Dr Lin Kooi Ong

Dr Lin Kooi Ong

Post Doctoral Research Fellow

School of Biomedical Sciences and Pharmacy

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.

Dr Lin Kooi Ong

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

Read more

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

  • catecholamines
  • Neuroscience
  • Medical Biochemistry
  • Neurodegeneration
  • Stress Biology
  • Biomedical Imaging
  • Tyrosine Hydroxylase
  • Post-stroke cognitive impairment
  • Catecholamines
  • Brain Plasticity
  • Growth Hormone
  • Stroke Recovery

Languages

  • English (Fluent)
  • Malay (Fluent)

Fields of Research

Code Description Percentage
110999 Neurosciences not elsewhere classified 50
110199 Medical Biochemistry and Metabolomics not elsewhere classified 50

Professional Experience

UON Appointment

Title Organisation / Department
Post Doctoral Research Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/03/2012 - 31/12/2014 Research Associate University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Professional appointment

Dates Title Organisation / Department
1/03/2018 -  Editorial Board Neuroscience Research Notes
Malaysia
30/06/2017 -  Review Editor Frontiers in Neuroendocrine Science
Switzerland
12/12/2015 -  Early Career Researcher Representative School of Biomedical Sciences Research Committee
Australia
1/07/2014 - 1/07/2016 Deputy Newcastle ASMR Convenor and Co-Secretary - Australian Society for Medical Research Australian Society for Medical Research (ASMR)
Australia

Awards

Recipient

Year Award
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
Edit

Publications

For publications that are currently unpublished or in-press, details are shown in italics.

Highlighted Publications

Year Citation Altmetrics Link
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]
DOI 10.3934/medsci.2017.1.1
Co-authors Michael Nilsson, Rohan Walker
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]

© 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.

DOI 10.1177/0271678X16654920
Citations Scopus - 3Web of Science - 4
Co-authors Michael Nilsson, Rohan Walker
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]
DOI 10.1161/STROKEAHA.117.020557
Co-authors Sarah Johnson, Michael Nilsson, Andrew Bivard, Rohan Walker

Chapter (1 outputs)

Year Citation Altmetrics Link
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]
Co-authors Michael Nilsson, Rohan Walker

Journal article (29 outputs)

Year Citation Altmetrics Link
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, (2018)
DOI 10.1016/j.neuroscience.2018.07.034
Co-authors Rohan Walker, Michael Nilsson
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)

© 2018 Lillicrap, Garcia-Esperon, Walker, Ong, Nilsson, Spratt, Levi, Parsons, Isgaard and Bivard. Introduction: The incidence of pituitary dysfunction after severe ischemic strok... [more]

© 2018 Lillicrap, Garcia-Esperon, Walker, Ong, Nilsson, Spratt, Levi, Parsons, Isgaard and Bivard. Introduction: The incidence of pituitary dysfunction after severe ischemic stroke is unknown, however given the increasing attention to pituitary dysfunction after neurological injuries such as traumatic brain injury, this may represent a novel area of research in stroke. Methods: We perform an arginine and human growth hormone releasing hormone challenge on ischemic stroke patients within a week of symptom onset. Results: Over the study period, 13 patients were successfully tested within a week of stroke (baseline NIHSS 10, range 7-16). Overall, 9(69%) patients had a poor response, with 7(54%) of these patients meeting the criteria for had human growth hormone deficiency. Other measures of pituitary function were within normal ranges. Conclusion: After major ischemic stroke, low GH levels are common and may play a role in stroke recovery.

DOI 10.3389/fneur.2018.00713
Co-authors Mark Parsons, Neil Spratt, Andrew Bivard, Rohan Walker, Michael Nilsson
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]
DOI 10.1161/STROKEAHA.117.020557
Co-authors Sarah Johnson, Michael Nilsson, Andrew Bivard, Rohan Walker
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]

© 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.

DOI 10.1016/j.bbi.2017.11.014
Citations Scopus - 1Web of Science - 1
Co-authors Sarah Johnson, Mahmoud Abdolhoseini Uon, Rohan Walker, Michael Nilsson
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]

© 2017 Elsevier B.V. A poor nutritional environment during early development has long been known to increase disease susceptibility later in life. We have previously shown that ra... [more]

© 2017 Elsevier B.V. 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.

DOI 10.1016/j.mce.2017.11.014
Co-authors Phil Dickson
2018 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.', J Cereb Blood Flow Metab, 271678X18797346 (2018)
DOI 10.1177/0271678X18797346
Co-authors Michael Nilsson, Rohan Walker, Mahmoud Abdolhoseini Uon
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]
DOI 10.3934/medsci.2017.1.1
Co-authors Michael Nilsson, Rohan Walker
2017 Ong LK, Nilsson M, Walker FR, 'Authors' response re: "Reconsidering the role of glial cells in chronic stress-induced dopa-minergic neurons loss within the substantia nigra? Friend of foe?" by Ong et al. Brain Behavior and Immunity, 2016', BRAIN BEHAVIOR AND IMMUNITY, 60 384-384 (2017)
DOI 10.1016/j.bbi.2016.11.029
Co-authors Michael Nilsson, Rohan Walker
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]
DOI 10.1038/srep40475
Citations Scopus - 2Web of Science - 2
Co-authors Phil Dickson, Deborah Hodgson, Peter Dunkley
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]

© 2016 Wiley Periodicals, Inc. Immune activation can alter the activity of adrenal chromaffin cells. The effect of immune activation by lipopolysaccharide (LPS) on the regulation ... [more]

© 2016 Wiley Periodicals, Inc. 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.

DOI 10.1002/jcb.25839
Co-authors Phil Dickson, Peter Dunkley, Matt Dun, Nikki Verrills
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]

© 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.

DOI 10.1177/0271678X16654920
Citations Scopus - 3Web of Science - 4
Co-authors Michael Nilsson, Rohan Walker
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]

© 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.

DOI 10.1016/j.bbi.2016.10.001
Citations Scopus - 7Web of Science - 10
Co-authors Phil Dickson, Michael Nilsson, Rohan Walker, Sarah Johnson
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]
DOI 10.1177/0271678x17696100
Citations Scopus - 5Web of Science - 5
Co-authors Rohan Walker, Michael Nilsson, Sarah Johnson
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]

© 2017 IBRO 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 ... [more]

© 2017 IBRO 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.

DOI 10.1016/j.neuroscience.2017.03.005
Citations Scopus - 3Web of Science - 2
Co-authors Sarah Johnson, Michael Nilsson, Rohan Walker
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]

© 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 P2Y12receptor, 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 P2Y12to the soma.

DOI 10.1002/glia.23201
Citations Web of Science - 2
Co-authors Mahmoud Abdolhoseini Uon, Michael Nilsson, Rohan Walker, Sarah Johnson
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]

© 2016 Published by Elsevier B.V. All rights reserved. The mechanistic target of rapamycin complex 1 (mTORC1) regulates synaptic protein synthesis and therefore synaptic function ... [more]

© 2016 Published by Elsevier B.V. All rights reserved. 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.

DOI 10.1016/j.ejphar.2016.05.013
Citations Scopus - 4Web of Science - 4
Co-authors Christopher Dayas, Douglas Smith, Phil Dickson
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]

© 2016 The Royal Society of Chemistry. Manganese (Mn) is an essential trace element required for a range of physiological processes, but Mn can also be neurotoxic especially durin... [more]

© 2016 The Royal Society of Chemistry. 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-1Mn, 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-1Mn, 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-1Mn, 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.

DOI 10.1039/c5mt00265f
Citations Scopus - 5Web of Science - 5
Co-authors Phil Dickson, Peter Dunkley
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]
DOI 10.1038/npp.2014.16
Citations Scopus - 13Web of Science - 12
Co-authors Phil Dickson, Douglas Smith, Christopher Dayas
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]
DOI 10.1111/jnc.12482
Citations Scopus - 19Web of Science - 18
Co-authors Phil Dickson, Peter Dunkley
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]
DOI 10.1007/s11064-013-0985-4
Citations Scopus - 7Web of Science - 6
Co-authors Peter Dunkley
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]
DOI 10.1371/journal.pone.0057700
Citations Scopus - 33Web of Science - 27
Co-authors Eugene Nalivaiko, Phil Dickson, Deborah Hodgson, Peter Dunkley
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]
DOI 10.1016/j.bbr.2011.08.038
Citations Scopus - 39Web of Science - 32
Co-authors Deborah Hodgson, Rohan Walker
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]
Citations Scopus - 10Web of Science - 9
Co-authors Deborah Hodgson, Peter Dunkley, Phil Dickson
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]
Citations Scopus - 22Web of Science - 18
Co-authors Peter Dunkley, Phil Dickson
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]
DOI 10.1016/j.neuroscience.2011.06.087
Citations Scopus - 14Web of Science - 14
Co-authors Peter Dunkley, Phil Dickson
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]
DOI 10.1007/s11064-010-0255-7
Citations Scopus - 12Web of Science - 12
Co-authors Peter Dunkley, Rohan Walker, Phil Dickson
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]
DOI 10.1016/j.bbi.2011.03.014
Citations Scopus - 4Web of Science - 4
Co-authors Jay Horvat, Deborah Hodgson, Philip Hansbro, Roger Smith, Olivia Wynne
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]
DOI 10.1016/j.neuint.2010.05.009
Citations Scopus - 18Web of Science - 16
Co-authors Jennifer Schneider, Peter Dunkley, Phil Dickson
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]
DOI 10.1016/j.toxicon.2007.03.014
Citations Scopus - 19Web of Science - 16
Co-authors Jennifer Schneider, Geoffrey Isbister
Show 26 more journal articles

Conference (17 outputs)

Year Citation Altmetrics Link
2017 English C, Janssen H, Crowfoot G, Walker R, Patterson A, Callister R, et al., 'Does breaking up sitting time after stroke improve glucose control? (bust-stroke)', INTERNATIONAL JOURNAL OF STROKE (2017)
Co-authors Amanda Patterson, Robin Callister, Coralie English, Rohan Walker, Christopher Oldmeadow, Neil Spratt
2017 English C, Janssen H, Crowfoot G, Walker R, Patterson A, Callister R, et al., 'Breaking up sitting time after stroke improves blood pressure (bust-stroke)', INTERNATIONAL JOURNAL OF STROKE (2017)
Co-authors Robin Callister, Amanda Patterson, Neil Spratt, Christopher Oldmeadow, Rohan Walker, Coralie English
2017 Zalewska K, Ong LK, Pietrogrande G, Johnson SJ, Nilsson M, Walker FR, 'Oral corticosterone administration alone is sufficient to simulate the actions of chronic stress on glial cells but not on vasculature', GLIA, Edinburgh, SCOTLAND (2017)
Co-authors Rohan Walker, Michael Nilsson
2015 Ong LK, Briggs G, Guan L, Dunkley P, Dickson P, 'Inflammation and dopamine synthesis in neurodegeneration', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Co-authors Peter Dunkley, Phil Dickson
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]
Co-authors Phil Dickson, Peter Dunkley
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]
Co-authors Peter Dunkley, Eugene Nalivaiko, Deborah Hodgson
2012 Ong LK, Guan L, Bobrovskaya L, Dickson PW, Dunkley PR, 'Neurobiological consequences of acute footshock stress', Journal of Neurochemistry, Kobe, Japan (2012) [E3]
Co-authors Peter Dunkley, Phil Dickson
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]
Co-authors Deborah Hodgson, Peter Dunkley, Eugene Nalivaiko
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]
Co-authors Deborah Hodgson, Rohan Walker
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]
Co-authors Deborah Hodgson, Roger Smith, Jay Horvat, Philip Hansbro
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]
DOI 10.1016/j.bbi.2011.07.014
Co-authors Deborah Hodgson
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]
DOI 10.1093/jac/dkq221
Citations Scopus - 3
Co-authors Peter Dunkley, Phil Dickson
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]
DOI 10.1016/j.autneu.2009.05.191
Co-authors Phil Dickson, Peter Dunkley
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]
DOI 10.1016/j.autneu.2009.05.228
Co-authors Peter Dunkley
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]
DOI 10.1016/j.autneu.2009.05.192
Co-authors Peter Dunkley
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]
Co-authors Peter Dunkley, Phil Dickson
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]
DOI 10.1111/j.1471-4159.2009.06242.x
Co-authors Phil Dickson, Peter Dunkley, Rohan Walker
Show 14 more conferences
Edit

Grants and Funding

Summary

Number of grants 14
Total funding $283,133

Click on a grant title below to expand the full details for that specific grant.


20181 grants / $22,000

Growth hormone As Neurorestorative Therapy After Stroke$22,000

Funding body: Markey Insurance

Funding body Markey Insurance
Project Team Doctor Lin Kooi Ong, Professor Michael Nilsson, Associate Professor Rohan Walker, Professor Jorgen Isgaard
Scheme Research Funding
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800846
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

20176 grants / $154,851

Early Career Researcher (ECR) Higher Degree by Research (HDR) Scholarships$95,200

This program supports the University’s commitment to fostering and developing Early Career Researchers’ research and research leadership through the provision of fully funded Higher Degree by Research scholarships to applicants, attached to UON ECRs.

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, Ms Heidi Janssen, Doctor Dianne Marsden, Doctor Jodie Marquez, Associate Professor Coralie English, Associate Professor Rohan Walker
Scheme Medical Research Support Program (MRSP)
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1701224
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
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: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Conjoint Associate Professor Michael Pollack, Professor Michael Nilsson, Associate Professor Rohan Walker, Doctor Lin Kooi Ong
Scheme Research Grant
Role Investigator
Funding Start 2016
Funding Finish 2017
GNo G1600724
Type Of Funding C3112 - Aust Not for profit
Category 3112
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 Associate Professor Rohan Walker, Doctor Lin Kooi Ong, Doctor 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

Edit

Research Supervision

Number of supervisions

Completed0
Current2

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2017 PhD The Glymphatic System: A Brain Waste Clearance Pathway as a Potential Target for Post-Stroke Cognitive Impairment PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Principal Supervisor
2016 PhD Post-stroke cognitive impairment: an exploration of the neuropathology and functional outcomes PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
Edit

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 38
United States 4
Malaysia 2
Sweden 2
Brazil 1
More...
Edit

News

Brain fertiliser nurtures new hope for stroke survivors

May 25, 2018

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

Post Doctoral Research Fellow
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email linkooi.ong@newcastle.edu.au
Phone (02) 49215736
Links Research Networks
Twitter

Office

Room HMRI Lvl 3 East Kookaburra Circuit
Edit