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Sharn Perry

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Sharn Perry

Lecturer
Wicking Dementia Research & Education Centre

Room 417C , Medical Science 1 (level 4)

Dr Sharn Perry is a neuroscientist and Lecturer with the Wicking Dementia Research and Education Centre in the College of Health and Medicine. Her research interests include the motor system and spinal cord, particularly how nerve cells communicate to control movement and gait.

Biography

Before relocating back to her home town of Hobart, Sharn worked as a postdoctoral researcher in the Developmental Genetics Unit at Uppsala University, Sweden. Her PhD and postdoctoral research work investigated how different spinal cord interneuron populations function to control and modulate motor behaviours such as walking and swimming. Sharn is currently employed as a lecturer with the Wicking Dementia Research and Education Centre.

Career summary

Qualifications

PhD

Deciphering the Locomotor Network: The role of Spinal cord interneurons

Uppsala University

Sweden

2016

BBiomedSc (1st Class Hons)

Physiology

The University of Adelaide

Australia

2010

BBiomedSc

 

The University of Adelaide

Australia

2009

Languages (other than English)

Conversational Swedish

Memberships

Professional practice

Golden Key International Honour Society

Teaching

Neuroscience, Physiology, Spinal cord, Interneurons, Dementia, Electrophysiology, Motor systems, Histology

Teaching expertise

Sharn’s teaching portfolio includes unit coordination, lecturing, tutoring and student supervision across a range of units and courses encompassing everything from basic neuroscience and research techniques, to electrophysiology and motor systems, and central nervous system histology at both undergraduate and master levels.

Teaching responsibility

CAD110 – Negotiated Study in Understanding Dementia

(http://www.utas.edu.au/courses/chm/units/cad110-negotiated-study-in-understanding-dementia)

View more on Dr Sharn Perry in WARP

Expertise

Electrophysiology Techniques

Mouse behaviour experiments  

Motor Circuits

Spinal Cord

Central Nervous System

Fields of Research

  • Cellular nervous system (320902)
  • Neurology and neuromuscular diseases (320905)
  • Neurosciences (320999)
  • Central nervous system (320903)
  • Cell development, proliferation and death (310102)
  • Artificial intelligence (460299)
  • Peripheral nervous system (320906)
  • Neurogenetics (310511)

Research Objectives

  • Clinical health (200199)
  • Treatment of human diseases and conditions (200105)
  • Other health (209999)
  • Expanding knowledge in the biomedical and clinical sciences (280103)
  • Prevention of human diseases and conditions (200104)
  • Diagnosis of human diseases and conditions (200101)

Publications

Total publications

3

Journal Article

(3 outputs)
YearCitationAltmetrics
2019Perry S, Larhammar M, Viellard J, Nagaraja C, Hilscher MM, et al., 'Characterization of Dmrt3-Derived Neurons Suggest a Role within Locomotor Circuits', Journal of Neuroscience, 39, (10) pp. 1771-1782. ISSN 0270-6474 (2019) [Refereed Article]

DOI: 10.1523/JNEUROSCI.0326-18.2018 [eCite] [Details]

Citations: Scopus - 13Web of Science - 13

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2018Aresh B, Freitag FB, Perry SE, Blumel E, Lau J, et al., 'Spinal cord interneurons expressing the gastrin-releasing peptide receptor convey itch through VGLUT2-mediated signaling', Pain, 158, (5) pp. 945-961. ISSN 0304-3959 (2018) [Refereed Article]

DOI: 10.1097/j.pain.0000000000000861 [eCite] [Details]

Citations: Scopus - 38Web of Science - 36

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2015Perry S, Gezelius H, Larhammar M, Hilscher MM, Lamotte d Incamps B, et al., 'Firing properties of Renshaw cells defined by Chrna2 are modulated by hyperpolarizing and small conductance ion currents Ih and ISK', European Journal of Neuroscience, 41, (7) pp. 889-900. ISSN 0953-816X (2015) [Refereed Article]

DOI: 10.1111/ejn.12852 [eCite] [Details]

Citations: Scopus - 17Web of Science - 19

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Grants & Funding

Funding Summary

Number of grants

8

Total funding

$1,962,506

Projects

Now this is an exciting project!: Exciting tools to excite neurons will excite students (2022)$4,969
Description
Donation RecordNeuronal hyperexcitability, often followed by excitotoxicity, is an established pathophysiological process in multiple neurodegenerative diseases including amyotrophic lateral sclerosis 1, Alzheimers disease 2, and Batten disease 3 each of these diseases are a major focus on the Project Team. Currently, we use application of the excitotoxin kainic acid to neurons to simulate excitotoxicity, and while we have learnt much from this approach, it is an exogenous agent and may therefore not fully model excitotoxicity occurring in neurodegenerative disease. Recent advances in electrophysiology have provided an elegant approach to stimulation of neurons, and which enable modelling of disease-driven intrinsic hyperexcitability. Chemogenetics employs Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) in combination with the pharmacologically inert clozapine-N-oxide (CNO) to induce membrane depolarisation in cells that express excitatory DREADD receptors 4, mimicking hyperexcitability independently of external inputs. We wish to establish DREADD/chemogenetics technology at the Wicking Centre. To support application of DREADDs across multiple projects, Perry and Cook will collaboratively establish this technology through supervision of two higher degree by research students, who will undertake the laboratory work as part of their PhD studies.
Funding
Donation via University of Tasmania Foundation ($4,969)
Scheme
Donation - Individual
Administered By
University of Tasmania
Research Team
Perry SE; Cook A
Year
2022
To die or not to die: What is the mechanism of axon degeneration in ALS? (2022)$99,491
Description
Axons are long processes that allow for communication between our nerve cells and muscles to enable movement. During MND, nerve cell axons degenerate, leading to loss of motor function and mortality; the mechanism of which we do not understand. In this project, we will use human iPSC-derived nerve cells to investigate what pathways are involved in axon degeneration through omics approaches, including RNA-seq and proteomics. By understanding why axons are vulnerable, and what pathways dysfunction during MND, we can design novel therapies to prevent and treat axon degeneration in MND.
Funding
Motor Neurone Disease Research Australia ($99,491)
Scheme
Grant - Innovator
Administered By
University of Tasmania
Research Team
Phipps AJ; Atkinson RAK; Perry SE; King AE; Cook AL
Year
2022
Isogenic iPSC models with CLN3 variants for high throughput drug screening (2021)$49,400
Description
To advance therapeutic strategies for Batten disease, we will use our existing isogenic iPSC models with CLN3 variants to:Aim 1: Measure CLN3-dependent changes in neuronal network activity using multielectrode arrays.Aim 2: Quantify CLN3-dependent changes in lysosomal, mitochondrial and autophagy function in neurons.Aim 3: Identify CNS-penetrant drugs that exhibit efficacy against CLN3-variant associated neuron changes.
Funding
Batten Disease Support and Research Association ($49,400)
Scheme
Grant-Research
Administered By
University of Tasmania
Research Team
Cook AL; Hewitt A; King AE; Perry SE
Year
2021
Why do we have SARM 1 protein if knocking it out prevents axons degenerating? (2020 - 2022)$597,651
Description
Loss of axonal connections between nerve cells results in reduced cognitive function and memory loss. Axons, like cells, can orchestrate their own death mechanisms and the SARM1 protein mediates Wallerian degeneration the best known axon death pathway. It is not yet understood, why neurons have evolved to have this axon degeneration pathway; whether it is aberrantly activate in neurodegenerative disease or whether it protects the nervous system from adverse nerve cell connections. By using a combination of methods, including axon injury and neurodegeneration mouse models, and human stem cell research, we will identify the exact role of SARM1 in the response to injury and neurodegeneration and determine whether blocking axons from this protein is beneficial or harmful. Our team is comprised of world leaders in investigating axon pathology, degeneration and regeneration in neurodegenerative disease and injury, and outcomes of this research will advance treatment of diseases such as dementia and motor-neuron disease.
Funding
National Health & Medical Research Council ($597,651)
Scheme
Grant-Ideas
Administered By
University of Tasmania
Research Team
King AE; Canty A; Cook AL; Perry SE
Period
2020 - 2022
Grant Reference
1187156
Proteomic analysis of exosomes from iPS cell-derived neurons with mislocalised TDP-43 (2019)$99,665
Description
Our overarching hypothesis is that TDP-43 mislocalisation leads to altered axonal and exosomal protein expression, and which may underpin the mechanism of TDP-43 pathological spread leading to neurodegeneration of motor circuits in ALS. To begin testing this hypothesis, we have designed experiments to address three Specific Aims:Aim 1: To characterize human iPS cell-based models of TDP-43 mislocalisationAim 2: To quantify proteins differentially expressed in axons and exosomes of iPS cell-derived neurons with and without TDP-43 mislocalisationAim 3: To quantify transmission of TDP-43 mislocalisation and altered phosphorylation in a human cerebral organoid model
Funding
Motor Neurone Disease Research Australia ($99,665)
Scheme
Grant - Innovator
Administered By
University of Tasmania
Research Team
Cook AL; King AE; Atkinson RAK; Perry SE; Hewitt A
Year
2019
HDAC6 inhibition to rescue axon degeneration in ALS (2019 - 2022)$997,046
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
Do Renshaw cells have a role in amyotrophic lateral sclerosis disease progression (2019)$15,814
Description
Amyotrophic lateral sclerosis (ALS) is a debilitating disease that results in the degeneration and eventual death of motor neurons in the brain and spinal cord. Currently, there are no effective treatments to slow or stop disease progression, and as such, patients experience a rapid progression of deteriorating motor symptoms prior to their death. We do not have a solid understanding of what causes motor neurons to be especially vulnerable to degeneration, however, we know that an increase in motor neuron activity, drives the disease forward. To better understand why motor neurons are targeted to become over active, we need to broaden our investigation of ALS mechanisms to other cell populations within motor circuits to examine how these cells might contribute to the biological mechanisms causing the disease. This project focuses on investigating how a population of spinal cord cells, known as Renshaw cells, might contribute to motor neuron degeneration and ALS disease mechanisms. We will use experimental mouse models that i) target Renshaw cells and ii) mimic ALS disease processes, and establish novel techniques to grow spinal cord cells in a dish. We will use these methods to identify and investigate the vulnerability and degeneration of Renshaw cells in response to ALS disease mechanisms, and what consequence this has on motor neuron degeneration.
Funding
University of Tasmania ($15,814)
Scheme
Grant-Research Enhancement Program
Administered By
University of Tasmania
Research Team
Perry SE; Atkinson RAK; King AE
Year
2019
Towards Axon Protection in ALS (2018)$98,470
Description
Nerve cells communicate with each other and their targets, such as muscle, via long processes called axons. In motor neuron disease these nerve cell processes degenerate and are lost, resulting in a loss of movement. Several mechanisms or axon degeneration have been recently identified, but we dont know which of these mechanisms is involved in motor neuron disease. In this project, we will use two models to determine which mechanisms of axon degeneration are involved in nerve process loss in motor neuron disease. This will allow us to determine which molecules to target for therapeutic intervention.
Funding
Motor Neurone Disease Research Australia ($98,470)
Scheme
Grant-In-Aid
Administered By
University of Tasmania
Research Team
King AE; Perry SE; Leung JY
Year
2018

Research Supervision

Since 2014, Dr Perry has supervised undergraduate and graduate students from Uppsala University including 4 undergraduate Medical students in summer internship positions and 2 Master’s students completing their graduate research projects. Sharn is currently supervising one Honours student at the University of Tasmania.

Current

5

Current

DegreeTitleCommenced
PhDDevelop a Novel Device for Regular Monitoring of Blood Biomarkers in Dementia2019
PhDDoes Obesity Exacerbate Neuroinflammation and Alter the Efficacy of Anti-inflammatory Treatment Following Experimental TBI?2020
PhDInvestigating the Role of SARM1 in Axon Degeneration using Human Induced Pluripotent Stem Cells2021
PhDInvestigating the Role of TDP-43 in Synaptic Dysfunction in ALS2021
PhDDo Renshaw Cells Drive Disease in ALS?2022