Dr Lin Kooi Ong
Honorary Associate Lecturer
School of Biomedical Sciences and Pharmacy
- Email:linkooi.ong@newcastle.edu.au
- Phone:(02) 49215736
An objective analysis of the impact of stress
A fascination with human biology and the desire to understand how the body works led Dr Lin Kooi Ong to biomedical science – and now neuroscience where he’s exploring the impact of stress on our health.
As Lin was concluding his undergraduate degree in biomedical science he connected with Professor Peter Dunkley who was the inspiration who honed Lin’s interest in the workings of the brain. Working with Peter first on his Honours year, and then his PhD, Lin’s fascination with the way that the brain works has driven him to specialise in neuroscience research.
“A lot of the basic science about the brain is still unexplored and unknown. We know it’s there, but what’s really happening in the brain with its network and cells all the way to the molecular level?” Lin asks.
With his research, Lin is focused on an increasingly common 21st century health problem – persistent stress. “A lot of people will say ‘Oh, I’m so stressed!’ but, as a neuroscientist with a biochemistry background, I’m really interested in defining what stress is and how it impacts on our health and wellbeing.”
Lin explains that the concept of stress can be confusing as the term is often used interchangeably with distress. “Stress, in a biological way, is the destruction of homeostasis – it impacts on our cell balance. Whereas distress is more of an emotionally unpleasant feeling.”
“As a scientist, I like things to be objective,” Lin says. “We need to be able to classify something such as a physical stressor: which is any threat which has a direct effect on your body or your cells.”
Lin’s research is exploring the parts of the brain which are activated during stress: primarily the catecholaminergic systems such as the locus coeruleus, the ventral tegmental area and the substantia nigra. These neurons transmit dopamine, noradrenaline and adrenaline as chemical messengers or neurotransmitters. “When you are stressed different parts of the brain region get fired up and stimulated. In the short term there are benefits to this, it keeps us alert and prepared for any danger,” Lin explains.
However, when stress is prolonged the effects on the body can be detrimental. During a period of stress the heart rate and blood pressure can be elevated and we get an adrenaline rush. “A small amount of stress is positive, it can improve our resilience and make us adapt to the next stressful event. But if the stress or distress load is high and it remains so for a long time, then it starts to shut down our body system.”
The potential health outcomes associated long-term stress are bleak, with stroke, heart disease and even Parkinson’s disease linked to long-term stress.
Could stress be a risk factor for Parkinson’s disease?
In late 2016 Lin and his team published results from a study linking stress to the development of Parkinson’s disease. With many neurodegenerative diseases, around five – ten per cent of the risk is due to genetic factors, but the remaining 90 per cent is due to idiopathic or unknown factors. “What’s causing the neurodegeneration is still unexplored and researchers are still trying to tease out what are the main components that really cause the brain to slowly die off.”
Taking literature from military doctors who documented Parkinson’s-like symptoms in soldiers after the war, Lin and the team recreated this in the lab through inducing mild stress in mouse modelling. The results showed that after six weeks parts of the brain starts to die off. “This part of the brain controls the motor functions so it’s an important discovery,” Lin adds.
“We think that chronic stress would be a potential risk factor for the development of Parkinson’s disease. It’s not surprising, because while 20 or 30 years ago a lot of neurodegenerative diseases only occurred in people aged over 60, but now it’s getting pushed earlier to around 40-years-old.”
“Age is always a risk factor for neurodegenerative diseases and many other diseases. As you age your body replenishes itself more slowly and all the biological systems get slower. But when you chronically stress the body for long enough the ageing process gets shifted to a younger age,” Lin explains. “So it’s not surprising to see younger people getting stroke, developing hypertension, Parkinson’s and dementia.”
Stress and stroke
The impact of stress on stroke is another area that Lin’s working on because not only does stress have an effect on increasing the risk of stroke, but it can also play a role in making rehabilitation even more difficult.
“One of the things that our lab is doing is using two-way Translational Research to use basic science to investigate what happens in the clinical population, fit it back into basic scientific modelling to investigate potential therapeutic responses, then move it forward to the human population,” Lin says. “So basically moving from bench, to bedside, and bedside to bench. Back and forward.”
Over the course of last few years, Lin and his team used preclinical models to replicate ongoing stress in brain repair after stroke in humans. “We have published many critical preclinical studies (Sage 2016, Sage 2017, Neuroscience 2017) providing evidence that chronic stress is bad for stroke recovery.”
“Excitingly, we are also working on a number of potential therapeutic interventions for stroke recovery. While in their early phases, these interventions, appear to promote neuroplasticity and ameliorate post-stroke cognitive decline.”
It’s hoped that this work will allow the team to develop enough evidence-based research to allow them to move forwards in the public health sphere. One option is through the development of public health campaigns for stress reduction, something Lin feels could be very useful.
Collaborations and ‘hair-brained’ ideas
The NHMRC Centre for Research Excellence in Stroke Recovery and Rehabilitation and the John Hunter Hospital Charitable Trust support Lin in developing and validating a way to measure stress load in an objective and very non-invasive manner – through hair! “One of the things about the stress hormone, cortisol is that it’s deposited in hair, we can extract and measure its levels,” Lin says. “If we take the average hair growing speed, which is around a centimetre a month, this allows us to look at stress periods in a retrospective way.”
“This is a more objective way of measuring stress than asking volunteers in a questionnaire – and also removes limitations around memory and recall,” Lin explains.
We are now working with the Hunter New England Area Health service, in collaboration with researchers at the Florey Institute, to implement the first longitudinal study of stress levels in stroke survivors using an objective biometric evaluation. This work aligns well with the new HMRI Stroke Register where the leading stroke researchers in the Hunter can work with volunteers who are prepared to collaborate with our researchers who are looking to understand stroke.
Lin is collaborating with a range of leading researchers in the Hunter such as Professor Michael Nilsson, Associate Professor Rohan Walker, Associate Professor Coralie English, Associate Professor Phillip Dickson and Professor Deb Hodgson on a wide array of projects around stroke and neuroscience. “We are so lucky to have all these inspiring leaders in our university,” Lin says. “We need to think big and collaboration for leading change in medical research.”
As an early career researcher, Lin’s passionate about ensuring promoting the work that our ECRs do, particularly in the community. Lin is Early Career Researcher Representative for the School of Biomedical Science and Pharmacy Research Committee and was previously the Deputy Newcastle Convenor of the Australian Society for Medical Research (ASMR). “This group of researchers need to be promoted so that government, the public and institutions can see the valuable work they’re doing and keep that work in Australia.”
“I’m a big fan of this quote from the Australian of the year, Professor Alan Mackay-Sim, ‘We must invest in young scientists,’” says Lin.
Also passionate about funding, Lin can see the evidence of public donations from the community in the work our researchers do at HMRI. “Sometimes even a small donation can spark a breakthrough and lead to real changes in health and wellbeing,” Lin concludes.
An objective analysis of the impact of stress
A fascination with human biology and the desire to understand how the body works led Dr Lin Kooi Ong to biomedical science
Career Summary
Biography
Dr Lin Kooi Ong is a Post-Doctoral Research Fellow within the Stroke Recovery Research Group (co-directed by Professor Michael Nilsson and A/Professor Frederick Rohan Walker), University of Newcastle Priority Research Centre in Stroke and Brain Injury and NHMRC Centre for Research Excellence in Stroke Recovery and Rehabilitation (jointly by Florey Institute of Neuroscience and Mental Health and Hunter Medical Research Institute). He graduated with a PhD in Medical Biochemistry (Supervisors; Emeritus Professor Peter Dunkley, A/Professor Phillip Dickson and Dr Larisa Bobrovskaya) in 2012 and completed 2-year Post-Doctoral training (funded by HMRI) in 2014.
Dr Ong’s research expertise is in translational stroke research, with a particular focus on understanding the biological mechanisms of post-stroke cognitive impairment, investigating the impact of chronic stress on stroke recovery, and developing and testing novel interventions to enhance brain repair after stroke.Highlights include:
1. Post-stroke cognitive impairment and secondary neurodegeneration
2. The impact of chronic stress on stroke recovery
3. Growth hormone as therapeutic opportunity to promote stroke recovery
Dr Ong has published 31 peer reviewed articles (12 as first author), 1 book chapter and over 26 conference abstracts. His work has been cited >300 times. Dr Ong’s contributions to the field have been recognized by over 20 grants/awards/scholarships (totalling > $300K). He has received multiple seed funding from the university/institute and philanthropic funding to investigate the relationship between chronic stress, cognitive performance and brain function in health and disease. On many of these multidisciplinary applications, he has been lead investigator. He also received 8 travel awards, including highly competitive award from the International Brain Research Organization (2014 & 2015). Dr Ong has presented his work over 20 times at national and international conferences and institutions. Highlights include; invited seminar at Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil (2015), oral presentation at Asia Pacific Stroke Conference, Brisbane (2016), invited seminar at University of Malaya, National University of Malaysia, and Universiti Putra Malaysia, oral presentation at Australasian Neuroscience Society Meeting, Sydney (2017), and invited seminar at Queensland Brain Institute and oral presentation at Stroke Rehabilitation workshop, Sydney (2018).
Since 2016, Dr Ong is the Early Career Researcher (ECR) Representative for the School of Biomedical Science and Pharmacy Research Committee. He served as an assessor for the Honours program and PhD Advisory Committee. He is on the Editorial Board for newly establish journal - Neuroscience Research Notesand Review Editor for Frontiers in Neuroendocrine Science. He has reviewed over 30 manuscripts for leading journals of his field. He also served as an external assessor for NHMRC Project Grant (2016 & 2018). In 2015/16, Dr Ong was elected as the Deputy Newcastle Convenor of the Australian Society for Medical Research. In 2017, Dr Ong participated in the Stroke Research Consumer Forum involving researchers, stroke survivors and policy makers to discuss around the theme “Stroke Prevention, Recovery and Cure”. He has delivered community engagement presentations to stroke survivors, caregivers and general audiences, including at ASMR Newcastle Gala Dinner, Working Age Group Stroke meeting (2017), Spotlight on Stroke and Pint of Science, Newcastle (2018).
Dr Ong is currently supervising 2 PhD students. Since his PhD, he has mentored and provided technical support of 2 undergraduate, 3 honours, 11 PhD students and 3 professional staffs. If you are interested in joining the research group or support current research please contact lin.ong@uon.edu.au or linkooi.ong@newcastle.edu.au
Research Expertise
Dr Ong uses a multidisciplinary approach to understand the relationship between chronic stress, cognitive performance and brain function in health and disease. He has extensive experience in a wide range of technical repertoire including pre-clinical modellings (stroke, neurodegeneration, stress paradigms, neurodevelopment), behavioural/functional assessments (cognitive and mood assessments, motor testings), rodent stereotaxic surgery, cell culture, advanced imaging techniques, histology analysis, and biochemical assays including immunoprecipitation, protein functional assays, oxidative stress assays, Western blotting, ELISA, HPLC, multiplex immunoassays. To enhance the alignment of pre-clinical and clinical research, Dr Ong has embedded the state of the art touchscreen platform to objectively assess cognitive function. His diverse training in medical biochemistry and neuroscience has placed him in a unique position to involve in clinical trials. He provide expertise in the analysis of human biological samples, including blood, saliva and hair. Highlights include: the establishment of hair cortisol as measurement of cumulative stress biologically and blood biomarkers (growth factors, inflammatory markers and neurotoxic waste proteins).
Teaching Expertise
Musculoskeletal Anatomy (HUBS1105, MEDI1015, MEDI3018), Human Bioscience (HUBS1401), Human Molecular Science (HUBS3206), Human Biochemistry and Cell Biology (HUBS2205, HUBS2207), Neuroscience (HUBS3402), Experimental Design and Laboratory Skills in Medical Research (HUBS2407)
Collaborations
Dr Ong has established successful multidisciplinary collaboration at both national and international levels. He has strong links with researchers, clinicians, allied health professionals and statisticians along the translational research pipeline. Highlights include:
Professor Jorgen Isgaard, University of Gothenburg - Growth hormone as neurorestorative therapy after stroke
A/Professor Michael Pollack, Director of Rehabilitation Medicine, Hunter New England - Monitoring stress load after stroke
Dr Heidi Janssen, Hunter New England Health - Assessment of hair cortisol from SLAM-TIA (Service change and supporting lifestyle and activity modification after transient ischemic attack )
A/Professor Coralie English - Assessment of blood metabolites from BUST-stroke (Breaking Up Sitting Time after stroke)
A/Professor Phillip Dickson and E/Professor Peter Dunkley - The role of inflammation in the development of Parkinson's disease
Professor Sarah Johnson - Computer automated histology and immunohistochemistry analysis
Professor Deborah Hodgson, A/Professor Sarah Spencer and Dr Luba Sominsky - The role of environmental factors on brain development
Qualifications
- PhD (Medical Biochemistry), University of Newcastle
- Bachelor of Biomedical Sciences, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
Keywords
- Biomedical Imaging
- Brain Plasticity
- Catecholamines
- Growth Hormone
- Medical Biochemistry
- Neurodegeneration
- Neuroscience
- Post-stroke cognitive impairment
- Stress Biology
- Stroke Recovery
- Tyrosine Hydroxylase
- catecholamines
Languages
- English (Fluent)
- Malay (Fluent)
Professional Experience
Academic appointment
Dates | Title | Organisation / Department |
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1/3/2012 - 31/12/2014 | Research Associate | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Professional appointment
Dates | Title | Organisation / Department |
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1/3/2018 - | Editorial Board | Neuroscience Research Notes Malaysia |
30/6/2017 - | Review Editor | Frontiers in Neuroendocrine Science Switzerland |
12/12/2015 - | Early Career Researcher Representative | School of Biomedical Sciences Research Committee Australia |
1/7/2014 - 1/7/2016 | Deputy Newcastle ASMR Convenor and Co-Secretary - Australian Society for Medical Research | Australian Society for Medical Research (ASMR) Australia |
Awards
Recipient
Year | Award |
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2015 |
IBRO World Congress Young Investigator Training Program (YITP) International Brain Research Organization |
2014 |
International Brain Research Organization International Travel Grant International Brain Research Organization |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Highlighted Publications
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2018 |
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]
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2020 |
Gyawali P, Chow WZ, Hinwood M, Kluge M, English C, Ong LK, et al., 'Opposing Associations of Stress and Resilience With Functional Outcomes in Stroke Survivors in the Chronic Phase of Stroke: A Cross-Sectional Study', FRONTIERS IN NEUROLOGY, 11 (2020) [C1]
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Chapter (2 outputs)
Year | Citation | Altmetrics | Link | ||
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2022 |
Ong L, Ilicic M, Hood R, Warren K, Coupland K, 'Targeting Adult Neurogenesis for Brain Recovery After Stroke: The Next Frontier in Stroke Medicine', Regenerative Therapies in Ischemic Stroke Recovery, Springer, Singapore (2022)
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2016 |
Walker FR, Ong L, Nilsson M, 'Chronic Stress-induced Changes in Microglia in Determining Vulnerability to Mood Disorders', PRIMER OF PSYCHONEUROIMMUNOLOGY RESEARCH, PsychoNeuroImmunology Research Society, Los Angeles, CA 119-124 (2016) [B1]
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Journal article (54 outputs)
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2023 |
Hood RJ, Sanchez-Bezanilla S, Beard DJ, Rust R, Turner RJ, Stuckey SM, et al., 'Leakage beyond the primary lesion: A temporal analysis of cerebrovascular dysregulation at sites of hippocampal secondary neurodegeneration following cortical photothrombotic stroke', Journal of Neurochemistry, 167 733-752 (2023) [C1] We have previously demonstrated that a cortical stroke causes persistent impairment of hippocampal-dependent cognitive tasks concomitant with secondary neurodegenerative processes... [more] We have previously demonstrated that a cortical stroke causes persistent impairment of hippocampal-dependent cognitive tasks concomitant with secondary neurodegenerative processes such as amyloid-ß accumulation in the hippocampus, a region remote from the primary infarct. Interestingly, there is emerging evidence suggesting that deposition of amyloid-ß around cerebral vessels may lead to cerebrovascular structural changes, neurovascular dysfunction, and disruption of blood¿brain barrier integrity. However, there is limited knowledge about the temporal changes of hippocampal cerebrovasculature after cortical stroke. In the current study, we aimed to characterise the spatiotemporal cerebrovascular changes after cortical stroke. This was done using the photothrombotic stroke model targeting the motor and somatosensory cortices of mice. Cerebrovascular morphology as well as the co-localisation of amyloid-ß with vasculature and blood¿brain barrier integrity were assessed in the cortex and hippocampal regions at 7, 28 and 84 days post-stroke. Our findings showed transient cerebrovascular remodelling in the peri-infarct area up to 28 days post-stroke. Importantly, the cerebrovascular changes were extended beyond the peri-infarct region to the ipsilateral hippocampus and were sustained out to 84 days post-stroke. When investigating vessel diameter, we showed a decrease at 84 days in the peri-infarct and CA1 regions that were exacerbated in vessels with amyloid-ß deposition. Lastly, we showed sustained vascular leakage in the peri-infarct and ipsilateral hippocampus, indicative of a compromised blood¿brain-barrier. Our findings indicate that hippocampal vasculature may represent an important therapeutic target to mitigate the progression of post-stroke cognitive impairment.
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2023 |
Kwa EK, Cheong SK, Ong LK, Lee PF, 'Development of audio-guided deep breathing and auditory Go/No-Go task on evaluating its impact on the wellness of young adults: a pilot study.', Biomed Tech (Berl), (2023) [C1]
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2023 |
Chen KF, Maran S, Tan WS, Ong LK, Abidin SAZ, Othman I, et al., 'Meta-analysis of studies on protection provided by different prophylactic agents, their routes of administration and incubation times against nodavirus infection in Macrobrachium rosenbergii', Aquaculture, 565 (2023) [C1] White tail disease caused by Macrobrachium rosenbergii nodavirus (MrNV) and extra small virus (XSV) is an infection that primarily affects giant freshwater prawns, Macrobrachium r... [more] White tail disease caused by Macrobrachium rosenbergii nodavirus (MrNV) and extra small virus (XSV) is an infection that primarily affects giant freshwater prawns, Macrobrachium rosenbergii, which in turn causes significant economic losses in aquaculture farms worldwide. In response, different prophylactic agents have been studied to improve resistance to this infection. This meta-analysis aims to assess the effectiveness of different prophylactic agents in promoting shrimp survival. Embase, Google Scholar, PubMed, and Scopus search engines were used to search for relevant articles from 2000 to 2022. Articles were screened to only select articles studying crustaceans being given prophylaxis before the disease challenge. Treatments were analyzed on overall survival, and we performed subgroup analysis of treatment type, administration routes, treatment incubation time pre-infection, and whether the prophylactic agents were derived from MrNV, XSV, or a mixture of both. Between the 3 major prophylaxis types, DNA/RNA prophylaxis, viral protein-based prophylaxis, and supplements, all conferred protection against MrNV infection, though no differences between groups were observed. A shorter incubation period (= 7 days) conferred better protection, and prophylactic agents from MrNV origin were found to be more effective. A high degree of heterogeneity was detected between studies, necessitating future large-scale studies addressing possible bias.
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2022 |
Sanchez-Bezanilla S, Beard DJ, Hood RJ, Åberg ND, Crock P, Walker FR, et al., 'Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice.', Neural plasticity, 2022 9983042 (2022) [C1]
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2021 |
Gasparotto J, Senger MR, de Sá Moreira ET, Brum PO, Kessler FGC, Peixoto DO, et al., 'Neurological impairment caused by Schistosoma mansoni systemic infection exhibits early features of idiopathic neurodegenerative disease', Journal of Biological Chemistry, 297 (2021) [C1] Schistosomiasis, a neglected tropical disease caused by trematodes of the Schistosoma genus, affects over 250 million people around the world. This disease has been associated wit... [more] Schistosomiasis, a neglected tropical disease caused by trematodes of the Schistosoma genus, affects over 250 million people around the world. This disease has been associated with learning and memory deficits in children, whereas reduced attention levels, impaired work capacity, and cognitive deficits have been observed in adults. Strongly correlated with poverty and lack of basic sanitary conditions, this chronic endemic infection is common in Africa, South America, and parts of Asia and contributes to inhibition of social development and low quality of life in affected areas. Nonetheless, studies on the mechanisms involved in the neurological impairment caused by schistosomiasis are scarce. Here, we used a murine model of infection with Schistosoma mansoni in which parasites do not invade the central nervous system to evaluate the consequences of systemic infection on neurologic function. We observed that systemic infection with S. mansoni led to astrocyte and microglia activation, expression of oxidative stress-induced transcription factor Nrf2, oxidative damage, Tau phosphorylation, and amyloid-ß peptide accumulation in the prefrontal cortex of infected animals. We also found impairment in spatial learning and memory as evaluated by the Morris water maze task. Administration of anthelmintic (praziquantel) and antioxidant (N-acetylcysteine plus deferoxamine) treatments was effective in inhibiting most of these phenotypes, and the combination of both treatments had a synergistic effect to prevent such changes. These data demonstrate new perspectives toward the understanding of the pathology and possible therapeutic approaches to counteract long-term effects of systemic schistosomiasis on brain function.
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2021 |
Zalewska K, Hood RJ, Pietrogrande G, Sanchez-Bezanilla S, Ong LK, Johnson SJ, et al., 'Corticosterone administration alters white matter tract structure and reduces gliosis in the sub-acute phase of experimental stroke', International Journal of Molecular Sciences, 22 (2021) [C1] White matter tract (WMT) degeneration has been reported to occur following a stroke, and it is associated with post-stroke functional disturbances. White matter pathology has been... [more] White matter tract (WMT) degeneration has been reported to occur following a stroke, and it is associated with post-stroke functional disturbances. White matter pathology has been suggested to be an independent predictor of post-stroke recovery. However, the factors that influence WMT remodeling are poorly understood. Cortisol is a steroid hormone released in response to prolonged stress, and elevated levels of cortisol have been reported to interfere with brain recovery. The objective of this study was to investigate the influence of corticosterone (CORT; the rodent equivalent of cortisol) on WMT structure post-stroke. Photothrombotic stroke (or sham surgery) was induced in 8-week-old male C57BL/6 mice. At 72 h, mice were exposed to standard drinking water ± CORT (100 µg/mL). After two weeks of CORT administration, mice were euthanised and brain tissue collected for histological and biochemical analysis of WMT (particularly the corpus cal-losum and corticospinal tract). CORT administration was associated with increased tissue loss within the ipsilateral hemisphere, and modest and inconsistent WMT reorganization. Further, a structural and molecular analysis of the WMT components suggested that CORT exerted effects over axons and glial cells. Our findings highlight that CORT at stress-like levels can moderately influence the reorganization and microstructure of WMT post-stroke.
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2021 |
Sanchez-Bezanilla S, Hood RJ, Collins-Praino LE, Turner RJ, Walker FR, Nilsson M, Ong LK, 'More than motor impairment: A spatiotemporal analysis of cognitive impairment and associated neuropathological changes following cortical photothrombotic stroke', Journal of Cerebral Blood Flow and Metabolism, 41 2439-2455 (2021) [C1] There is emerging evidence suggesting that a cortical stroke can cause delayed and remote hippocampal dysregulation, leading to cognitive impairment. In this study, we aimed to in... [more] There is emerging evidence suggesting that a cortical stroke can cause delayed and remote hippocampal dysregulation, leading to cognitive impairment. In this study, we aimed to investigate motor and cognitive outcomes after experimental stroke, and their association with secondary neurodegenerative processes. Specifically, we used a photothrombotic stroke model targeting the motor and somatosensory cortices of mice. Motor function was assessed using the cylinder and grid walk tasks. Changes in cognition were assessed using a mouse touchscreen platform. Neuronal loss, gliosis and amyloid-ß accumulation were investigated in the peri-infarct and ipsilateral hippocampal regions at 7, 28 and 84 days post-stroke. Our findings showed persistent impairment in cognitive function post-stroke, whilst there was a modest spontaneous motor recovery over the investigated period of 84 days. In the peri-infarct region, we detected a reduction in neuronal loss and decreased neuroinflammation over time post-stroke, which potentially explains the spontaneous motor recovery. Conversely, we observed persistent neuronal loss together with concomitant increased neuroinflammation and amyloid-ß accumulation in the hippocampus, which likely accounts for the persistent cognitive dysfunction. Our findings indicate that cortical stroke induces secondary neurodegenerative processes in the hippocampus, a region remote from the primary infarct, potentially contributing to the progression of post-stroke cognitive impairment.
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2021 |
Zhao Z, Hood RJ, Ong LK, Pietrogrande G, Sanchez Bezanilla S, Warren KE, et al., 'Exploring How Low Oxygen Post Conditioning Improves Stroke-Induced Cognitive Impairment: A Consideration of Amyloid-Beta Loading and Other Mechanisms', FRONTIERS IN NEUROLOGY, 12 (2021) [C1]
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2021 |
Lee NT, Ong LK, Gyawali P, Nassir CMNCM, Mustapha M, Nandurkar HH, Sashindranath M, 'Role of purinergic signalling in endothelial dysfunction and thrombo-inflammation in ischaemic stroke and cerebral small vessel disease', Biomolecules, 11 (2021) [C1] The cerebral endothelium is an active interface between blood and the central nervous system. In addition to being a physical barrier between the blood and the brain, the endothel... [more] The cerebral endothelium is an active interface between blood and the central nervous system. In addition to being a physical barrier between the blood and the brain, the endothelium also actively regulates metabolic homeostasis, vascular tone and permeability, coagulation, and movement of immune cells. Being part of the blood¿brain barrier, endothelial cells of the brain have specialized morphology, physiology, and phenotypes due to their unique microenvironment. Known cardiovascular risk factors facilitate cerebral endothelial dysfunction, leading to impaired vasodilation, an aggravated inflammatory response, as well as increased oxidative stress and vascular proliferation. This culminates in the thrombo-inflammatory response, an underlying cause of ischemic stroke and cerebral small vessel disease (CSVD). These events are further exacerbated when blood flow is returned to the brain after a period of ischemia, a phenomenon termed ischemia-reperfusion injury. Purinergic signaling is an endogenous molecular pathway in which the enzymes CD39 and CD73 catabolize extracellular adenosine triphosphate (eATP) to adenosine. After ischemia and CSVD, eATP is released from dying neurons as a damage molecule, triggering thrombosis and inflammation. In contrast, adenosine is anti-thrombotic, protects against oxidative stress, and suppresses the immune response. Evidently, therapies that promote adenosine generation or boost CD39 activity at the site of endothelial injury have promising benefits in the context of atherothrombotic stroke and can be extended to current CSVD known pathomechanisms. Here, we have reviewed the rationale and benefits of CD39 and CD39 therapies to treat endothelial dysfunction in the brain.
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2021 |
Chen KF, Tan WS, Ong LK, Zainal Abidin SA, Othman I, Tey BT, Lee RFS, 'The Macrobrachium rosenbergii nodavirus: a detailed review of structure, infectivity, host immunity, diagnosis and prevention', Reviews in Aquaculture, 13 2117-2141 (2021) [C1] The Macrobrachium rosenbergii nodavirus causes white tail disease, which primarily infects giant freshwater prawns, Macrobrachium rosenbergii. The infection leads to almost 100% m... [more] The Macrobrachium rosenbergii nodavirus causes white tail disease, which primarily infects giant freshwater prawns, Macrobrachium rosenbergii. The infection leads to almost 100% mortality in post-larvae, causing significant economic losses in aquaculture farms. To develop effective measures against outbreaks, a good understanding of the virus is essential. In this review, we discuss key aspects of the Macrobrachium rosenbergii nodavirus including its structure, mechanisms of transmission and infection and common strategies for detection and prevention of outbreaks. Structurally, cryogenic electron microscopy revealed that the nodavirus has a T¿=¿3 icosahedral structure with dimeric blade-like spikes on its surface. Homology modelling comparing wild-type and enzymatically cleaved Macrobrachium rosenbergii nodavirus-like particles revealed the significance of these spikes or protruding domains for binding. In vitro and in vivo studies have identified key aspects of Macrobrachium rosenbergii nodavirus infectivity, including (i) the viral binding targets such as transglutaminase and caveolin-1, (ii) utilisation of B2-like proteins in promoting infectivity and intracellular migration, (iii) replication mechanisms and (iv) co-infection with the extra small virus. Though susceptible at a post-larvae stage, adult Macrobrachium rosenbergii is immune to Macrobrachium rosenbergii nodavirus infection. During outbreaks, polymerase chain reaction and in situ hybridisation-based detection techniques are commonly used to identify infected populations. Currently, the most useful strategies for an outbreak are physical biosecurity measures and prophylaxis such as vaccination and immunostimulants. Finally, critical gaps in research include development of immortalised shrimp cell models, elucidation of time-resolved protein changes post-infection and development of therapies to treat infections to mitigate economic losses during outbreaks.
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2021 |
Stuckey SM, Ong LK, Collins-Praino LE, Turner RJ, 'Neuroinflammation as a Key Driver of Secondary Neurodegeneration Following Stroke?', Int J Mol Sci, 22 (2021) [C1]
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2021 |
Ong LK, Briggs GD, Guan L, Dunkley PR, Dickson PW, 'Peripheral inflammation induces long-term changes in tyrosine hydroxylase activation in the substantia nigra', NEUROCHEMISTRY INTERNATIONAL, 146 (2021) [C1]
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2021 |
Nassir CMNCM, Ghazali MM, Hashim S, Idris NS, Yuen LS, Hui WJ, et al., 'Diets and Cellular-Derived Microparticles: Weighing a Plausible Link With Cerebral Small Vessel Disease', FRONTIERS IN CARDIOVASCULAR MEDICINE, 8 (2021) [C1]
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2020 |
Sanchez-Bezanilla S, Aberg ND, Crock P, Walker FR, Nilsson M, Isgaard J, Ong LK, 'Growth Hormone Promotes Motor Function after Experimental Stroke and Enhances Recovery-Promoting Mechanisms within the Peri-Infarct Area', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21 (2020) [C1]
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2020 |
Sanchez-Bezanilla S, Aberg ND, Crock P, Walker FR, Nilsson M, Isgaard J, Ong LK, 'Growth Hormone Treatment Promotes Remote Hippocampal Plasticity after Experimental Cortical Stroke', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21 (2020) [C1]
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2020 |
Gyawali P, Hinwood M, Chow WZ, Kluge M, Ong LK, Nilsson M, Walker FR, 'Exploring the relationship between fatigue and circulating levels of the pro-inflammatory biomarkers interleukin-6 and C-reactive protein in the chronic stage of stroke recovery: A cross-sectional study', Brain, Behavior, & Immunity - Health, 9 (2020)
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2020 |
Chow WZ, Ong LK, Kluge MG, Gyawali P, Walker FR, Nilsson M, 'Similar cognitive deficits in mice and humans in the chronic phase post-stroke identified using the touchscreen-based paired-associate learning task', SCIENTIFIC REPORTS, 10 (2020) [C1]
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2020 |
Gyawali P, Chow WZ, Hinwood M, Kluge M, English C, Ong LK, et al., 'Opposing Associations of Stress and Resilience With Functional Outcomes in Stroke Survivors in the Chronic Phase of Stroke: A Cross-Sectional Study', FRONTIERS IN NEUROLOGY, 11 (2020) [C1]
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2019 |
Sanchez-Bezanilla S, TeBay C, Nilsson M, Walker FR, Ong LK, 'Visual discrimination impairment after experimental stroke is associated with disturbances in the polarization of the astrocytic aquaporin-4 and increased accumulation of neurotoxic proteins', Experimental Neurology, 318 232-243 (2019) [C1] Numerous clinical studies have documented the high incidence of cognitive impairment after stroke. However, there is only limited knowledge about the underlying mechanisms. Intere... [more] Numerous clinical studies have documented the high incidence of cognitive impairment after stroke. However, there is only limited knowledge about the underlying mechanisms. Interestingly, there is emerging evidence suggesting that cognitive function after stroke may be affected due to reduced waste clearance and subsequent accumulation of neurotoxic proteins. To further explore this potential association, we utilised a model of experimental stroke in mice. Specifically, a photothrombotic vascular occlusion targeting motor and sensory parts of the cerebral cortex was induced in young adult mice, and changes in cognition were assessed using a touchscreen platform for pairwise visual discrimination. The results showed that the execution of the visual discrimination task was impaired in mice 10 to 14 days post-stroke compared to sham. Stroke also induced significant neuronal loss within the peri-infarct, thalamus and the CA1 sub-region of the hippocampus. Further, immunohistochemical and protein analyses of the selected brain regions revealed an increased accumulation and aggregation of both amyloid-ß and a-synuclein. These alterations were associated with significant disturbances in the aquaporin-4 protein expression and polarization at the astrocytic end-feet. The results suggest a link between the increased accumulation of neurotoxic proteins and the stroke-induced cognitive impairment. Given that the neurotoxic protein accumulation appeared alongside changes in astrocytic aquaporin-4 distribution, we suggest that the function of the waste clearance pathways in the brain post-stroke may represent a therapeutic target to improve brain recovery.
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2019 |
Pietrogrande G, Zalewska K, Zhao Z, Abdolhoseini M, Chow WZ, Sanchez-Bezanilla S, et al., 'Low oxygen post conditioning prevents thalamic secondary neuronal loss caused by excitotoxicity after cortical stroke', SCIENTIFIC REPORTS, 9 (2019) [C1]
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2019 |
Sanchez-Bezanilla S, Nilsson M, Walker FR, Ong LK, 'Can We Use 2,3,5-Triphenyltetrazolium Chloride-Stained Brain Slices for Other Purposes? The Application of Western Blotting', FRONTIERS IN MOLECULAR NEUROSCIENCE, 12 (2019) [C1]
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2019 |
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]
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2018 |
Lillicrap T, Garcia-Esperon C, Walker FR, Ong LK, Nilsson M, Spratt N, et al., 'Growth Hormone Deficiency Is Frequent After Recent Stroke', FRONTIERS IN NEUROLOGY, 9 (2018) [C1]
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2018 |
English C, Janssen H, Crowfoot G, Bourne J, Callister R, Dunn A, et al., 'Frequent, short bouts of light-intensity exercises while standing decreases systolic blood pressure: Breaking Up Sitting Time after Stroke (BUST-Stroke) trial', International Journal of Stroke, 13 932-940 (2018) [C1] Background: Stroke survivors sit for long periods each day. Uninterrupted sitting is associated with increased risk of cardiovascular disease. Breaking up uninterrupted sitting wi... [more] Background: Stroke survivors sit for long periods each day. Uninterrupted sitting is associated with increased risk of cardiovascular disease. Breaking up uninterrupted sitting with frequent, short bouts of light-intensity physical activity has an immediate positive effect on blood pressure and plasma clotting factors in healthy, overweight, and type 2 diabetic populations. Aim: We examined the effect of frequent, short bouts of light-intensity physical activity on blood pressure and plasma fibrinogen in stroke survivors. Methods: Prespecified secondary analyses from a three-armed randomized, within-participant, crossover trial. Participants were 19 stroke survivors (nine female, aged 68 years old, 90% able to walk independently). The experimental conditions were sitting for 8 h uninterrupted, sitting with 3 min bouts of light-intensity exercise while standing every 30 min, or sitting with 3 min of walking every 30 min. Blood pressure was measured every 30 min over 8 h and plasma fibrinogen at the beginning, middle, and end of each day. Intention-to-treat analyses were performed using linear mixed models including fixed effects for condition, period, and order, and a random intercept for participant to account for repeated measures and missing data. Results: Sitting with 3 min bouts of light-intensity exercise while standing every 30 min decreased systolic blood pressure by 3.5 mmHg (95% CI 1.7¿5.4) compared with sitting for 8 h uninterrupted. For participants not taking antihypertensive medications, sitting with 3 min of walking every 30 min decreased systolic blood pressure by 5.0 mmHg (95% CI -7.9 to 2.0) and sitting with 3 min bouts light-intensity exercise while standing every 30 min decreased systolic blood pressure by 4.2 mmHg (95% CI -7.2 to -1.3) compared with sitting for 8 h uninterrupted. There was no effect of condition on diastolic blood pressure (p = 0.45) or plasma fibrinogen levels (p = 0.91). Conclusion: Frequent, short bouts of light-intensity physical activity decreases systolic blood pressure in stroke survivors. However, before translation into clinical practice, the optimal duration and timing of physical activity bouts needs to be determined. Clinical trial registration: Australian and New Zealand Clinical Trials Registry http://www.anzctr.org.au ANZTR12615001189516.
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2018 |
English C, Janssen H, Crowfoot G, Callister R, Dunn A, Mackie P, et al., 'Breaking up sitting time after stroke (BUST-stroke)', International Journal of Stroke, 13 921-931 (2018) [C1] Objectives: People with stroke sit for long periods each day, which may compromise blood glucose control and increase risk of recurrent stroke. Studies in other populations have f... [more] Objectives: People with stroke sit for long periods each day, which may compromise blood glucose control and increase risk of recurrent stroke. Studies in other populations have found regular activity breaks have a significant immediate (within-day) positive effect on glucose metabolism. We examined the effects of breaking up uninterrupted sitting with frequent, short bouts of light-intensity physical activity in people with stroke on post-prandial plasma glucose and insulin. Methods: Randomized within-participant crossover trial. We included people between 3 months and 10 years post-stroke, ambulant with minimal assistance and not taking diabetic medication other than metformin. The three experimental conditions (completed in random order) were: sitting for 8 h uninterrupted, sitting with 3 min bouts of light-intensity exercise while standing every 30 min, or sitting with 3 min of walking every 30 min. Meals were standardized and bloods were collected half- to one-hourly via an intravenous cannula. Results: A total of 19 participants (9 female, mean [SD] age 68.2 [10.2]) completed the trial. The majority (n = 12, 63%) had mild stroke symptoms (National Institutes of Stroke Scale score 0¿13). There was no significant effect of experimental condition on glucose (mean [SD] positive incremental area [+iAUC] mmol·L·h-1 under the curve during sitting 42.3 [29.5], standing 47.4 [23.1], walking 44.6 [26.5], p = 0.563) or insulin (mean + iAUC pmol·L·h-1 sitting 14,161 [7,560], standing 14,043 [8,312], walking 14,008 [8,269], p = 0.987). Conclusion: Frequent, short bouts of light-intensity physical activity did not have a significant effect on post-prandial plasma glucose and insulin in this sample of people with stroke. Further studies are needed to identify strategies that improve inactivity-related glucose metabolism after stroke.
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2018 |
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]
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2018 |
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] 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... [more] 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.
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2018 |
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] 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 init... [more] 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.
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2018 |
Sominsky L, Ong LK, Ziko I, Dickson PW, Spencer SJ, 'Neonatal overfeeding increases capacity for catecholamine biosynthesis from the adrenal gland acutely and long-term in the male rat', Molecular and Cellular Endocrinology, 470 295-303 (2018) [C1] A poor nutritional environment during early development has long been known to increase disease susceptibility later in life. We have previously shown that rats that are overfed a... [more] A poor nutritional environment during early development has long been known to increase disease susceptibility later in life. We have previously shown that rats that are overfed as neonates (i.e. suckled in small litters (4 pups) relative to control conditions (12 pups)) show dysregulated hypothalamic-pituitary-adrenal axis responses to immune stress in adulthood, particularly due to an altered capacity of the adrenal to respond to an immune challenge. Here we hypothesised that neonatal overfeeding similarly affects the sympathomedullary system, testing this by investigating the biochemical function of tyrosine hydroxylase (TH), the first rate-limiting enzyme in the catecholamine synthesis. We also examined changes in adrenal expression of the leptin receptor and in mitogen-activated protein kinase (MAPK) signalling. During the neonatal period, we saw age-dependent changes in TH activity and phosphorylation, with neonatal overfeeding stimulating increased adrenal TH specific activity at postnatal days 7 and 14, along with a compensatory reduction in total TH protein levels. This increased TH activity was maintained into adulthood where neonatally overfed rats exhibited increased adrenal responsiveness 30 min after an immune challenge with lipopolysaccharide, evident in a concomitant increase in TH protein levels and specific activity. Neonatal overfeeding significantly reduced the expression of the leptin receptor in neonatal adrenals at postnatal day 7 and in adult adrenals, but did not affect MAPK signalling. These data suggest neonatal overfeeding alters the capacity of the adrenal to synthesise catecholamines, both acutely and long term, and these effects may be independent of leptin signalling.
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2017 |
Ong LK, Walker FR, Nilsson M, 'Is Stroke a Neurodegenerative Condition? A Critical Review of Secondary Neurodegeneration and Amyloid-beta Accumulation after Stroke', AIMS MEDICAL SCIENCE, 4 1-16 (2017) [C1]
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2017 |
Ong LK, Fuller EA, Sominsky L, Hodgson DM, Dunkley PR, Dickson PW, 'Early life peripheral lipopolysaccharide challenge reprograms catecholaminergic neurons', SCIENTIFIC REPORTS, 7 (2017) [C1]
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2017 |
Ong LK, Page S, Briggs GD, Guan L, Dun MD, Verrills NM, et al., 'Peripheral Lipopolysaccharide Challenge Induces Long-Term Changes in Tyrosine Hydroxylase Regulation in the Adrenal Medulla', Journal of Cellular Biochemistry, 118 2096-2107 (2017) [C1] Immune activation can alter the activity of adrenal chromaffin cells. The effect of immune activation by lipopolysaccharide (LPS) on the regulation of tyrosine hydroxylase (TH) in... [more] Immune activation can alter the activity of adrenal chromaffin cells. The effect of immune activation by lipopolysaccharide (LPS) on the regulation of tyrosine hydroxylase (TH) in the adrenal medulla in vivo was determined between 1 day and 6 months after LPS injection. The plasma levels of eleven cytokines were reduced 1 day after LPS injection, whereas the level for interleukin-10 was increased. The levels of all cytokines remained at control levels until 6 months when the levels of interleukin-6 and -4 were increased. One day after LPS injection, there was a decrease in TH-specific activity that may be due to decreased phosphorylation of serine 31 and 40. This decreased phosphorylation of serine 31 and 40 may be due to an increased activation of the protein phosphatase PP2A. One week after LPS injection, there was increased TH protein and increased phosphorylation of serine 40 that this was not accompanied by an increase in TH-specific activity. All TH parameters measured returned to basal levels between 1 month and 3 months. Six months after injection there was an increase in TH protein. This was associated with increased levels of the extracellular regulated kinase isoforms 1 and 2. This work shows that a single inflammatory event has the capacity to generate both short-term and long-term changes in TH regulation in the adrenal medulla of the adult animal. J. Cell. Biochem. 118: 2096¿2107, 2017. © 2016 Wiley Periodicals, Inc.
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2017 |
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] 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 ne... [more] 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.
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2017 |
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] 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. ... [more] 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.
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2017 |
Zhao Z, Ong LK, Johnson S, Nilsson M, Walker FR, 'Chronic stress induced disruption of the peri-infarct neurovascular unit following experimentally induced photothrombotic stroke.', Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 37 3709-3724 (2017) [C1]
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2017 |
Zalewska K, Ong LK, Johnson SJ, Nilsson M, Walker FR, 'Oral administration of corticosterone at stress-like levels drives microglial but not vascular disturbances post-stroke', Neuroscience, 352 30-38 (2017) [C1] Exposure to chronic stress following stroke has been shown, both clinically and pre-clinically, to impact negatively on the recovery process. While this phenomenon is well establi... [more] Exposure to chronic stress following stroke has been shown, both clinically and pre-clinically, to impact negatively on the recovery process. While this phenomenon is well established, the specific mechanisms involved have remained largely unexplored. One obvious signaling pathway through which chronic stress may impact on the recovery process is via corticosterone, and its effects on microglial activity and vascular remodeling. In the current study, we were interested in examining how orally delivered corticosterone at a stress-like concentration impacted on microglial activity and vascular remodeling after stroke. We identified that corticosterone administration for two weeks following stroke significantly increased tissue loss and decreased the weight of the spleen and thymus. We also identified that corticosterone administration significantly altered the expression of the key microglial complement receptor, CD11b after stroke. Corticosterone administration did not alter the expression of the vessel basement membrane protein, Collagen IV after stroke. Together, these results suggest that corticosterone is likely to represent only one of the major stress signals responsible for driving the negative impacts of chronic stress on recovery.
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2017 |
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] 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 neurod... [more] 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.
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2016 |
James MH, Quinn RK, Ong LK, Levi EM, Smith DW, Dickson PW, Dayas CV, 'Rapamycin reduces motivated responding for cocaine and alters GluA1 expression in the ventral but not dorsal striatum', European Journal of Pharmacology, 784 147-154 (2016) [C1] The mechanistic target of rapamycin complex 1 (mTORC1) regulates synaptic protein synthesis and therefore synaptic function and plasticity. A role for mTORC1 has recently been dem... [more] The mechanistic target of rapamycin complex 1 (mTORC1) regulates synaptic protein synthesis and therefore synaptic function and plasticity. A role for mTORC1 has recently been demonstrated for addiction-related behaviors. For example, central or intra-accumbal injections of the mTORC1 inhibitor rapamycin attenuates several indices of cocaine-seeking including progressive ratio (PR) responding and reinstatement. These behavioral effects are associated with decreased mTORC1 activity and synaptic protein translation in the nucleus accumbens (NAC) and point to a possible therapeutic role for rapamycin in the treatment of addiction. Currently, it is unclear whether similar behavioral and biochemical effects can be achieved by administering rapamycin systemically, which represents a more clinically-appropriate route of administration. Here, we assessed the effects of repeated, systemic administration of rapamycin (10 mg/kg, i.p.) on PR responding for cocaine. We also assessed whether systemic rapamycin was associated with changes in measures of mTORC1 activity and GluA1 expression in the ventral and dorsal striatum. We report that systemic rapamycin treatment reduced PR breakpoints to levels comparable to intra-NAC rapamycin. Systemic rapamycin treatment also reduced phosphorylated p70S6K and GluA1 AMPARs within the NAC but not dorsal striatum. Thus, systemic administration of rapamycin is as effective at reducing drug seeking behavior and measures of mTORC1 activity compared to direct accumbal application and may therefore represent a possible therapeutic option in the treatment of addiction. Possible caveats of this treatment approach are discussed.
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2016 |
Peres TV, Ong LK, Costa AP, Eyng H, Venske DKR, Colle D, et al., 'Tyrosine hydroxylase regulation in adult rat striatum following short-term neonatal exposure to manganese', Metallomics, 8 597-604 (2016) [C1] Manganese (Mn) is an essential trace element required for a range of physiological processes, but Mn can also be neurotoxic especially during development. Excess levels of Mn accu... [more] Manganese (Mn) is an essential trace element required for a range of physiological processes, but Mn can also be neurotoxic especially during development. Excess levels of Mn accumulate preferentially in the striatum and can induce a syndrome called manganism, characterized by an initial stage of psychiatric disorder followed by motor impairment. In the present study, we investigated the effects of Mn exposure on the developing dopaminergic system, specifically tyrosine hydroxylase (TH) protein and phosphorylation levels in the striatum of rats. Neonatal rats were exposed to Mn intraperitoneally (ip) from post-natal day 8 up to day 12 (PND8-12). Striatal tissue was analysed on PND14 or PND70, to detect either short-term or long-term effects induced by Mn exposure. There was a dose dependent increase in TH protein levels in the striatum at PND14, reaching significance at 20 mg kg-1 Mn, and this correlated with an increase in TH phosphorylation at serines 40, 31 and 19. However, in the striatum at PND70, a time by which Mn levels were no longer elevated, there was a dose dependent decrease in TH protein levels, reaching significance at 20 mg kg-1 Mn, and this correlated with TH phosphorylation at Ser40 and Ser19. There was however a significant increase in phosphorylation of TH at serine 31 at 20 mg kg-1 Mn, which did not correlate with TH protein levels. Taken together our findings suggest that neonatal Mn exposure can have both short-term and long-term effects on the regulation of TH in the striatal dopaminergic system.
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2014 |
James MH, Quinn RK, Ong LK, Levi EM, Charnley JL, Smith DW, et al., 'mTORC1 inhibition in the nucleus accumbens 'protects' against the expression of drug seeking and 'relapse' and is associated with reductions in GluA1 AMPAR and CAMKIIa levels.', Neuropsychopharmacology, 39 1694-1702 (2014) [C1]
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2014 |
Ong LK, Guan L, Damanhuri H, Goodchild AK, Bobrovskaya L, Dickson PW, Dunkley PR, 'Neurobiological consequences of acute footshock stress: effects on tyrosine hydroxylase phosphorylation and activation in the rat brain and adrenal medulla', JOURNAL OF NEUROCHEMISTRY, 128 547-560 (2014) [C1]
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2013 |
Bobrovskaya L, Maniam J, Ong LK, Dunkley PR, Morris MJ, 'Early Life Stress and Post-Weaning High Fat Diet Alter Tyrosine Hydroxylase Regulation and AT1 Receptor Expression in the Adrenal Gland in a Sex Dependent Manner', NEUROCHEMICAL RESEARCH, 38 826-833 (2013) [C1]
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2013 |
Sominsky L, Fuller EA, Bondarenko E, Ong LK, Averell L, Nalivaiko E, et al., 'Functional Programming of the Autonomic Nervous System by Early Life Immune Exposure: Implications for Anxiety', PLOS ONE, 8 (2013) [C1]
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2012 |
Sominsky Bar L, Walker AK, Ong LK, Tynan R, Walker FR, Hodgson DM, 'Increased microglial activation in the rat brain following neonatal exposure to a bacterial mimetic', Behavioural Brain Research, 226 351-356 (2012) [C1]
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2012 |
Ong LK, Sominsky L, Dickson PW, Hodgson DM, Dunkley PR, 'The sustained phase of Tyrosine hydroxylase activation in vivo', Neurochemical Research, 37 1938-1943 (2012) [C1]
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2012 |
Damanhuri HA, Burke PGR, Ong LK, Bobrovskaya L, Dickson PW, Dunkley PR, Goodchild AK, 'Tyrosine hydroxylase phosphorylation in catecholaminergic brain regions: A marker of activation following acute hypotension and glucoprivation', Plos One, 7 1-19 (2012) [C1]
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2011 |
Ong LK, Guan L, Stutz B, Dickson PW, Dunkley PR, Bobrovskaya L, 'The effects of footshock and immobilization stress on tyrosine hydroxylase phosphorylation in the rat locus coeruleus and adrenal gland', Neuroscience, 192 20-27 (2011) [C1]
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2011 |
Ong LK, Bobrovskaya L, Walker FR, Day TA, Dickson PW, Dunkley PR, 'The effect of social defeat on tyrosine hydroxylase phosphorylation in the rat brain and adrenal gland', Neurochemical Research, 36 27-33 (2011) [C1]
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2011 |
Wynne OL, Horvat JC, Kim RY, Ong LK, Smith R, Hansbro PM, et al., 'Neonatal respiratory infection and adult re-infection: Effect on glucocorticoid and mineralocorticoid receptors in the hippocampus in BALB/c mice', Brain Behavior and Immunity, 25 1214-1222 (2011) [C1]
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2010 |
Bobrovskaya L, Damanhuri HA, Ong LK, Schneider JJ, Dickson PW, Dunkley PR, Goodchild AK, 'Signal transduction pathways and tyrosine hydroxylase regulation in the adrenal medulla following glucoprivation: An in vivo analysis', Neurochemistry International, 57 162-167 (2010) [C1]
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2007 |
O'Leary MA, Schneider JJ, Krishnan BP, Lavis C, McKendry A, Ong LK, Isbister GK, 'Cross-neutralisation of Australian brown and tiger snake venoms with commercial antivenoms: Cross-reactivity or antivenom mixtures?', Toxicon, 50 206-213 (2007) [C1]
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Conference (23 outputs)
Year | Citation | Altmetrics | Link | ||||||||
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2019 |
Bezanilla SS, Nilsson M, Walker F, Ong L, 'Cortical photothrombotic stroke induces cognitive deficits and is associated with an increased levels of neurotoxic proteins accumulation', JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, Yokohama, JAPAN (2019)
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2019 |
Gyawali P, Chow WZ, Ong LK, Nilsson M, Walker RF, 'Increased Resiliency is Associated With Better Recovery Trajectory Among Community Dwelling Stroke Survivors', STROKE, Honolulu, HI (2019)
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2019 |
Zhao Z, Ong LK, Hood R, Pietrogrande G, Sanchez Bezanilla S, Warren K, et al., 'Low oxygen post-conditioning improves cognition and reduces amyloid beta accumulation post-stroke in mice' (2019)
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2016 |
Walker F, Jones K, Zhao Z, Ong LK, Kluge M, Zalewska K, et al., 'Secondary neurodegeneration after stroke is exacerbated by stress: A new opportunity for preserving viable brain tissue', BRAIN BEHAVIOR AND IMMUNITY (2016)
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2015 |
Ong LK, Briggs G, Guan L, Dunkley P, Dickson P, 'Inflammation and dopamine synthesis in neurodegeneration', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
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2014 |
Ong LK, Briggs GD, Dunkley PR, Dickson PW, 'The role of inflammation and dopamine synthesis in Parkinson's disease', JOURNAL OF NEUROCHEMISTRY, Kaohsiung, TAIWAN (2014) [E3]
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2012 |
Sominsky Bar L, Fuller AE, Bondarenko E, Ong LK, Clark VR, Bobrovskaya L, et al., 'Neonatal programming of the autonomic nervous system by immunological challenge: Implications for anxiety', Abstracts of the 21st Annual Meeting of the International Behavioral Neuroscience Society, Kona, Hawaii (2012) [E3]
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2012 |
Ong LK, Guan L, Bobrovskaya L, Dickson PW, Dunkley PR, 'Neurobiological consequences of acute footshock stress', Journal of Neurochemistry, Kobe, Japan (2012) [E3]
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2012 |
Sominsky Bar L, Fuller EA, Bondarenko E, Ong LK, Clark VR, Bobrovskaya L, et al., 'Neonatal immune challenge induces anxiety in adulthood and is associated with functional alterations to the autonomic nervous system', Brain, Behavior, and Immunity, San Diego, CA (2012) [E3]
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2011 |
Sominsky Bar L, Walker AK, Ong LK, Tynan R, Walker FR, Hodgson DM, 'Epigenetic inheritance of anxiety-like behaviour in rats - Role of early life exposure to a bacterial mimetic', Journal of Developmental Origins of Health and Disease, Portland, Oregon (2011) [E3]
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2011 |
Wynnea O, Horvat JC, Kim RY, Ong LK, Smith R, Hansbro PM, et al., 'Sex differences in the effect of neonatal infection and adult re-infection on hippocampal corticosterone receptors and stress response outcomes', Brain, Behavior, and Immunity, Chicago, Illinois (2011) [E3]
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2011 |
Ong LK, Sominsky L, Walker AK, Hodgson DM, Goodchild AK, Bobrovskaya L, et al., 'SUSTAINED PHOSPHORYLATION OF TYROSINE HYDROXYLASE AT SERINE 40 IN VIVO', JOURNAL OF NEUROCHEMISTRY (2011)
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2011 |
Sominsky Bar L, Walker AK, Ong LK, Walker FR, Hodgson DM, 'Postnatal exposure to a bacterial mimetic increases microglial activation and histone H3 acetylation in rats', Brain, Behavior, and Immunity, Chicago, Illinois (2011) [E3]
|
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2010 |
Ong LK, Guan L, Stutz B, Dickson PW, Dunkley PR, Bobrovskaya L, 'Tyrosine hydroxylase phosphorylation in response to footshock and restraint stress', Journal of Neurochemistry, Phuket, Thailand (2010) [E3]
|
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2009 |
Bobrovskaya L, Damanhuri H, Ong LK, Dickson PW, Dunkley PR, Goodchild AK, 'The effect of glucoprivation on tyrosine hydroxylase phosphorylation in adrenals of Sprague-Dawley rats', Autonomic Neuroscience: Basic and Clinical, Sydney, NSW (2009) [E3]
|
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2009 |
Damanhuri H, Ong LK, Bobrovskaya L, Dunkley PR, Goodchild AK, 'Activation of tyrosine hydroxylase in the A8, A9 and A10 cell groups following hypotension and glucoprivation in Sprague Dawley rat', Autonomic Neuroscience: Basic and Clinical, Sydney, NSW (2009) [E3]
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2009 |
Ong LK, Maniam J, Dunkley PR, Bobrovskaya L, Morris MJ, 'The effect of voluntary exercise and high fat diet on tyrosine hydroxylase phosphorylation in male Sprague-Dawley rats exposed to early life stress', Autonomic Neuroscience: Basic and Clinical, Sydney, NSW (2009) [E3]
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2009 |
Bobrovskaya L, Ong LK, Walker RA, Day TA, Dickson PW, Dunkley PR, 'The effect of social stress on tyrosine hydroxylase phosphorylation', ANS 2009 Abstracts: Posters, Canberra, ACT (2009) [E3]
|
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2009 |
Ong LK, Bobrovskaya L, Walker FR, Day TA, Dickson PW, Dunkley PR, 'The effect of social conflict on tyrosine hydroxylase phosphorylation in catecholamine-producing cells from sprague-dawley rats', Journal of Neurochemistry, Busan, Korea (2009) [E3]
|
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Show 20 more conferences |
Preprint (3 outputs)
Year | Citation | Altmetrics | Link | |||||
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2023 |
Hood RJ, Sanchez-Bezanilla S, Beard DJ, Rust R, Turner RJ, Stuckey SM, et al., 'Leakage beyond the primary infarction: A temporal analysis of cerebrovascular dysregulation at sites of hippocampal secondary neurodegeneration following cortical photothrombotic stroke (2023)
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2021 |
Cheong MWL, Chong CW, Gan SH, Ong LK, Wang LS, Saw PS, et al., 'Distal Technologies for Prediabetes: A Systematic Review and Meta-Analysis (Preprint) (2021)
|
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2018 |
Zhao Z, Ong LK, Pietrogrande G, Bezanilla SS, Warren K, Ilicic M, et al., 'Low oxygen post conditioning improves stroke-induced cognitive impairment (2018)
|
Grants and Funding
Summary
Number of grants | 15 |
---|---|
Total funding | $293,133 |
Click on a grant title below to expand the full details for that specific grant.
20182 grants / $32,000
Growth hormone As Neurorestorative Therapy After Stroke$22,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Lin Kooi Ong, Professor Michael Nilsson, Professor Rohan Walker, Professor Jorgen Isgaard |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1800846 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
The glymphatic system: A brain waste clearance pathway as a potential target for post-stroke cognitive impairment$10,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Miss Sonia Sanchez Bezanilla, Doctor Lin Kooi Ong, Professor Rohan Walker, Professor Michael Nilsson |
Scheme | Greaves Family Postgraduate Top Up Scholarship in Medical Research |
Role | Lead |
Funding Start | 2018 |
Funding Finish | 2018 |
GNo | G1801355 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20176 grants / $154,851
Early Career Researcher (ECR) Higher Degree by Research (HDR) Scholarships$95,200
Funding body: The University of Newcastle
Funding body | The University of Newcastle |
---|---|
Scheme | Early Career Researcher HDR Candidate Scholarship |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2020 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
The glymphatic system – waste clearance system of the brain$15,000
Funding body: Faculty of Health and Medicine, University of Newcastle
Funding body | Faculty of Health and Medicine, University of Newcastle |
---|---|
Project Team | Lin Kooi Ong |
Scheme | Mary Costello Alzheimer’s Research Pilot Grant |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2018 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
Breaking Up Sitting Time After Stroke – BUST-Stroke$13,000
Funding body: Priority Research Centre for Stroke and Brain Injury, University of Newcastle
Funding body | Priority Research Centre for Stroke and Brain Injury, University of Newcastle |
---|---|
Project Team | Gary Crowfoot, Paul Mackie, Corallie English , Lin Kooi Ong, Rohan Walker, David Dunstan |
Scheme | Research Support Funding |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
Service change and Supporting Lifestyle and Activity Modification after TIA (S+SLAM-TIA)$11,755
Funding body: Priority Research Centre for Stroke and Brain Injury, University of Newcastle
Funding body | Priority Research Centre for Stroke and Brain Injury, University of Newcastle |
---|---|
Scheme | Research Support Funding |
Role | Investigator |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
Growth hormone as neurorestorative therapy after stroke$10,000
Funding body: Priority Research Centre for Stroke and Brain Injury, University of Newcastle
Funding body | Priority Research Centre for Stroke and Brain Injury, University of Newcastle |
---|---|
Project Team | Lin Kooi Ong, Michael Nilsson, Rohan Walker |
Scheme | Research Support Funding |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
Assessment for stroke recovery$9,896
Funding body: NSW Ministry of Health
Funding body | NSW Ministry of Health |
---|---|
Project Team | Doctor Lin Kooi Ong, Doctor Gary Crowfoot, Doctor Heidi Janssen, Doctor Dianne Marsden, Doctor Jodie Marquez, Professor Coralie English, Professor Rohan Walker |
Scheme | Medical Research Support Program (MRSP) |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1701224 |
Type Of Funding | C2400 – Aust StateTerritoryLocal – Other |
Category | 2400 |
UON | Y |
20162 grants / $39,686
Development and implementation of improved monitoring of psychological stress loads in patients recovering from stroke$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Conjoint Associate Professor Michael Pollack, Professor Michael Nilsson, Professor Rohan Walker, Doctor Lin Kooi Ong |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2016 |
Funding Finish | 2017 |
GNo | G1600724 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
Research Advantage Early Career Researcher Equipment Grant $19,686
Funding body: Research Advantage
Funding body | Research Advantage |
---|---|
Project Team | Lin Kooi Ong, Lucy Murtha, Gary Crowfoot |
Scheme | the Research Advantage Early Career Researcher Equipment Grant |
Role | Lead |
Funding Start | 2016 |
Funding Finish | 2016 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20153 grants / $37,000
Blocking the negative effects of stress on the brain to promote better healing of the brain after stroke$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Professor Rohan Walker, Doctor Lin Kooi Ong, Associate Professor Ming Yang, Professor Sarah Johnson |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | G1501384 |
Type Of Funding | Grant - Aust Non Government |
Category | 3AFG |
UON | Y |
The role of neuroinflammation in development of stroke-induced secondary neurodegeneration$9,000
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Lin Kooi Ong, Frederick Rohan Walker, Michael Nilsson |
Scheme | Pilot Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
IBRO - Young Investigator Travel Program $8,000
Funding body: International Brain Research Organisation
Funding body | International Brain Research Organisation |
---|---|
Scheme | Young Investigator Travel Program |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | |
Type Of Funding | International - Competitive |
Category | 3IFA |
UON | N |
20141 grants / $5,000
The role of inflammation and dopamine synthesis in the development of Parkinson’s disease$5,000
Funding body: University of Newcastle - Faculty of Health and Medicine
Funding body | University of Newcastle - Faculty of Health and Medicine |
---|---|
Project Team | Lin Kooi Ong, Phillip Dickson, Peter Dunkley |
Scheme | Pilot Grant |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20131 grants / $24,596
Ultra-Low Temperature Cryogenic Freezer$24,596
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Doctor Jude Weidenhofer, Doctor Rick Thorne, Associate Professor Kathryn Skelding, Associate Professor Nikki Verrills, Professor Pradeep Tanwar, Associate Professor Phillip Dickson, Professor Murray Cairns, Professor Hubert Hondermarck, Professor Xu Dong Zhang, Associate Professor Estelle Sontag, Doctor Chen Chen Jiang, Prof LIZ Milward, Doctor Jean-Marie Sontag, Associate Professor Paul Tooney, Doctor Severine Roselli Dayas, Professor Matt Dun, Professor Chris Dayas, Doctor Lin Kooi Ong, Professor Dirk Van Helden, Mr Ben Copeland, Doctor Gabrielle Briggs, Emeritus Professor Leonie Ashman, Emeritus Professor John Rostas |
Scheme | Equipment Grant |
Role | Investigator |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1201189 |
Type Of Funding | Other Public Sector - Commonwealth |
Category | 2OPC |
UON | Y |
Research Supervision
Number of supervisions
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2020 | PhD | Functional Deficits after Stroke: The Key Underlying Mechanisms and the Therapeutic Potential of Growth Hormone | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Principal Supervisor |
2020 | PhD | Investigation of Cognition After Stroke - A Translational Approach | PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
Research Collaborations
The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.
Country | Count of Publications | |
---|---|---|
Australia | 69 | |
Malaysia | 24 | |
Singapore | 9 | |
Sweden | 7 | |
United States | 6 | |
More... |
News
News • 12 Oct 2018
Brain fertiliser nurtures new hope for stroke survivors
A hormone already at our fingertips could provide a simple answer for a first-of-its-kind treatment to promote ‘brain fertilisers’ and significantly improve quality of life for stroke survivors, potentially even months or years after experiencing a stroke.
Dr Lin Kooi Ong
Position
Honorary Associate Lecturer
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Contact Details
linkooi.ong@newcastle.edu.au | |
Phone | (02) 49215736 |
Links |
Research Networks |
Office
Room | HMRI Lvl 3 East Kookaburra Circuit |
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