Dr Murielle Kluge
Strategy and Research Coordinator
School of Biomedical Sciences and Pharmacy
- Phone: (02) 4921 8672
I work within the newly formed “Virtual Reality (VR) in Teaching” group at UON. We develop and evaluate of community-focused teaching and training solutions using mixed reality (XR) technology, for a range of applications.
In my role, I am at the intersection between science and technology and their real-world applications. I facilitate and drive the creation of new training and teaching solutions and the subsequent evaluation of their impact and effectiveness. My work is highly diverse and spans a variety of sectors. I focus on synthesising knowledge through complex partnerships between technology experts, clinical psychologists, educators, academics and industry groups. With my strong science and research background, I bring a highly process-oriented approach to the team.
Previous Experience and Research Focus:
I came to Australia in 2014, on a research scholarship with Professor Rohan Walker and completed my PhD in Neuroscience in 2018. My research focused on the contribution of microglia (immune cells of the brain) to the chronic phases after stroke. I remain very passionate about neuro-molecular mechanisms, specifically the involvement of my favourite cell type (microglia cells), in processes such as stress, inflammation and stroke. Since completing my PhD studies, I have transitioned from basic science research to focus on the effects of stress on a larger system: the human being as a whole.
I passionately believe that stress management strategies are an essential and basic life skill, which can and should be taught throughout an individual’s lifetime. Just as exercise and a healthy diet are now indisputably considered essential to wellbeing, effective stress management strategies also contribute to a person’s overall health. Despite substantial scientific evidence to the contrary, public perception persists with the myth that stress resiliency is inherited rather than a developed skill. However, the ability to effectively deal with stress effectively in our day-to-day lives can be trained. These skills are unfortunately often not taught, and existing training approaches are often unstructured, informal and not evidence-based. My primary research goal is to move us away from the stigma currently attached to stress management training. I utilise novel technologies to create effective teaching platforms (e.g. virtual reality) that facilitate knowledge transfer and provide evidence-based skills training in stress management, both broadly and for specific applications.
- Doctor of Philosophy in Anatomy, University of Newcastle
- Master of Science, Philipps University of Marburg, Germany
- Evaluation of novel teaching modalities
- Microglia Cell Activation, Motility and Migration
- Stress and Stress Management Skills
- Teaching Platforms and Technologies
- digital simulation technology
- German (Mother)
- English (Fluent)
Fields of Research
|130101||Continuing and Community Education||50|
|150307||Innovation and Technology Management||50|
|Dates||Title||Organisation / Department|
Strategy and Research Cooardinator
Using innovate ways to teach, learn and train.
|Faculty of Health and Medicine, The University of Newcastle
School of Biomedical Science and Pharmacy
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (11 outputs)
Abdolhoseini M, Kluge MG, Walker FR, Johnson SJ, 'Segmentation, Tracing, and Quantification of Microglial Cells from 3D Image Stacks', SCIENTIFIC REPORTS, 9 (2019) [C1]
Hinwood M, Kluge MG, Ilicic M, Walker FR, 'Understanding microglial involvement in stress-induced mood disturbance: a modulator of vulnerability?', Current Opinion in Behavioral Sciences, 28 98-104 (2019) [C1]
© 2019 Elsevier Ltd Evidence demonstrating that microglial mediated neuroimmune disturbances play a central role in the aetiology of mood pathology have transformed the landscape ... [more]
© 2019 Elsevier Ltd Evidence demonstrating that microglial mediated neuroimmune disturbances play a central role in the aetiology of mood pathology have transformed the landscape within psychiatric neuroscience. This article will place in context these recent developments and will place a particular focus on considering how microglia may contribute to shaping the operating environment of the CNS to foster susceptibility and resilience to psychopathology. Specifically, we will consider contributions from microglial priming, microglial modulation of synaptic plasticity, glial modulation of glutamatergic tone, and finally the role of neuroinflammatory disturbances in cerebrovascular integrity. Although much has been revealed about neuroimmune contributions to mood state and psychological health, our understanding of core mechanisms is still very much in a state of flux and it is likely that new insights will continue to shape our understanding well into the future.
Abdolhoseini M, Kluge MG, Walker FR, Johnson SJ, 'Segmentation of Heavily Clustered Nuclei from Histopathological Images', SCIENTIFIC REPORTS, 9 (2019) [C1]
Kluge MG, Abdolhoseini M, Zalewska K, Ong LK, Johnson SJ, Nilsson M, Walker FR, 'Spatiotemporal analysis of impaired microglia process movement at sites of secondary neurodegeneration post-stroke', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 39 2456-2470 (2019) [C1]
Jones KA, Maltby S, Plank MW, Kluge M, Nilsson M, Foster PS, Walker FR, 'Peripheral immune cells infiltrate into sites of secondary neurodegeneration after ischemic stroke', Brain, Behavior, and Immunity, 67 299-307 (2018) [C1]
© 2017 Elsevier Inc. Experimental stroke leads to microglia activation and progressive neuronal loss at sites of secondary neurodegeneration (SND). These lesions are remote from, ... [more]
© 2017 Elsevier Inc. Experimental stroke leads to microglia activation and progressive neuronal loss at sites of secondary neurodegeneration (SND). These lesions are remote from, but synaptically connected to, primary infarction sites. Previous studies have demonstrated that immune cells are present in sites of infarction in the first hours and days after stroke, and are associated with increased neurodegeneration in peri-infarct regions. However, it is not known whether immune cells are also present in more distal sites where SND occurs. Our study aimed to investigate whether immune cells are present in sites of SND and, if so, how these cell populations compare to those in the peri-infarct zone. Cells were isolated from the thalamus, the main site of SND, and remaining brain tissue 14 days post-stroke. Analysis was performed using flow cytometry to quantify microglia, myeloid cell and lymphocyte numbers. We identified a substantial infiltration of immune cells in the ipsilateral (stroked) compared to the contralateral (control) thalamus, with a significant increase in the percentage of CD4+ and CD8+ T cells. This result was further quantified using immunofluorescent labelling of fixed tissue. In the remaining ipsilateral hemisphere tissue, there were significant increases in the frequency of CD4+ and CD8+ T lymphocytes, B lymphocytes, Ly6G+ neutrophils and both Ly6G-Ly6CLO and Ly6G-Ly6CHI monocytes. Our results indicate that infiltrating immune cells persist in ischemic tissue after the acute ischemic phase, and are increased in sites of SND. Importantly, immune cells have been shown to play pivotal roles in both damage and repair processes after stroke. Our findings indicate that immune cells may also be involved in the pathogenesis of SND and further clinical studies are warranted to characterise the nature of inflammatory cell infiltrates in human disease.
Ong LK, Chow WZ, Tebay C, Kluge M, Pietrogrande G, Zalewska K, et al., 'Growth Hormone Improves Cognitive Function After Experimental Stroke', STROKE, 49 1257-+ (2018) [C1]
Kluge MG, Jones K, Kooi Ong L, Gowing EK, Nilsson M, Clarkson AN, Walker FR, 'Age-dependent Disturbances of Neuronal and Glial Protein Expression Profiles in Areas of Secondary Neurodegeneration Post-stroke', Neuroscience, 393 185-195 (2018) [C1]
© 2018 Despite the fact that approximately 80% of strokes occur in those aged over 60 years, many pre-clinical stroke studies have been conducted in younger adult rodents, raising... [more]
© 2018 Despite the fact that approximately 80% of strokes occur in those aged over 60 years, many pre-clinical stroke studies have been conducted in younger adult rodents, raising debate about translation and generalizability of these results. We were interested in potential age differences in stroke-induced secondary neurodegeneration (SND). SND involves the death of neurons in areas remote from, but connected to, the site of infarction, as well as glial disturbances. Here we investigated potential differences in key parameters of SND in the thalamus, a major site of post-stroke SND. Protein expression profiles in young adult (2¿4 months) and aged (22¿23 months) mice were analyzed 28 days after a cortical stroke. Our results show that age reduced the expression of synaptic markers (PSD 95, Synapsin1) and increased Amyloid ß oligomer accumulation after stroke. Protein expression of several markers of glial activity remained relatively stable across age groups post-stroke. We have identified that age exacerbates the severity of SND after stroke. Our results, however, do not support a view that microglia or astrocytes are the main contributors to the enhanced severity of SND in aged mice.
Zalewska K, Pietrogrande G, Ong LK, Abdolhoseini M, Kluge M, Johnson SJ, et al., 'Sustained administration of corticosterone at stress-like levels after stroke suppressed glial reactivity at sites of thalamic secondary neurodegeneration', Brain, Behavior, and Immunity, 69 210-222 (2018) [C1]
© 2017 Elsevier Inc. Secondary neurodegeneration (SND) is an insidious and progressive condition involving the death of neurons in regions of the brain that were connected to but ... [more]
© 2017 Elsevier Inc. Secondary neurodegeneration (SND) is an insidious and progressive condition involving the death of neurons in regions of the brain that were connected to but undamaged by the initial stroke. Our group have published compelling evidence that exposure to psychological stress can significantly exacerbate the severity SND, a finding that has considerable clinical implications given that stroke-survivors often report experiencing high and unremitting levels of psychological stress. It may be possible to use one or more targeted pharmacological approaches to limit the negative effects of stress on the recovery process but in order to move forward with this approach the most critical stress signals have to be identified. Accordingly, in the current study we have directed our attention to examining the potential effects of corticosterone, delivered orally at stress-like levels. Our interest is to determine how similar the effects of corticosterone are to stress on repair and remodelling that is known to occur after stroke. The study involved 4 groups, sham and stroke, either administered corticosterone or normal drinking water. The functional impact was assessed using the cylinder task for paw asymmetry, grid walk for sensorimotor function, inverted grid for muscle strength and coordination and open field for anxiety-like behaviour. Biochemically and histologically, we considered disturbances in main cellular elements of the neurovascular unit, including microglia, astrocytes, neurons and blood vessels using both immunohistochemistry and western blotting. In short, we identified that corticosterone delivery after stroke results in significant suppression of key microglial and astroglial markers. No changes were observed on the vasculature and in neuronal specific markers. No changes were identified for sensorimotor function or anxiety-like behaviour. We did, however, observe a significant change in motor function as assessed using the inverted grid walk test. Collectively, these results suggest that pharmacologically targeting corticosterone levels in the future may be warranted but that such an approach is unlikely to limit all the negative effects associated with exposure to chronic stress.
Ong LK, Zhao Z, Kluge M, Walker FR, Nilsson M, 'Chronic stress exposure following photothrombotic stroke is associated with increased levels of amyloid beta accumulation and altered oligomerisation at sites of thalamic secondary neurodegeneration in mice', Journal of Cerebral Blood Flow and Metabolism, 37 1338-1348 (2017) [C1]
© Author(s) 2016. Exposure to severe stress following stroke is recognised to complicate the recovery process. We have identified that stress can exacerbate the severity of post-s... [more]
© Author(s) 2016. Exposure to severe stress following stroke is recognised to complicate the recovery process. We have identified that stress can exacerbate the severity of post-stroke secondary neurodegeneration in the thalamus. In this study, we investigated whether exposure to stress could influence the accumulation of the neurotoxic protein Amyloid-b. Using an experimental model of focal cortical ischemia in adult mice combined with exposure to chronic restraint stress, we examined changes within the contra-and ipsilateral thalamus at six weeks post-stroke using Western blotting and immunohistochemical approaches. Western blotting analysis indicated that stroke was associated with a significant enhancement of the 25 and 50 kDa oligomers within the ipsilateral hemisphere and the 20 kDa oligomer within the contralateral hemisphere. Stroked animals exposed to stress exhibited an additional increase in multiple forms of Amyloid-beta oligomers. Immunohistochemistry analysis confirmed that stroke was associated with a significant accumulation of Amyloid-beta within the thalami of both hemispheres, an effect that was exacerbated in stroke animals exposed to stress. Given that Amyloid-beta oligomers, most notably the 30-40 and 50 kDa oligomers, are recognised to correlate with accelerated cognitive decline, our results suggest that monitoring stress levels in patients recovering from stroke may merit consideration in the future.
Ong LK, Zhao Z, Kluge M, TeBay C, Zalewska K, Dickson PW, et al., 'Reconsidering the role of glial cells in chronic stress-induced dopaminergic neurons loss within the substantia nigra? Friend or foe?', Brain, Behavior, and Immunity, 60 117-125 (2017) [C1]
© 2016 Elsevier Inc. Exposure to psychological stress is known to seriously disrupt the operation of the substantia nigra (SN) and may in fact initiate the loss of dopaminergic ne... [more]
© 2016 Elsevier Inc. Exposure to psychological stress is known to seriously disrupt the operation of the substantia nigra (SN) and may in fact initiate the loss of dopaminergic neurons within the SN. In this study, we aimed to investigate how chronic stress modified the SN in adult male mice. Using a paradigm of repeated restraint stress (an average of 20¿h per week for 6¿weeks), we examined changes within the SN using western blotting and immunohistochemistry. We demonstrated that chronic stress was associated with a clear loss of dopaminergic neurons within the SN. The loss of dopaminergic neurons was accompanied by higher levels of oxidative stress damage, indexed by levels of protein carbonylation and strong suppression of both microglial and astrocytic responses. In addition, we demonstrated for the first time, that chronic stress alone enhanced the aggregation of a-synuclein into the insoluble protein fraction. These results indicate that chronic stress triggered loss of dopaminergic neurons by increasing oxidative stress, suppressing glial neuroprotective functions and enhancing the aggregation of the neurotoxic protein, a-synuclein. Collectively, these results reinforce the negative effects of chronic stress on the viability of dopaminergic cells within the SN.
Kluge MG, Kracht L, Abdolhoseini M, Ong LK, Johnson SJ, Nilsson M, Walker FR, 'Impaired microglia process dynamics post-stroke are specific to sites of secondary neurodegeneration', GLIA, 65 1885-1899 (2017) [C1]
© 2017 Wiley Periodicals, Inc. Stroke induces tissue death both at the site of infarction and at secondary sites connected to the primary infarction. This latter process has been ... [more]
© 2017 Wiley Periodicals, Inc. Stroke induces tissue death both at the site of infarction and at secondary sites connected to the primary infarction. This latter process has been referred to as secondary neurodegeneration (SND). Using predominantly fixed tissue analyses, microglia have been implicated in regulating the initial response at both damage sites post-stroke. In this study, we used acute slice based multiphoton imaging, to investigate microglia dynamic process movement in mice 14 days after a photothrombotic stroke. We evaluated the baseline motility and process responses to locally induced laser damage in both the peri-infarct (PI) territory and the ipsilateral thalamus, a major site of post-stroke SND. Our findings show that microglia process extension toward laser damage within the thalamus is lost, yet remains robustly intact within the PI territory. However, microglia at both sites displayed an activated morphology and elevated levels of commonly used activation markers (CD68, CD11b), indicating that the standardly used fixed tissue metrics of microglial ¿activity¿ are not necessarily predictive of microglia function. Analysis of the purinergic P2Y12 receptor, a key regulator of microglia process extension, revealed an increased somal localization on nonresponsive microglia in the thalamus. To our knowledge, this is the first study to identify a non-responsive microglia phenotype specific to areas of SND post-stroke, which cannot be identified by the classical assessment of microglia activation but rather the localization of P2Y12 to the soma.
|Show 8 more journal articles|
Conference (1 outputs)
Abdolhoseini M, Klugen MG, Walker FR, Johnson SJ, 'Neuron image synthesizer via gaussian mixture model and perlin noise', 2019 IEEE 16th International Symposium On Biomedical Imaging (ISBI 2019), Venice, ITALY (2019) [E1]
Simulation Technology Evaluation Pilot Program (STEP1) 2019 - 2021
STEP1 is University wide program and key initiative of the NEW Education Framework brought to life by the former DVC-A Darrell Evans .
It is a prospective return on investment research program to consider the merits of introducing innovative, new technologies into existing degree programs within the University of Newcastle. This pilot project supports, manages and evaluates the development of at least 4 different simulation technology teaching tools. The program is supported by the DVC-A's office and lead by Professor Rohan Walker.
A Cost-Effective Virtual Reality Approach To Assess And Train Cognitive Resilience (Performance EDGE) 2017 - 2021
This project is an ADF funded project within the Defence Health Annual Grants Foundation Research Innovation program. The project centers around the development of a virtual reality (VR) approach to train stress management techniques. The VR training tool, termed Performance EDGE, will focus on knowledge transfer, repetitive skills training and consolidation of established stress-management skills and includes biofeedback technology to capture physiological responses. Scientific leads and chef investigators on the project are A/Prof Eugene Nalivaiko and Prof Frederick Rohan Walker. The project includes a number of pilot trials and user testing as well as the evaluation of effectiveness.
Dr Murielle Kluge
Strategy and Research Coordinator
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine