for National Science Week fundraising event – Headway Brain Break, 2013
- Guest speaker for MND Tasmania AGM – Motor neuron degeneration in MND, 2013
- Presentation at MND Victoria Sympoisuim – MND Research in Tasmania, 2012
- Guest speaker for Biota Teacher's Association Conference – Can the brain repair itself following injury? 2011
View more on Dr Catherine Blizzard in WARP
Expertise
- Frontotemporal Dementia
- Neurodegeneration
- Neuroplasticity
- Amyotrophic Lateral Sclerosis
- Traumatic Brain Injury
Awards
- Young Investigator International Training Program Fellowship (1 of 2 Australians selected)– Federation of European Neuroscience Society, 2014
- Cosmopolitan Australian's Role Model of the Year, 2013
- Southern Cross Young Achiever of the Year – Science/Technology, 2012
- International travel award – International Brain Research Organisation, 2011
- National Student Oral Presentation Prize – Dementia and Neurodegenerative Diseases Conference, Sydney Australia, 2010
- Menzies Institute For Medical Research - Doctoral Student of the year, 2010
- National travel award – Australian Neuroscience Society, 2010
- National Student Poster Presentation Prize – ASMR Neurogenetics National Meeting, 2009
- Student Oral Presentation Prize – University of Tasmania's Sharing Excellence in Research Conference, 2009
- Tasmanian Medical Student of the Year – ASMR, 2008
Current projects
- Synaptic dysfunction in Frontotemporal Dementia and Amyotrophic Lateral Sclerosis
- The role of interneurons in Amyotrophic Lateral Sclerosis (collaborator)
- Interneurons and Traumatic Brain Injury (collaborator)
- Targeted axonal protection in Amyotrophic Lateral Sclerosis (collaborator)
Fields of Research
- Neurology and neuromuscular diseases (320905)
- Cellular nervous system (320902)
- Central nervous system (320903)
- Cell neurochemistry (310104)
- Immunogenetics (incl. genetic immunology) (320406)
- Health services and systems (420399)
- Peripheral nervous system (320906)
- Cardiology (incl. cardiovascular diseases) (320101)
- Cognitive neuroscience (520203)
Research Objectives
- Clinical health (200199)
- Treatment of human diseases and conditions (200105)
- Expanding knowledge in the biological sciences (280102)
- Diagnosis of human diseases and conditions (200101)
- Health related to ageing (200502)
- Prevention of human diseases and conditions (200104)
- Expanding knowledge in the biomedical and clinical sciences (280103)
Publications
Since starting my lab in 2017 (in addition to taking two maternity leaves) I have published seven senior author papers. The senior author original research papers I have published have all been in quality quartile 1 journals, placing them in the top 25% of my discipline. I have made a high-level contribution to all outputs. I have published in Journals such as Science, Cerebral Cortex and Neuropath and Applied Neuro. My work has been cited 1200 times (google scholar).
Total publications
48
Journal Article
(30 outputs)Year | Citation | Altmetrics |
---|---|---|
2021 | Dyer MS, Woodhouse A, Blizzard CA, 'Cytoplasmic human TDP-43 mislocalization induces widespread dendritic spine loss in mouse upper motor neurons', Brain Sciences, 11, (7) pp. 1-16. ISSN 2076-3425 (2021) [Refereed Article] DOI: 10.3390/brainsci11070883 [eCite] [Details] Citations: Scopus - 2Web of Science - 2 Co-authors: Dyer MS; Woodhouse A | |
2020 | Clark JA, Chuckowree JA, Dyer MS, Dickson TC, Blizzard CA, 'Epothilone D alters normal growth, viability and microtubule dependent intracellular functions of cortical neurons in vitro', Scientific Reports, 10, (1) Article 918. ISSN 2045-2322 (2020) [Refereed Article] DOI: 10.1038/s41598-020-57718-z [eCite] [Details] Citations: Scopus - 9Web of Science - 9 Co-authors: Clark JA; Chuckowree JA; Dyer MS; Dickson TC | |
2020 | Dyer MS, Reale LA, Lewis KE, Walker AK, Dickson TC, et al., 'Mislocalisation of TDP‐43 to the cytoplasm causes cortical hyperexcitability and reduced excitatory neurotransmission in the motor cortex', Journal of Neurochemistry, 157, (4) pp. 1300-1315. ISSN 0022-3042 (2020) [Refereed Article] DOI: 10.1111/jnc.15214 [eCite] [Details] Citations: Scopus - 8Web of Science - 10 Co-authors: Dyer MS; Reale LA; Lewis KE; Walker AK; Dickson TC; Woodhouse A | |
2020 | Zhu Z, Chuckowree JA, Musgrove R, Dickson TC, Blizzard CA, 'The pathologic outcomes and efficacy of epothilone treatment following traumatic brain injury is determined by age', Neurobiology of Aging, 93 pp. 85-96. ISSN 0197-4580 (2020) [Refereed Article] DOI: 10.1016/j.neurobiolaging.2020.03.023 [eCite] [Details] Citations: Scopus - 3Web of Science - 4 Co-authors: Chuckowree JA; Musgrove R; Dickson TC | |
2019 | Jiang T, Handley EE, Brizuela MD, Dawkins E, Lewis KE, et al., 'Amyotrophic lateral sclerosis mutant TDP-43 may cause synaptic dysfunction through altered dendritic spine function', Disease Models & Mechanisms, 12, (5) Article dmm038109. ISSN 1754-8403 (2019) [Refereed Article] DOI: 10.1242/dmm.038109 [eCite] [Details] Citations: Scopus - 16Web of Science - 17 Co-authors: Handley EE; Brizuela MD; Dawkins E; Lewis KE; Clark RM; Dickson TC | |
2018 | Chuckowree JA, Zhu Z, Brizuela MD, Lee KM, Blizzard CA, et al., 'The microtubule-modulating drug Epothilone D alters dendritic spine morphology in a mouse model of mild traumatic brain injury', Frontiers in Cellular Neuroscience, 12 Article 223. ISSN 1662-5102 (2018) [Refereed Article] DOI: 10.3389/fncel.2018.00223 [eCite] [Details] Citations: Scopus - 14Web of Science - 15 Co-authors: Chuckowree JA; Brizuela MD; Lee KM; Dickson TC | |
2018 | Clark JA, Blizzard CA, Breslin MC, Yeaman EJ, Lee KM, et al., 'Epothilone D accelerates disease progression in the SOD1G93A mouse model of amyotrophic lateral sclerosis', Neuropathology and Applied Neurobiology, 44, (6) pp. 590-605. ISSN 0305-1846 (2018) [Refereed Article] DOI: 10.1111/nan.12473 [eCite] [Details] Citations: Scopus - 15Web of Science - 13 Co-authors: Clark JA; Breslin MC; Yeaman EJ; Chuckowree JA; Dickson TC | |
2018 | Clark RM, Brizuela M, Blizzard CA, Dickson TC, 'Reduced excitability and increased neurite complexity of cortical interneurons in a familial mouse model of amyotrophic lateral sclerosis', Frontiers in Cellular Neuroscience, 12 Article 328. ISSN 1662-5102 (2018) [Refereed Article] DOI: 10.3389/fncel.2018.00328 [eCite] [Details] Citations: Scopus - 7Web of Science - 7 Co-authors: Clark RM; Dickson TC | |
2017 | Brizuela MD, Blizzard CA, Chuckowree JA, Pitman KA, Young KM, et al., 'Mild traumatic brain injury leads to decreased inhibition and a differential response of calretinin positive interneurons in the injured cortex', Journal of Neurotrauma, 34, (17) pp. 2504-2517. ISSN 0897-7151 (2017) [Refereed Article] DOI: 10.1089/neu.2017.4977 [eCite] [Details] Citations: Scopus - 16Web of Science - 16 Co-authors: Brizuela MD; Chuckowree JA; Pitman KA; Young KM; Dickson T | |
2017 | Clark RM, Blizzard CA, Young KM, King AE, Dickson TC, 'Calretinin and Neuropeptide Y interneurons are differentially altered in the motor cortex of the SOD1G93A mouse model of ALS', Scientific Reports, 7 Article 44461. ISSN 2045-2322 (2017) [Refereed Article] DOI: 10.1038/srep44461 [eCite] [Details] Citations: Scopus - 22Web of Science - 21 Co-authors: Clark RM; Young KM; King AE; Dickson TC | |
2017 | Yap YC, King AE, Guijt RM, Jiang T, Blizzard CA, et al., 'Mild and repetitive very mild axonal stretch injury triggers cystoskeletal mislocalization and growth cone collapse', PLoS One, 12, (5) Article e0176997. ISSN 1932-6203 (2017) [Refereed Article] DOI: 10.1371/journal.pone.0176997 [eCite] [Details] Citations: Scopus - 22Web of Science - 20 Co-authors: Yap YC; King AE; Guijt RM; Breadmore MC; Dickson TC | |
2016 | Blizzard CA, Lee KM, Dickson TC, 'Inducing chronic excitotoxicity in the mouse spinal cord to investigate lower motor neuron degeneration', Frontiers in Neuroscience, 10 Article 76. ISSN 1662-453X (2016) [Refereed Article] DOI: 10.3389/fnins.2016.00076 [eCite] [Details] Citations: Scopus - 11Web of Science - 9 Co-authors: Lee KM; Dickson TC | |
2016 | Clark JA, Southam KA, Blizzard CA, King AE, Dickson TC, 'Axonal degeneration, distal collateral branching and neuromuscular junction architecture alterations occur prior to symptom onset in the SOD1G93A mouse model of amyotrophic lateral sclerosis', Journal of Chemical Neuroanatomy, 76, (Pt A) pp. 35-47. ISSN 0891-0618 (2016) [Refereed Article] DOI: 10.1016/j.jchemneu.2016.03.003 [eCite] [Details] Citations: Scopus - 48Web of Science - 46 Co-authors: Clark JA; Southam KA; King AE; Dickson TC | |
2016 | Clark JA, Yeaman EJ, Blizzard CA, Chuckowree JA, Dickson TC, 'A Case for Microtubule Vulnerability in Amyotrophic Lateral Sclerosis: Altered Dynamics During Disease', Frontiers in Cellular Neuroscience, 10 Article 204. ISSN 1662-5102 (2016) [Refereed Article] DOI: 10.3389/fncel.2016.00204 [eCite] [Details] Citations: Scopus - 33Web of Science - 30 Co-authors: Clark JA; Yeaman EJ; Chuckowree JA; Dickson TC | |
2016 | Handley EE, Pitman KA, Dawkins E, Young KM, Clark RM, et al., 'Synapse dysfunction of layer V pyramidal neurons precedes neurodegeneration in a mouse model of TDP-43 proteinopathies', Cerebral Cortex, 27, (7) pp. 3630-3647. ISSN 1047-3211 (2016) [Refereed Article] DOI: 10.1093/cercor/bhw185 [eCite] [Details] Citations: Scopus - 39Web of Science - 39 Co-authors: Handley EE; Pitman KA; Dawkins E; Young KM; Clark RM; Dickson TC | |
2015 | Blizzard CA, Southam KA, Dawkins E, Lewis KE, King AE, et al., 'Identifying the primary site of pathogenesis in amyotrophic lateral sclerosis - vulnerability of lower motor neurons to proximal excitotoxicity', Disease Models & Mechanisms, 8, (3) pp. 215-224. ISSN 1754-8403 (2015) [Refereed Article] DOI: 10.1242/dmm.018606 [eCite] [Details] Citations: Scopus - 27Web of Science - 28 Co-authors: Southam KA; Dawkins E; Lewis KE; King AE; Clark JA; Dickson TC | |
2015 | Brizuela MD, Blizzard CA, Chuckowree JA, Dawkins E, Gasperini RJ, et al., 'The microtubule-stabilizing drug Epothilone D increases axonal sprouting following transection injury in vitro', Molecular and Cellular Neurosciences, 66, (Part B) pp. 129-140. ISSN 1044-7431 (2015) [Refereed Article] DOI: 10.1016/j.mcn.2015.02.006 [eCite] [Details] Citations: Scopus - 32Web of Science - 31 Co-authors: Brizuela MD; Chuckowree JA; Dawkins E; Gasperini RJ; Young KM; Dickson TC | |
2015 | Clark R, Blizzard C, Dickson T, 'Inhibitory dysfunction in amyotrophic lateral sclerosis: future therapeutic opportunities', Neurodegenerative Disease Management, 5, (6) pp. 511-525. ISSN 1758-2024 (2015) [Refereed Article] DOI: 10.2217/nmt.15.49 [eCite] [Details] Citations: Scopus - 10Web of Science - 11 Co-authors: Clark R; Dickson T | |
2015 | Radford R, Rcom-H'cheo-Gauthier A, Wong MB, Eaton ED, Quilty M, et al., 'The degree of astrocyte activation in multiple system atrophy is inversely proportional to the distance to α-synuclein inclusions', Molecular and Cellular Neuroscience, 65 pp. 68-81. ISSN 1044-7431 (2015) [Refereed Article] DOI: 10.1016/j.mcn.2015.02.015 [eCite] [Details] Citations: Scopus - 41Web of Science - 38 Co-authors: Eaton ED; Quilty M; Vickers JC; West AK; Dickson TC | |
2013 | Blizzard CA, King AE, Vickers J, Dickson T, 'Cortical murine neurons lacking the neurofilament light chain protein have an attenuated response to injury in vitro', Journal of Neurotrauma, 30, (22) pp. 1908-1918. ISSN 0897-7151 (2013) [Refereed Article] DOI: 10.1089/neu.2013.2850 [eCite] [Details] Citations: Scopus - 8Web of Science - 7 Co-authors: King AE; Vickers J; Dickson T | |
2013 | Southam KA, King AE, Blizzard CA, McCormack GH, Dickson TC, 'Microfluidic primary culture model of the lower motor neuron-neuromuscular junction circuit', Journal of Neuroscience Methods, 218, (2) pp. 164-169. ISSN 0165-0270 (2013) [Refereed Article] DOI: 10.1016/j.jneumeth.2013.06.002 [eCite] [Details] Citations: Scopus - 79Web of Science - 73 Co-authors: Southam KA; King AE; McCormack GH; Dickson TC | |
2012 | Hosie KA, King AE, Blizzard CA, Vickers JC, Dickson TC, 'Chronic excitotoxin-induced axon degeneration in a compartmented neuronal culture model', ASN Neuro, 4, (1) Article e00076. ISSN 1759-0914 (2012) [Refereed Article] DOI: 10.1042/AN20110031 [eCite] [Details] Citations: Scopus - 42Web of Science - 37 Co-authors: Hosie KA; King AE; Vickers JC; Dickson TC | |
2012 | King AE, Blizzard CA, Southam KA, Vickers JC, Dickson TC, 'Degeneration of axons in spinal white matter in G93A mSOD1 mouse characterized by NFL and alpha internexin immunoreactivity', Brain Research, 1465 pp. 90-100. ISSN 0006-8993 (2012) [Refereed Article] DOI: 10.1016/j.brainres.2012.05.018 [eCite] [Details] Citations: Scopus - 17Web of Science - 13 Co-authors: King AE; Southam KA; Vickers JC; Dickson TC | |
2011 | Blizzard CA, Chuckowree JA, King AE, Hosie KA, McCormack GH, et al., 'Focal Damage to the Adult Rat Neocortex Induces Wound Healing Accompanied by Axonal Sprouting and Dendritic Structural Plasticity ', Cerebral Cortex, 21, (2) pp. 281-291. ISSN 1047-3211 (2011) [Refereed Article] DOI: 10.1093/cercor/bhq091 [eCite] [Details] Citations: Scopus - 31Web of Science - 32 Co-authors: Chuckowree JA; King AE; Hosie KA; McCormack GH; Chapman JA; Vickers JC; Dickson TC | |
2011 | King AE, Dickson TC, Blizzard CA, Woodhouse A, Foster SS, et al., 'Neuron-glia interactions underlie ALS-like axonal cytoskeletal pathology', Neurobiology of Aging: Experimental and Clinical Research, 32, (3) pp. 459-469. ISSN 0197-4580 (2011) [Refereed Article] DOI: 10.1016/j.neurobiolaging.2009.04.004 [eCite] [Details] Citations: Scopus - 27Web of Science - 24 Co-authors: King AE; Dickson TC; Woodhouse A; Foster SS; Chung RS; Vickers JC | |
2010 | Murchison EP, Tovar C, Hsu A, Bender HS, Kheradpour P, et al., 'The Tasmanian Devil Transcriptome Reveals Schwann Cell Origins of a Clonally Transmissible Cancer ', Science, 327, (5961) pp. 84-87. ISSN 0036-8075 (2010) [Refereed Article] DOI: 10.1126/science.1180616 [eCite] [Details] Citations: Scopus - 172Web of Science - 154 Co-authors: Tovar C; Obendorf D; Kreiss A; Woods GM | |
2009 | Blizzard CA, King AE, Haas MA, O'Toole DA, Vickers JC, et al., 'Axonal shearing in mature cortical neurons induces attempted regeneration and the reestablishment of neurite polarity', Brain Research: International Multidisciplinary Journal Devoted to Fundamental Research in The Brain Sciences, 1300, (November) pp. 24-36. ISSN 0006-8993 (2009) [Refereed Article] DOI: 10.1016/j.brainres.2009.08.059 [eCite] [Details] Citations: Scopus - 2Web of Science - 3 Co-authors: King AE; Haas MA; O'Toole DA; Vickers JC; Dickson TC | |
2009 | Vickers JC, King AE, Woodhouse A, Kirkcaldie MT, Staal JA, et al., 'Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous system ', Brain Research Bulletin, 80, (4-5) pp. 217-223. ISSN 0361-9230 (2009) [Refereed Article] DOI: 10.1016/j.brainresbull.2009.08.004 [eCite] [Details] Citations: Scopus - 53Web of Science - 51 Co-authors: Vickers JC; King AE; Woodhouse A; Kirkcaldie MT; Staal JA; McCormack GH; Musgrove RE; Mitew S; Liu Y; Chuckowree JA; Bibari O; Dickson TC | |
2007 | Blizzard CA, Haas MA, Vickers JC, Dickson TC, 'Cellular dynamics underlying regeneration of damaged axons differs from initial axon development', European Journal of Neuroscience, 26, (5) pp. 1100-1108. ISSN 0953-816X (2007) [Refereed Article] DOI: 10.1111/j.1460-9568.2007.05750.x [eCite] [Details] Citations: Scopus - 24Web of Science - 23 Co-authors: Haas MA; Vickers JC; Dickson TC | |
2007 | King AE, Dickson TC, Blizzard CA, Foster SS, Chung RS, et al., 'Excitotoxicity mediated by non-NMDA receptors causes distal axonopathy in long-term cultured spinal motor neurons', European Journal of Neuroscience, 26, (8) pp. 2151-2159. ISSN 0953-816X (2007) [Refereed Article] DOI: 10.1111/j.1460-9568.2007.05845.x [eCite] [Details] Citations: Scopus - 31Web of Science - 25 Co-authors: King AE; Dickson TC; Foster SS; Chung RS; West AK; Chuah MI; Vickers JC |
Chapter in Book
(1 outputs)Year | Citation | Altmetrics |
---|---|---|
2015 | Southam KA, King AE, Blizzard CA, McCormack GH, Dickson T, 'A Novel In Vitro Primary Culture Model of the Lower Motor Neuron-Neuromuscular Junction Circuit', Microfluidic and Compartmentalized Platforms for Neurobiological Research, Springer, E Biffi (ed), United States, pp. 181-193. ISBN 978-1-4939-2509-4 (2015) [Other Book Chapter] DOI: 10.1007/978-1-4939-2510-0_11 [eCite] [Details] Citations: Scopus - 1 Co-authors: Southam KA; King AE; McCormack GH; Dickson T |
Conference Publication
(17 outputs)Year | Citation | Altmetrics |
---|---|---|
2014 | Blizzard CA, Handley E, Dawkins E, Clark R, Fielder T, et al., 'Synaptic alterations in the TDP-A315T mouse model of Amyotrophic Lateral Sclerosis', 25th International Symposium on ALS/MND, 5-7 December, Brussels, Belgium (2014) [Conference Extract] DOI: 10.3109/21678421.2014.960187/259 [eCite] [Details] Co-authors: Handley E; Dawkins E; Clark R; Fielder T; Dickson T | |
2012 | Blizzard C, King AE, Hosie KA, Dickson TC, 'Site-specific excitotoxin exposure in vivo leads to neuronal excitotoxicity and axonal dysfunction', 32nd Annual Meeting Australian Neuroscience Society, January 2012, Gold Coast, Australia (2012) [Conference Extract] Co-authors: King AE; Hosie KA; Dickson TC | |
2012 | Blizzard C, King AE, Vickers JC, Dickson TC, 'Site specific excitotoxicity: a model of amyotrophic lateral sclerosis', 32nd Annual Meeting Australian Neuroscience Society, January 2012, Gold Coast, Australia (2012) [Conference Extract] Co-authors: King AE; Vickers JC; Dickson TC | |
2012 | King AE, Blizzard C, Mitew S, Dickson TC, 'Investigating the role of interneurons in neurological disease', DANDIS, January, 2012, Queensland, Australia (2012) [Conference Extract] Co-authors: King AE; Mitew S; Dickson TC | |
2012 | Southam K, Blizzard C, Vickers JC, Dickson TC, King AE, 'Modelling site specific excitotixicity in vitro', University of Tasmania Sharing Excellence in Research meeting, September 2012, Hobart, Australia (2012) [Conference Extract] Co-authors: Southam K; Vickers JC; Dickson TC; King AE | |
2011 | Blizzard C, King AE, Hosie KA, Dickson TC, 'Modelling site-specific excitotoxicity in vivo', 22nd International Symposium on ALS/MND, November 2011, Sydney, Australia (2011) [Conference Extract] Co-authors: King AE; Hosie KA; Dickson TC | |
2011 | Hosie KA, King AE, Blizzard C, Vickers JC, Dickson TC, 'Modelling ALS pathology in vitro', 22nd Symposium on ALS/MND, November 2011, Sydney, Australia (2011) [Conference Extract] Co-authors: Hosie KA; King AE; Vickers JC; Dickson TC | |
2011 | King AE, Hosie KA, Vickers JC, Blizzard C, Dickson TC, 'An in vitro investigation of the role of interneurons in the development of ALS', 22nd Symposium on ALS/MND, November 2011, Sydney, Australia (2011) [Conference Extract] Co-authors: King AE; Hosie KA; Vickers JC; Dickson TC | |
2010 | Blizzard CA, Chuckowree JA, King AE, Hosie KA, Chapman JA, et al., 'Focal damage to the neocortex induces dendritic structural plasticity', Australian Neuroscience Society/Australian Physiological Society, January, Sydney, Australia (2010) [Conference Extract] Co-authors: Chuckowree JA; King AE; Hosie KA; Chapman JA; Vickers JC; Dickson TC | |
2010 | Blizzard CA, Chuckowree JA, King AE, Hosie KA, Chapman JA, et al., 'Focal damage to the neocortex induces dendritic structural plasticity', Proceedings of the Dementia, Ageing and Neurodegenerative Diseases Group Conference 2010, 30 January 2010, Sydney, Australia (2010) [Conference Extract] Co-authors: Chuckowree JA; King AE; Hosie KA; Chapman JA; Vickers JC; Dickson TC | |
2009 | Blizzard CA, Chuckowree JA, King AE, McCormack GH, Chapman JA, et al., 'Acute neocortical injury induces axonal sprouting and dendritic remodelling', ASMR National Scientific Conference, Neurogenetics on the Apple Isle, February, Hobart (2009) [Conference Extract] Co-authors: Chuckowree JA; King AE; McCormack GH; Chapman JA; Vickers JC; Dickson TC | |
2008 | Blizzard C, Chuckowree JA, McCormack GH, Chapman JA, King AE, et al., 'Delayed morphological alterations in a subpopulation of interneurons in the peri-wound region following focal damage to the adult rat neocortex', Neuroscience, 15-19 November 2008, Washington DC (2008) [Conference Extract] Co-authors: Chuckowree JA; McCormack GH; Chapman JA; King AE; Vickers JC; Dickson TC | |
2008 | King AE, Dickson TC, Blizzard CA, Foster SS, Woodhouse A, et al., 'Neuron-glia interactions underlying axonal health in an in vitro spinal culture model of relevance to ALS', Amyotrophic Lateral Sclerosis, 19th Symposium on ALS/MND, 3-5 November, Birmingham, pp. 85. (2008) [Conference Extract] Co-authors: King AE; Dickson TC; Foster SS; Woodhouse A; Chung RS; Vickers JC | |
2008 | Vickers JC, King AE, Blizzard CA, Woodhouse A, Foster SS, et al., 'Murine spinal neurons in vitro develop proximal axonal transport abnormalities and swellings that are similar to early axonal changes in amyotrophic lateral sclerosis', Society for Neuroscience, 15-19 November, Washington, DC (2008) [Conference Extract] Co-authors: Vickers JC; King AE; Woodhouse A; Foster SS; Chung RS; Dickson TC | |
2007 | King AE, Dickson TC, Blizzard CA, Foster SS, Chung RS, et al., 'ALS-like axonal pathology in cultured spinal motor neurons', Amyotrophic Lateral Sclerosis, 18th Symposium on ALS/MND, 1-3 December, Toronto, pp. 191. (2007) [Conference Extract] Co-authors: King AE; Dickson TC; Foster SS; Chung RS; West AK; Chuah MI; Vickers JC | |
2007 | King AE, Dickson TC, Blizzard CA, Foster SS, Chung RS, et al., 'ALS-like pathology in cultured spinal motor neurons following excitoxicity', IBRO International Conference, 12-17 July, Melbourne (2007) [Conference Extract] Co-authors: King AE; Dickson TC; Foster SS; Chung RS; West AK; Chuah MI; Vickers JC | |
2006 | Vickers JC, King AE, Dickson TC, Chung RS, Chuckowree JA, et al., 'In vitro models of the key pathological changes in axons associated with neurodegenerative disease and acquired brain injury', 4th Congress of Federation of Asian-Oceanain Neuroscience Societies, November, Hong Kong (2006) [Conference Extract] Co-authors: Vickers JC; King AE; Dickson TC; Chung RS; Chuckowree JA; Haas MA; Staal JA; Woodhouse A; West AK; Chuah I; McCormack G |
Grants & Funding
Dr Blizzard has shown great capacity to fund her research. In addition fellowship scholarships, she has received grant funding in excess of $290,000 from a range of nationally competitive granting schemes including the Brain Foundation (CIA (2014) - $35,000) and the Motor Neuron Disease Research Institute of Australia (CIA (2014) - $85,000).
Funding Summary
Number of grants
25
Total funding
Projects
- Description
- Amyotrophic lateral sclerosis (ALS) is an unrelenting and fatal disease in which motor neurons of the motor cortex and spinal cord rapidly degenerate. One of the earliest detectable clinical markers of ALS is hyperexcitability. We have discovered that upper motor neurons in the motor cortex and lower motor neurons in the spinal cord, may be differentially vulnerable to pathogenic effects of hyperexcitability, and possibly the resulting excitotoxicity. Furthermore we have evidence to suggest that age and sex, two important patient demographic variables in ALS also may influence the vulnerability of motor neurons to excitotoxicity. This indicates that a blanket treatment approach toward excitotoxicity in ALS may not be appropriate for the protection of all motor neurons. An innovative and potentially more effective strategy is to specifically tailor treatment to the differential changes that are occurring in the brain and spinal cord through disease progression.With leading-edge experimental design in appropriate models this project will determine how age and sex impacts excitotoxicity in mouse models of ALS (Aim 1), if upper and lower motor neurons are differentially vulnerable to disease using mouse models and patient derived induced pluripotent stem cells (Aim 2) and whether diffuse sub-threshold transcranial magnetic stimulation, a non-invasive form of central nervous system network stimulation, can regionally treat upper and lower motor neurons to halt disease progression in mouse models of ALS (Aim 3).This project brings together a team of CIs and AIs that have a demonstrated excellence in all aspects necessary for this project. The CI team (Catherine Blizzard and Tracey Dickson) have a long and productive collaborative track record; 29 publications and $3.5 million in funding together. This is the first time a disease treatment has been trialled in ALS that applies approaches tailored to address pathology in distinct regions of the corticomotor system.
- Funding
- National Health & Medical Research Council ($624,821)
- Scheme
- Grant-Ideas
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Dickson TC
- Period
- 2022 - 2024
- Grant Reference
- 2013024
- Description
- Amyotrophic lateral sclerosis (ALS) is a devastating and universally fatal late onset motor neuron disease for which there are currently no effective treatments or cure. Development of effective therapeutics for ALS is complicated by the fact that it shows substantial clinical heterogeneity, with a high degree of variability in susceptibility, site of onset of symptoms, age of onset, and severity and progression of disease. However, what underpins this heterogeneity is not understood. Here we will utilise a unique cohort of human tissue, alongside highly characterised transgenic model tissue, to investigate the role of individual glial populations in triggering inhibitory pathogenesis. The findings of this project will contribute important knowledge to the problem of clinical heterogeneity in ALS, and prove invaluable for the development of therapeutic candidates that can be targeted to the motor system during the symptomatic phase.
- Funding
- Motor Neurone Disease Research Australia ($98,339)
- Scheme
- Grant - Innovator
- Administered By
- University of Tasmania
- Research Team
- Dickson TC; Clark RM; Young K; Blizzard C
- Year
- 2022
- Description
- ALS is caused by a destruction of the neurons that are part of the motor system in the brain and spinal cord. It is not known how the disease moves through this system and we have few effective treatments to stop the spread. In Lauras PHD she aims to discover why one population of neurons can make another population stop working, ie. How the disease spreads, and test a non invasive intervention to stop this destruction from spreading. If we can better understand why the whole system fails and how to protection against this then we can develop new effective treatments for ALS.
- Funding
- Motor Neurone Disease Research Australia ($15,000)
- Scheme
- Scholarship-PhD Top-Up Grant
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Reale LA
- Period
- 2020 - 2022
- Description
- Deficits in neuroplasticity may be one of the earliest events in Frontotemporal Dementia (FTD). Our studies have identified that TDP-43, a frequently aggregated protein in FTD specifically affects neuroplasticity at the dendrite spine in mouse models of FTD. Furthermore we have identified that this pathogenic mechanism is likely due to the translocation of TDP-43 into the cytoplasm. It is now time to unravel the role of mislocalised TDP-43 in neuroplasticity deficits that may drive FTD and perform vital pilot investigations to determine if we can modulate these circuitry deficits non-invasively using transcranial magnetic stimulation (TMS). We will address the hypothesis: Neuroplasticity deficits are an early disease causing event in FTD that can be modulated with TMS using novel mouse models and multiphoton live imaging. This project will be lead by Dr Catherine Blizzard in conjunction with Dr Kaylene Young, who will strategically use the Dementia Australia funding to unravel the earliest changes in neuroplasticity that may drive FTD and generate the pilot data necessary to provide evidence for a large-scale pre clinical trial investigating novel ways to ameliorate neuroplasticity deficits that characterises FTD.
- Funding
- Dementia Australia Research Foundation Ltd ($75,000)
- Scheme
- Grant-Project Grants
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Young K; Lewis KE; Dickson TC
- Period
- 2019 - 2020
- Description
- Deficits in neuroplasticity may be one of the earliest events in Frontotemporal Dementia (FTD). Our studies have identified that TDP-43, a frequently aggregated protein in FTD specifically affects neuroplasticity at the dendrite spine in mouse models of FTD. Furthermore we have identified that this pathogenic mechanism is likely due to the translocation of TDP-43 into the cytoplasm. It is now time to unravel the role of mislocalised TDP-43 in neuroplasticity deficits that may drive FTD and perform vital pilot investigations to determine if we can modulate these circuitry deficits non-invasively using transcranial magnetic stimulation (TMS). We will address the hypothesis: Neuroplasticity deficits are an early disease causing event in FTD that can be modulated with TMS using novel mouse models and multiphoton live imaging. This project will be lead by Dr Catherine Blizzard in conjunction with Dr Kaylene Young, who will strategically use the Dementia Australia funding to unravel the earliest changes in neuroplasticity that may drive FTD and generate the pilot data necessary to provide evidence for a large-scale pre clinical trial investigating novel ways to ameliorate neuroplasticity deficits that characterises FTD
- Funding
- Motor Neurone Disease Research Australia ($99,700)
- Scheme
- Grant - Innovator
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Dickson TC
- Year
- 2019
- Description
- In the vast majority of ALS cases, pathological movement of a protein called TDP-43 from the cell nucleus into the outer parts of the cell occurs. The pathological mechanism of how mislocalised TDP-43 causes motor neuron death is not known.. My PhD project hypothesizes that the presence of TDP-43 in the cytoplasm affects the activity of neurons, which eventually causes their death. I will be identifying if alterations in activity are one of the earliest changes as a consequence of TDP-43 misprocessing and if we can potentially prevent this pathogenic mechanism from driving the onset and progression of ALS.
- Funding
- Motor Neurone Disease Research Australia ($11,250)
- Scheme
- Scholarship-PhD Top-Up Grant
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2019 - 2021
- Description
- We will test an HDAC6 inhibitor in models of ALS. We will investigate the HDA6 inhibitor activity of novel compounds
- Funding
- FightMND ($997,046)
- Scheme
- Grant - Drug Development Grant
- Administered By
- University of Tasmania
- Research Team
- King AE; Cook AL; Guven N; Van Den Bosch L; Dickson TC; Blizzard C; Vickers JC; Smith JA; Alty JE; Leung JY; Perry SE
- Period
- 2019 - 2022
- Description
- Proposed PhD project investigating the role of amyoloid upon axonal dystrophies in the progression of Alzheimers disease
- Funding
- Dementia Australia Research Foundation Ltd ($90,000)
- Scheme
- Grant-Scholarship
- Administered By
- University of Tasmania
- Research Team
- Young K; Blizzard C; Cullen CL; Sutherland BA
- Period
- 2018 - 2020
- Description
- Neuroplasticity describes the brains ability to remodel and make new circuits. This capacity, which is vital for all cognitive function is diminished as we age. Thus it is imperative to determine the mechanisms of neuroplasticity and understand how and why it changes throughout life. It is not know how both excitatory and inhibitory neurons contribute to neuroplasticity and how these dynamic alterations are controlled. This proposal will usesophisticated in vitro platforms; novel transgenic mouse crosses; in vivo live imaging and targeted high-coverage quantitative synaptosome protein comparisons to establish a program of research that will determine how neuroplasticity is controlled in both excitatory and inhibitory neurons.
- Funding
- Australian Research Council ($372,000)
- Scheme
- Fellowship-Discovery Early Career Researcher Award
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2017 - 2019
- Grant Reference
- DE170101514
- Description
- Disturbances in neuronal synapses may be an early event that potentially leads to the neuronal dysfunction and death that causes Amyotrophic Lateral Sclerosis (ALS). Mutations in the protein, transactive response DNA-binding protein 43 (TDP-43) causes a genetic form of ALS. TDP-43 has recently been shown to be involved in maintaining synapses between neurons; regulating the number and maturation of synapses. We will investigate how dysfunction TDP-43 protein alters synapses and determine how these synaptic changes can lead to the neuronal death that characterises ALS.
- Funding
- Motor Neurone Disease Research Australia ($249,861)
- Scheme
- Grant-Betty Laidlaw
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Woodhouse A; Walker A
- Year
- 2017
- Description
- Motor Neuron Disease (MND) is a rapidly progressing neurodegenerative disease. There are no cures and no effective treatments for MND, with people diagnosed having a median survival of only three years from symptom onset. Not knowing the cause of MND or how it progresses through the CNS have been immense barriers to the development of effective therapeutics. We have reached a critical time in MND research. Our research team has been dedicated to researching the mechanism of MND for the last ten years. We are now poised to transition my teams research efforts from determining the cause of this disease to using this knowledge to develop treatments. A critical pathway that our work and others have shown is key to MND is altered network excitability and subsequent excitotoxicity in the cortex. We have recent published and preliminary data that identifies that a critical potential point of intervention in this pathway is via the subclass of inhibitory cells that express neuropeptide Y (NPY). The overarching Aim for this Cure for MND Translational Research Grant is to now target this pathway to develop a treatment. By performing this world-first preclinical trial we will reveal further aspects of disease pathogenesis. Positive outcomes from these trials will identify a candidate compounds for progression to a human trial for the treatment of MND.
- Funding
- FightMND ($936,572)
- Scheme
- Grant-Translational Research Grant
- Administered By
- University of Tasmania
- Research Team
- Dickson TC; Blizzard C; Pebay A; Walker A; Blizzard CL; Rogers M; Hewitt A; Zosky GR
- Period
- 2017 - 2020
- Description
- This is a three year fellowship provided by donations to Menzies.Mark Bennett will advise once candidate accepted offer.
- Funding
- Menzies Institute for Medical Research ($420,000)
- Scheme
- Donation - Institutional
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2016 - 2018
- Description
- Amyotrophic Lateral Sclerosis (ALS) is incurable, caused by the death of motor neurons in the cortex and spinal cord. There is a desperate need to discover new therapeutic ways to stop this neuron death, ideally targeted at early changes in the disease to prevent the majority of cell loss. There is growing evidence that neuronal dysfunction in the cortex is occurring in ALS well before symptoms present. Disturbances in neuronal synapses may be one such early event that potentially leads to neuronal dysfunction and then death. Changes in synapses can have serious effects on neurons activity levels and if not controlled can cause neuron death. The RNA binding protein TDP-43 is likely to play a critical role in ALS as inappropriate localization of this protein is frequent in the disease and mutations in TDP-43 causes a genetic form of ALS. We have found that TDP-43 involved in maintaining synapses between neurons; regulating the number and maturation of spines. It is feasible that an early disease-causing event in ALS may be changes to synapses. We will investigate how different mutations of the TDP-43 protein determine the number and composition of spines as it happens in upper motor neurons of the cortex. This novel research program addresses an important gap in the current understanding of how synaptic changes can lead to neuron death in ALS and may open up a new target for drug intervention in this devastating disease.
- Funding
- Motor Neurone Disease Research Australia ($99,767)
- Scheme
- Grant-In-Aid
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Dickson TC
- Year
- 2016
- Description
- Amyotrophic Lateral Sclerosis (ALS) is a devastating disease that is caused by the death of motor neurons. There is a desperate need to discover new therapeutic ways to stop this neuron death, ideally targeted at early changes in the disease to prevent the majority of cell loss. Disturbances in neuronal synapses may be one such early event that potentially leads to neuronal dysfunction and then death. Synapses are specialised structures that allow neurons to communicate with each other. Changes in synapses can have serious effects on neurons activity levels and if not controlled can cause neuron death. Mutations in the protein, transactive response DNA-binding protein 43 (TDP-43) causes a genetic form of ALS. TDP-43 has recently been shown to be involved in maintaining synapses between neurons; regulating the number and maturation of spines. It is feasible that an early disease-causing event in ALS may be changes to synapses. This project will investigate how different mutations of the TDP-43 protein determines the number and composition of synapses in vitro using specialised compartmentalised primary neuronal cultures. This novel research program addresses an important gap in the current understanding of how synaptic changes can lead to neuron death in ALS and may open up a new target for drug intervention in this devastating disease.
- Funding
- Motor Neurone Disease Research Australia ($94,848)
- Scheme
- Grant-In-Aid
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Dickson TC
- Year
- 2015
- Description
- Changes in synapses can have serious effects on neurons and if notcontrolled can cause neuron death. TDP-43 has been shown to affect the number and maturation of synapses. It is feasible that an early disease-causing event in FTD may be changes to synapses.Emily will determine how TDP-43 changes lead to specific pre and post synaptic alterations in vitro using primary neurons.
- Funding
- Dementia Australia Research Foundation Ltd ($52,500)
- Scheme
- Grant-Scholarship
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2015 - 2017
- Funding
- Dementia Australia Research Foundation Ltd ($110,000)
- Scheme
- Fellowship-Postdoctoral Fellowship in Dementia
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2014 - 2015
- Description
- Frontotemporal dementia is a devastating disease affecting primarily the frontal and temporal part of the brain. It is the second most common form of dementia in people under the age of 65. In FTD proteins that play important functional roles in neurons inappropriately aggregate in the neuronal cyoplasm. This causes the neurons to stop working properly and eventually die. One protein that has been identified to do this is the transactive response DNA-binding protein 43 (TDP-43). The function of the protein is unknown. Understanding its function could provide clues as to what is causing FTD.
- Funding
- Brain Foundation ($35,000)
- Scheme
- Grant-Research
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Dickson TC
- Year
- 2014
- Description
- This novel research program addresses an important gap in the new current understanding of how synaptic changes can lead to neuron death in ALS and may open up a new target for drug intervention in this devastating disease.
- Funding
- Motor Neurone Disease Research Australia ($84,971)
- Scheme
- Grant-In-Aid
- Administered By
- University of Tasmania
- Research Team
- Blizzard C; Dickson TC
- Year
- 2014
- Funding
- University of Tasmania ($20,000)
- Scheme
- Grant-Research Enhancement (REGS)
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Year
- 2013
- Funding
- University of Tasmania ($2,500)
- Scheme
- Grant-Conference Support Scheme
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Year
- 2013
- Funding
- Motor Neurone Disease Research Australia ($78,307)
- Scheme
- Grant-In-Aid
- Administered By
- University of Tasmania
- Research Team
- King AE; Blizzard C; Dickson TC
- Year
- 2013
- Funding
- Motor Neurone Disease Research Australia ($8,000)
- Scheme
- Consultancy
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2012 - 2015
- Funding
- Royal Hobart Hospital Research Foundation ($6,508)
- Scheme
- Grant-Starter
- Administered By
- University of Tasmania
- Research Team
- Terblanche N; Blizzard C; King AE; Dickson TC; Skinner MW; Vickers JC
- Year
- 2012
- Funding
- Motor Neurone Disease Research Australia ($225,000)
- Scheme
- Fellowship-Bill Gole MND Research
- Administered By
- University of Tasmania
- Research Team
- Blizzard C
- Period
- 2011 - 2013
- Funding
- Masonic Medical Research Foundation Limited ($60,000)
- Scheme
- Scholarship
- Administered By
- University of Tasmania
- Research Team
- Vickers JC; Blizzard C
- Period
- 2007 - 2009
Research Supervision
I have seven PhD completions (three as primary supervisor) and my students have produced 14 original research publications and been awarded two international and five national presentation prizes and 10 travel grants.
Current
4
Completed
7
Current
Degree | Title | Commenced |
---|---|---|
PhD | Investigating the Role of Mislocalised TDP-43 in Cortical Hyperexcitability in ALS | 2018 |
PhD | Cuprizone Demyelination Modifies Neuron to Oligodendrocyte Progenitor Cell Synaptic Networks | 2018 |
PhD | Inhibitory Regulation of Motor Neurons: A new target mechanism for MND | 2018 |
PhD | Investigating the Role of TDP-43 in Synaptic Dysfunction in ALS | 2019 |
Completed
Degree | Title | Completed |
---|---|---|
Masters | Investigating Differential Cellular and Regional Vulnerability to Alpha-Synuclein Pathogenesis in the Cortex Candidate: Anastasia Jasmine Salter | 2021 |
PhD | Investigating the Influence of Risk Factors on the Cellular Changes After Mild Traumatic Brain Injury Candidate: Zhendan Zhu | 2020 |
PhD | Cellular Dysfunction in Amyotrophic Lateral Sclerosis: Investigating the role of TDP-43 Candidate: Tongcui Jiang | 2019 |
PhD | Neuroplasticity of the Dendritic Spine: Early dysfunction in amyotrophic lateral sclerosis Candidate: Emily Elizabeth Handley | 2019 |
PhD | Targeting Microtubules in the Distal Neuromuscular Circuitry to Improve Outcomes in Amyotrophic Lateral Sclerosis Candidate: Jayden Andrew Clark | 2017 |
PhD | Interneuron Dysfunction in Amyotrophic Lateral Sclerosis Candidate: Rosemary Maree Clark | 2017 |
PhD | Injury Induced Plasticity in Primary Neuronal Culture and the Mature Brain Candidate: Mariana Del Valle Brizuela | 2016 |