Profiles
Rachel Atkinson
Rachel Atkinson
Lecturer
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.
Biography
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
Qualifications
Degree | Thesis title | University | Country | Date of award |
PhD | Frontotemporal dementia/ Amyotrophic lateral sclerosis proteins in neurite health and dysfunction | University of Tasmania | Australia | Pending |
BBiotech and Med Res (1st Class Hons) | Frontotemporal dementia proteins in development: Insights into their normal role and relationship to disease | University of Tasmania | Australia | December, 2013 |
Teaching
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 www.utas.edu.au/courses/CAD101
View more on Dr Rachel Atkinson in WARP
Expertise
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)
- Clinical chemistry (incl. diagnostics) (320202)
- Neurosciences (320999)
- Neurogenetics (310511)
Research Objectives
- Clinical health (200199)
- Treatment of human diseases and conditions (200105)
- Expanding knowledge in the health sciences (280112)
- Prevention of human diseases and conditions (200104)
- Diagnosis of human diseases and conditions (200101)
- Expanding knowledge in the biomedical and clinical sciences (280103)
Publications
Total publications
11
Journal Article
(11 outputs)| Year | Citation | Altmetrics |
|---|---|---|
| 2023 | Kabir F, Atkinson R, Cook AL, Phipps AJ, King AE, 'The role of altered protein acetylation in neurodegenerative disease', Frontiers in Aging Neuroscience, 14 pp. 1-24. ISSN 1663-4365 (2023) [Refereed Article] DOI: 10.3389/fnagi.2022.1025473 [eCite] [Details] Co-authors: Kabir F; Cook AL; Phipps AJ; King AE | |
| 2021 | Atkinson 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 | |
| 2021 | Atkinson 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 - 6Web of Science - 3 Co-authors: Leung J; Bender J; Kirkcaldie M; Vickers J; King A | |
| 2020 | Liu Y, Hanson KA, McCormack G, Atkinson RAK, Dittmann J, et al., 'Enhanced anti-amyloid effect of combined leptin and pioglitazone in app/ps1 transgenic mice', Current Alzheimer Research, 17, (14) pp. 1294-1301. ISSN 1567-2050 (2020) [Refereed Article] DOI: 10.2174/1567205018666210218163857 [eCite] [Details] Citations: Scopus - 4Web of Science - 5 Co-authors: Liu Y; McCormack G; Dittmann J; Vickers JC; King AE | |
| 2018 | Woodhouse 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 - 6Web of Science - 6 Co-authors: Woodhouse A; Fernandez-Martos CM; Hanson KA; Collins JM; O'Mara AR; Terblanche N; Skinner MW; Vickers JC; King AE | |
| 2016 | Fernandez-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 - 30 Co-authors: Fernandez-Martos CM; Chuah MI; King AE; Vickers JC | |
| 2015 | Atkinson 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 - 22Web of Science - 27 Co-authors: Fernandez-Martos CM; Vickers JC; King AE | |
| 2015 | Fernandez-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 - 22Web of Science - 20 Co-authors: Fernandez-Martos CM; King AE; Woodhouse A; Vickers JC | |
| 2015 | Liu 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 - 11Web of Science - 10 Co-authors: Liu Y; Fernandez-Martos CM; Kirkcaldie MTK; Vickers JC; King AE | |
| 2015 | Soo 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 - 43Web of Science - 44 Co-authors: King AE | |
| 2014 | Farg 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 - 320Web of Science - 305 Co-authors: King AE |
Grants & Funding
Funding Summary
Number of grants
7
Total funding
Projects
- Description
- Donation account for Brian Marks Research Grant recipient.
- Funding
- Donation via University of Tasmania Foundation ($30,000)
- Scheme
- Donation - Individual
- Administered By
- University of Tasmania
- Research Team
- Atkinson RAK
- Year
- 2023
- Description
- In this project we want to investigate whether genetic risk and environmental interactions cause motor neurons to die and what cellular pathways are activated in response to genetic and environmental risk individually, and combined. We will use human cells to grow motor neurons in a dish, and genetically alter these neurons to carry genes associated with familial or sporadic ALS - this will be modelling the first 'step' in the multistep process. We will then expose these neurons to a variety of environmental factors known to be risk factors for ALS, including cholesterol, neurotoxins and increased cellular activity, that will contribute additional steps in this process. We will examine how the neurons respond to different gene-environment interactions by documenting changes to their shape, activity and function, cellular processes and protein expression, to identify key/signature pathways in these cells that are going wrong in disease. We will correlate our findings in cells to human ALS tissues and ALS mouse models. This work will help us understand how ALS develops and why cells are vulnerable to genetic and environmental interactions.
- Funding
- FightMND ($999,981)
- Scheme
- Grant-Discovery
- Administered By
- University of Tasmania
- Research Team
- Cook AL; Perry SE; King AE; Atkinson RAK; Phipps AJ
- Period
- 2022 - 2025
- 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
- Description
- This project looks at the effect of leptin resistance induced by high path diet on the neurodegenerative pathways induced by TDP-43.
- Funding
- Fundacion Hospital Nacional de Paraplejicos ($222,212)
- Scheme
- Consortium Agreement
- Administered By
- Fundacion Hospital Nacional de Paraplejicos
- Research Team
- Fernandez Martos C; King AE; Del Olmo Izquierdo N; Sreedharan J; Vickers JC; Atkinson RAK
- Period
- 2020 - 2022
- 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
- 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
- Description
- 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.
- Funding
- Dementia Australia Research Foundation Ltd ($90,000)
- Scheme
- Grant-Scholarship
- Administered By
- University of Tasmania
- Research Team
- King AE; Atkinson RAK; Vickers JC
- Period
- 2014 - 2016
Research Supervision
During her PhD, Rachel was heavily involved in the training of undergraduate, honours and postgraduate students in the laboratory.
Current
4
Completed
1
Current
| Degree | Title | Commenced |
|---|---|---|
| PhD | The Role of Wallerian Degeneration and Axon Loss in Dementia | 2019 |
| PhD | Developing Drugs to Protect Neuronal Connections in Neurodegenerative Diseases | 2020 |
| PhD | Investigating the Role of SARM1 in Axon Degeneration using Human Induced Pluripotent Stem Cells | 2021 |
| PhD | Axon Alteration in ALS | 2023 |
Completed
| Degree | Title | Completed |
|---|---|---|
| PhD | Investigations of Excitotoxic Injury in the Visual System of Mice Candidate: James Alexander Bender | 2021 |