Rachel Atkinson

UTAS Home Dr Rachel Atkinson

Rachel Atkinson

Wicking Dementia Research & Education Centre

Room 417-22, Level 4 , Medical Science 1

+61 3 6226 4278 (phone)

Rachel Atkinson is a neuroscience lecturer in the Bachelor of Dementia Care. Her research interests are in frontotemporal dementia and amyotrophic lateral sclerosis and the proteins associated with these diseases.


Rachel carried out her undergraduate and postgraduate studies at the University of Tasmania. She submitted her PhD thesis in 2017 and is currently undertaking her first appointment as a balanced teaching/research academic in the Wicking Dementia Research and Education Centre at the University of Tasmania.

General Responsibilities

Rachel Atkinson is a neuroscience lecturer in the Bachelor of Dementia Care. Her research interests are in frontotemporal dementia and amyotrophic lateral sclerosis and the proteins associated with these diseases.

Career summary



Thesis title



Date of award


Frontotemporal dementia/ Amyotrophic lateral sclerosis proteins in neurite health and dysfunction

University of Tasmania



BBiotech and Med Res (1st Class Hons)

Frontotemporal dementia proteins in development: Insights into their normal role and relationship to disease

University of Tasmania


December, 2013


Neuroscience, dementia, ageing, neurodegeneration, human biology

Teaching expertise

Rachel has been involved in running practical sessions, carrying out tutorials and giving lectures for Human Biology, Histology and Neuroscience to medical, science and pharmacy students. She has also been a marker and tutor in the Bachelor of Dementia care for a range of units including: CAD110 (Negotiated Study in Understanding Dementia), CAD004 (Neurospeak – Understanding the Nervous System), CAD101 (Introduction to Ageing, the Brain and Dementia), CAD103 (Introduction to Dementia in Australia), CAD302 (Advanced Topics in the Neurobiology of Dementia) and CAD304 (Negotiated Project in Dementia).

Teaching responsibility

Unit Co-ordinator Introduction to the Brain, Ageing and Dementia

View more on Dr Rachel Atkinson in WARP


Tissue Culture

Molecular Biology (cloning) and construct design

Viral techniques

Behavioural studies in mice

Advanced microscopy

Research Themes

Rachel’s research aligns to the University’s research theme of Better Health and with the NHMRA priority areas of Dementia and Ageing Well. As a member of the Wicking Centre, her research is targeted towards better understanding of the cellular and molecular mechanisms which underpin dementia. Rachel’s particular interests include understanding the underlying causes of frontotemporal dementia and amyotrophic lateral sclerosis.

Frontotemporal dementia is the second most common cause of younger onset dementia, and amyotrophic lateral sclerosis is the most common form of motor neuron disease. A number of proteins have been implicated in playing roles in these diseases. Rachel’s research proposes that these proteins play a role in maintaining the long nerve processes of neurons, and, in disease this results in disconnection of neurons within the nervous system. In order to study these proteins, Rachel uses viruses, like those that infect humans, to inject cells in the brain and in the dish and cause them to express mutant forms of proteins involved in frontotemporal dementia. These techniques allow the mechanisms by which these proteins cause nerve cells to dysfunction to be further deciphered.

Current projects

Towards axon protection in ALS (Motor Neuron Disease Research Institute Australia funded project)

Staying connected: determining targets to protect neuronal circuitry in ALS (Motor Neuron Disease Research Institute Australia funded project)

Fields of Research

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

Research Objectives

  • Clinical health (200199)
  • Expanding knowledge in the health sciences (280112)
  • Treatment of human diseases and conditions (200105)
  • Expanding knowledge in the biomedical and clinical sciences (280103)
  • Prevention of human diseases and conditions (200104)
  • Diagnosis of human diseases and conditions (200101)


Total publications


Journal Article

(9 outputs)
2021Atkinson RAK, Fair HL, Wilson R, Vickers JC, King AE, 'Effects of TDP-43 overexpression on neuron proteome and morphology in vitro', Molecular and Cellular Neurosciences, 114 pp. 1-11. ISSN 1044-7431 (2021) [Refereed Article]

DOI: 10.1016/j.mcn.2021.103627 [eCite] [Details]

Co-authors: Fair HL; Wilson R; Vickers JC; King AE


2021Atkinson RAK, Leung J, Bender J, Kirkcaldie M, Vickers J, et al., 'TDP-43 mislocalization drives neurofilament changes in a novel model of TDP-43 proteinopathy', Disease Models & Mechanisms, 14, (2) pp. 1-14. ISSN 1754-8403 (2021) [Refereed Article]

DOI: 10.1242/dmm.047548 [eCite] [Details]

Citations: Scopus - 2Web of Science - 1

Co-authors: Leung J; Bender J; Kirkcaldie M; Vickers J; King A


2018Woodhouse A, Fernandez-Martos CM, Atkinson RAK, Hanson KA, Collins JM, et al., 'Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer's disease mice', BMC Anesthesiology, 18, (1) Article 47. ISSN 1471-2253 (2018) [Refereed Article]

DOI: 10.1186/s12871-018-0509-5 [eCite] [Details]

Citations: Scopus - 3Web of Science - 3

Co-authors: Woodhouse A; Fernandez-Martos CM; Hanson KA; Collins JM; O'Mara AR; Terblanche N; Skinner MW; Vickers JC; King AE


2016Fernandez-Martos CM, Atkinson RAK, Chuah MI, King AE, Vickers JC, 'Combination treatment with leptin and pioglitazone in a mouse model of Alzheimer's disease', Alzheimer's & Dementia: Translational Research & Clinical Interventions, 3, (1) pp. 92-106. ISSN 2352-8737 (2016) [Refereed Article]

DOI: 10.1016/j.trci.2016.11.002 [eCite] [Details]

Citations: Scopus - 22

Co-authors: Fernandez-Martos CM; Chuah MI; King AE; Vickers JC


2015Atkinson RA, Fernandez-Martos CM, Atkin J, Vickers JC, King AE, 'C9ORF72 expression and cellular localization over mouse development', Acta neuropathologica communications, 3 Article 59. ISSN 2051-5960 (2015) [Refereed Article]

DOI: 10.1186/s40478-015-0238-7 [eCite] [Details]

Citations: Scopus - 16Web of Science - 20

Co-authors: Fernandez-Martos CM; Vickers JC; King AE


2015Fernandez-Martos CM, King AE, Atkinson RAK, Woodhouse A, Vickers JC, 'Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease', Neurobiology of Aging, 36, (10) pp. 2757-2767. ISSN 0197-4580 (2015) [Refereed Article]

DOI: 10.1016/j.neurobiolaging.2015.07.003 [eCite] [Details]

Citations: Scopus - 20Web of Science - 18

Co-authors: Fernandez-Martos CM; King AE; Woodhouse A; Vickers JC


2015Liu Y, Atkinson RAK, Fernandez-Martos CM, Kirkcaldie MTK, Cui H, et al., 'Changes in TDP-43 expression in development, aging, and in the neurofilament light protein knockout mouse', Neurobiology of Aging: Experimental and Clinical Research, 36, (2) pp. 1151-1159. ISSN 0197-4580 (2015) [Refereed Article]

DOI: 10.1016/j.neurobiolaging.2014.10.001 [eCite] [Details]

Citations: Scopus - 10Web of Science - 9

Co-authors: Liu Y; Fernandez-Martos CM; Kirkcaldie MTK; Vickers JC; King AE


2015Soo KY, Sultana J, King AE, Atkinson RAK, Warraich ST, et al., 'ALS-associated mutant FUS inhibits macroautophagy which is restored by overexpression of Rab1', Cell Death Discovery, 1 Article 15030. ISSN 2058-7716 (2015) [Refereed Article]

DOI: 10.1038/cddiscovery.2015.30 [eCite] [Details]

Citations: Scopus - 36Web of Science - 39

Co-authors: King AE


2014Farg MA, Sundaramoorthy V, Sultana JM, Yang S, Atkinson RAK, et al., 'C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking', Human Molecular Genetics, 23, (13) Article ddu068. ISSN 0964-6906 (2014) [Refereed Article]

DOI: 10.1093/hmg/ddu068 [eCite] [Details]

Citations: Scopus - 276Web of Science - 272

Co-authors: King AE


Grants & Funding

Funding Summary

Number of grants


Total funding



A potential metabolic-targeted therapeutic for Amyotrophic lateral sclerosis (ALS): Leptin (2020 - 2022)$222,212
This project looks at the effect of leptin resistance induced by high path diet on the neurodegenerative pathways induced by TDP-43.
Fundación Hospital Nacional de Parapléjicos ($222,212)
Consortium Agreement
Administered By
Fundacin Hospital Nacional de Parapljicos
Research Team
Fernandez Martos C; King AE; Del Olmo Izquierdo N; Sreedharan J; Vickers JC; Atkinson RAK
2020 - 2022
Proteomic analysis of exosomes from iPS cell-derived neurons with mislocalised TDP-43 (2019)$99,665
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
Motor Neurone Disease Research Australia ($99,665)
Grant - Innovator
Administered By
University of Tasmania
Research Team
Cook AL; King AE; Atkinson RAK; Perry SE; Hewitt A
Do Renshaw cells have a role in amyotrophic lateral sclerosis disease progression (2019)$15,814
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.
University of Tasmania ($15,814)
Grant-Research Enhancement Program
Administered By
University of Tasmania
Research Team
Perry SE; Atkinson RAK; King AE
The role of FTLD proteins in neurite health, function and dysfunction (2014 - 2016)$90,000
In the last seven years a number of proteins have been identified that are pathologically or genetically associated with Frontotemporal Lobe Degeneration including TDP-43, FUS, C9ORF72 and progranulin. As ubiquitously expressed proteins it has been difficult to assess the role these proteins play in disease, particularly associated with ageing. This project proposes that the disease-associated roles are likely to stem from functions that are specific to neurons and/or glial cells. Accumulating evidence suggests that many of these proteins are involved in neurite outgrowth and cytoskeletal maintenance. This project will use a threefold approach to investigate the role of FTLD proteins in disease. First, it will utilize novel primary cell culture techniques that allow compartmentalization of the neuron to probe axonal and somatodenditic mechanisms. Second, it will utilize an in-vivo intraocular injection model to rapidly examine the effect of mutant and non-mutant proteins on downstream connectivity. Finally, it will investigate neurite pathology in human tissue. This project will provide mechanistic insight into the role of FTLD proteins in disease.
Dementia Australia Research Foundation Ltd ($90,000)
Administered By
University of Tasmania
Research Team
King AE; Atkinson RAK; Vickers JC
2014 - 2016

Research Supervision

During her PhD, Rachel was heavily involved in the training of undergraduate, honours and postgraduate students in the laboratory.




PhDInvestigations of Excitotoxic Injury in the Visual System of Mice2018
PhDThe Role of Wallerian Degeneration and Axon Loss in Dementia2019
PhDDeveloping Drugs to Protect Neuronal Connections in Neurodegenerative Diseases2020
PhDInvestigating the Role of SARM1 in Axon Degeneration using Human Induced Pluripotent Stem Cells2021