TREM-2, inflammation resolution and the transition from brain injury to repair after stroke
Lead Research Organisation:
University of Edinburgh
Department Name: The Roslin Institute
Abstract
Stroke is one of the most common causes of death and disability and is normally caused by a blockage in an artery carrying blood to the brain. Blockage of the artery triggers many processes that cause brain tissue to die and this leads to disability. Long term outcome after stroke and related brain disorders is influenced by the amount of initial brain damage and the capacity for surviving brain tissue to promote regeneration and repair. This is why understanding the factors that influence this balance between brain damage and repair after stroke is so important. Currently we have a poor understanding of this but recent research suggests that the immune system might be a crucial balancing influence.
The immune system produces an inflammatory response when the body is infected or injured, including when the brain is injured after a stroke. Research we and others have carried out previously in stroke patients and animal models of stroke has shown that inflammation can worsen brain damage and cause more disability. However, not all inflammation is bad because some brain repair processes are boosted by inflammation. These contrasting effects of inflammation mean that we need to find out how the bad, injury-causing effects of inflammation can be switched off without compromising the good effects of inflammation on brain repair and recovery.
Our recent research has identified a chemical made by inflammatory cells that we believe could help control the balance between good and bad inflammation in the brain after stroke. This chemical is called TREM-2. The most exciting thing about TREM-2 is that it seems to affect this balance by limiting the injury-promoting affects of inflammation but at the same time still supporting responses of brain cells needed for repair. To potentially take advantage of these properties of TREM-2 in future we need to find out a lot more about how TREM-2 works under the conditions that occur in the brain after stroke.
The overall aim of our research project is to build on our recent results and firmly establish how TREM-2 influences the balance of inflammation, injury and repair in the brain after stroke. To do this, we will address four key questions:
1. When and where is TREM-2 produced in the brain after stroke?
2. How does TREM-2 function affect the behaviour of inflammatory cells in the brain?
3. What effect does genetic deletion of TREM-2 have on inflammation, injury and repair?
4. What affect does boosting production of TREM-2 have on inflammation, injury and repair?
We expect that the answers to these questions will firmly show us if TREM-2 does limit injury-causing inflammation without compromising repair in the brain after stroke. More generally, the work will help us understand how the delicate balance of inflammation in the injured brain is controlled. Ultimately, we hope our findings can be used to help set up patient trials that will test if new treatments based on manipulating TREM-2 and more generally the balance of inflammation have potential to reduce death and disability in stroke patients.
The immune system produces an inflammatory response when the body is infected or injured, including when the brain is injured after a stroke. Research we and others have carried out previously in stroke patients and animal models of stroke has shown that inflammation can worsen brain damage and cause more disability. However, not all inflammation is bad because some brain repair processes are boosted by inflammation. These contrasting effects of inflammation mean that we need to find out how the bad, injury-causing effects of inflammation can be switched off without compromising the good effects of inflammation on brain repair and recovery.
Our recent research has identified a chemical made by inflammatory cells that we believe could help control the balance between good and bad inflammation in the brain after stroke. This chemical is called TREM-2. The most exciting thing about TREM-2 is that it seems to affect this balance by limiting the injury-promoting affects of inflammation but at the same time still supporting responses of brain cells needed for repair. To potentially take advantage of these properties of TREM-2 in future we need to find out a lot more about how TREM-2 works under the conditions that occur in the brain after stroke.
The overall aim of our research project is to build on our recent results and firmly establish how TREM-2 influences the balance of inflammation, injury and repair in the brain after stroke. To do this, we will address four key questions:
1. When and where is TREM-2 produced in the brain after stroke?
2. How does TREM-2 function affect the behaviour of inflammatory cells in the brain?
3. What effect does genetic deletion of TREM-2 have on inflammation, injury and repair?
4. What affect does boosting production of TREM-2 have on inflammation, injury and repair?
We expect that the answers to these questions will firmly show us if TREM-2 does limit injury-causing inflammation without compromising repair in the brain after stroke. More generally, the work will help us understand how the delicate balance of inflammation in the injured brain is controlled. Ultimately, we hope our findings can be used to help set up patient trials that will test if new treatments based on manipulating TREM-2 and more generally the balance of inflammation have potential to reduce death and disability in stroke patients.
Technical Summary
Inflammation may have both damaging and protective influences during acute and chronic neurodegeneration including after acute cerebral ischaemia/stroke. This duality of inflammation underlines the need to understand how toxic and beneficial inflammation is balanced in the injured brain. In particular, establishing how pro-injurious inflammation can be contained or resolved without compromising the capacity for endogenous or exogenously-triggered brain repair is essential.
Our recent data supporting this proposal show that Triggering Receptor Expressed on Myeloid cells-2 (TREM-2) may act as a critical molecular regulator restraining injurious inflammation and supporting repair e.g. we have shown that TREM-2 signalling in microglia and macrophages connects the removal of neurotoxic neutrophils with proliferation of neuronal precursors. However, the role of TREM-2 under the unique conditions of the ischaemic brain has not been studied previously.
The overriding aim of this proposal is to test the hypothesis that Triggering Receptor Expressed on Myeloid cells-2 (TREM-2) drives resolution of injurious inflammation and the transition from injury to repair in the brain after acute cerebral ischaemia. We will use a multi-modal approach including an experimental model of stroke, in vitro co-culture systems combining myeloid and neural cells and post-mortem brain tissue from stroke patients. We will exploit and generate novel tools that enable targeted deletion or augmentation of TREM-2 activity. These approaches will be used to determine expression patterns of TREM-2, the effects of TREM-2 on inflammatory cell phenotypes and the impact of TREM-2 deletion or overexpression on inflammatory profile and markers of injury and repair after stroke.
We expect our findings will provide a rational basis for developing effective immunomodulatory approaches for the treatment of stroke and other neurological conditions.
Our recent data supporting this proposal show that Triggering Receptor Expressed on Myeloid cells-2 (TREM-2) may act as a critical molecular regulator restraining injurious inflammation and supporting repair e.g. we have shown that TREM-2 signalling in microglia and macrophages connects the removal of neurotoxic neutrophils with proliferation of neuronal precursors. However, the role of TREM-2 under the unique conditions of the ischaemic brain has not been studied previously.
The overriding aim of this proposal is to test the hypothesis that Triggering Receptor Expressed on Myeloid cells-2 (TREM-2) drives resolution of injurious inflammation and the transition from injury to repair in the brain after acute cerebral ischaemia. We will use a multi-modal approach including an experimental model of stroke, in vitro co-culture systems combining myeloid and neural cells and post-mortem brain tissue from stroke patients. We will exploit and generate novel tools that enable targeted deletion or augmentation of TREM-2 activity. These approaches will be used to determine expression patterns of TREM-2, the effects of TREM-2 on inflammatory cell phenotypes and the impact of TREM-2 deletion or overexpression on inflammatory profile and markers of injury and repair after stroke.
We expect our findings will provide a rational basis for developing effective immunomodulatory approaches for the treatment of stroke and other neurological conditions.
Planned Impact
Academic research - as described in the academic beneficiaries section, we expect multiple groups will benefit including those in the neurobiology/degeneration, stroke, immunology and bone disorder fields. This reflects the position of TREM-2 as a molecule that functions at the interface of basic neurobiology, neurodegeneration and immunology. These groups include those in the UK and internationally and include our collaborators. These groups will benefit through the increased knowledge and understanding our research will bring that will impact on their own ability to make advances in understanding related biological mechanisms and disease processes. The general biomedical community will also benefit through a major new resource we will create (TREM-2 overexpressing mouse) and our training of researchers in highly skilled and sought-after techniques, notably whole animal physiology.
University teaching and education - our research findings will inform teaching content and practices by providing up-to-date information on scientific advances leading to a more relevant teaching experience equipping students with better knowledge and skills
Clinical/healthcare - our project will benefit clinicians and healthcare providers through advancing knowledge on potential new strategies for treatment and management of stroke and related neurological disorders. These groups would be able to use the data we generate to inform decisions on testing agents in clinical trials in patients. Our project may also impact on general policy and practice in the long-term through generating new concepts on how stroke patients can be treated and managed e.g. by targeting mechanisms in the sub-acute phase.
Industry - a key aim of our proposal is to generate an evidence base for new therapeutic strategies and targets for stroke and related conditions. This information will benefit biotech and pharmaceutical companies by informing their drug discovery and development pathways. Reciprocal benefits are possible through partnerships with industry and investment by companies in academia
Schools - through our research projects and engagement activities we are able to promote the awareness of how scientific research contributes to addressing important issues related to health and wellbeing. This can benefit schools through enriching the science curriculum and providing opinion and advice to pupils and teachers on careers in biomedical research
General public - although our proposed research is at the discovery stage it has the potential to impact on the health and well-being of the general population through identifying new ways to treat many more individuals affected by stroke and related neurological conditions. The benefit may take years to realise however our research has the potential to contribute a vital step in this process. Our research will also generate opportunities to increase public awareness of science and its role in reducing suffering associated with injury and disease
Policy makers - our work involves considerable use of in vivo approaches so has potential to generate new information influencing policy and practice relating to the use of animals in research
University teaching and education - our research findings will inform teaching content and practices by providing up-to-date information on scientific advances leading to a more relevant teaching experience equipping students with better knowledge and skills
Clinical/healthcare - our project will benefit clinicians and healthcare providers through advancing knowledge on potential new strategies for treatment and management of stroke and related neurological disorders. These groups would be able to use the data we generate to inform decisions on testing agents in clinical trials in patients. Our project may also impact on general policy and practice in the long-term through generating new concepts on how stroke patients can be treated and managed e.g. by targeting mechanisms in the sub-acute phase.
Industry - a key aim of our proposal is to generate an evidence base for new therapeutic strategies and targets for stroke and related conditions. This information will benefit biotech and pharmaceutical companies by informing their drug discovery and development pathways. Reciprocal benefits are possible through partnerships with industry and investment by companies in academia
Schools - through our research projects and engagement activities we are able to promote the awareness of how scientific research contributes to addressing important issues related to health and wellbeing. This can benefit schools through enriching the science curriculum and providing opinion and advice to pupils and teachers on careers in biomedical research
General public - although our proposed research is at the discovery stage it has the potential to impact on the health and well-being of the general population through identifying new ways to treat many more individuals affected by stroke and related neurological conditions. The benefit may take years to realise however our research has the potential to contribute a vital step in this process. Our research will also generate opportunities to increase public awareness of science and its role in reducing suffering associated with injury and disease
Policy makers - our work involves considerable use of in vivo approaches so has potential to generate new information influencing policy and practice relating to the use of animals in research
Organisations
- University of Edinburgh (Lead Research Organisation)
- UNIVERSITY OF EDINBURGH (Collaboration)
- University of Arizona (Collaboration)
- Complutense University of Madrid (Collaboration)
- Dementia Discovery Fund (Collaboration)
- University of Manchester (Collaboration)
- McGill University (Collaboration)
- University of Bordeaux (Collaboration)
- Alector (Collaboration)
- KING'S COLLEGE LONDON (Collaboration)
- MRC Harwell Institute (Collaboration)
People |
ORCID iD |
Barry McColl (Principal Investigator) |
Publications
Askew KE
(2024)
Inhibiting CSF1R alleviates cerebrovascular white matter disease and cognitive impairment.
in Glia
Daniels MJD
(2023)
Cystatin F (Cst7) drives sex-dependent changes in microglia in an amyloid-driven model of Alzheimer's disease.
in eLife
Davies CL
(2019)
Myeloid Cell and Transcriptome Signatures Associated With Inflammation Resolution in a Model of Self-Limiting Acute Brain Inflammation.
in Frontiers in immunology
Giles JA
(2015)
Requirement for interleukin-1 to drive brain inflammation reveals tissue-specific mechanisms of innate immunity.
in European journal of immunology
Giles JA
(2018)
Neutrophil infiltration to the brain is platelet-dependent, and is reversed by blockade of platelet GPIba.
in Immunology
Grabert K
(2016)
Microglial brain region-dependent diversity and selective regional sensitivities to aging.
in Nature neuroscience
Grabert K
(2018)
Macrophages
Graham LC
(2019)
Regional Molecular Mapping of Primate Synapses during Normal Healthy Aging.
in Cell reports
Greenhalgh AD
(2018)
Peripherally derived macrophages modulate microglial function to reduce inflammation after CNS injury.
in PLoS biology
Horsburgh K
(2018)
Small vessels, dementia and chronic diseases - molecular mechanisms and pathophysiology.
in Clinical science (London, England : 1979)
Keane L
(2021)
Inhibition of microglial EZH2 leads to anti-tumoral effects in pediatric diffuse midline gliomas.
in Neuro-oncology advances
Kirby C
(2023)
Association between circulating inflammatory biomarkers and functional outcome or perihaematomal oedema after ICH: a systematic review & meta-analysis
in Wellcome Open Research
Kirby C
(2023)
Association between circulating inflammatory biomarkers and functional outcome or perihaematomal oedema after ICH: a systematic review & meta-analysis.
in Wellcome open research
Loan JJ
(2022)
Secondary injury and inflammation after intracerebral haemorrhage: a systematic review and meta-analysis of molecular markers in patient brain tissue.
in Journal of neurology, neurosurgery, and psychiatry
Maysami S
(2015)
Prolonged diet-induced obesity in mice modifies the inflammatory response and leads to worse outcome after stroke.
in Journal of neuroinflammation
McCulloch L
(2017)
Adrenergic-mediated loss of splenic marginal zone B cells contributes to infection susceptibility after stroke.
in Nature communications
McCulloch L
(2019)
Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence.
in F1000Research
McCulloch L
(2017)
Corrigendum: Adrenergic-mediated loss of splenic marginal zone B cells contributes to infection susceptibility after stroke.
in Nature communications
McCulloch L
(2019)
Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence
in F1000Research
McCulloch L
(2018)
Experimental Stroke Differentially Affects Discrete Subpopulations of Splenic Macrophages.
in Frontiers in immunology
McFall A
(2020)
UK consensus on pre-clinical vascular cognitive impairment functional outcomes assessment: Questionnaire and workshop proceedings.
in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
McNamara NB
(2023)
Microglia regulate central nervous system myelin growth and integrity.
in Nature
McQueen J
(2017)
Pro-death NMDA receptor signaling is promoted by the GluN2B C-terminus independently of Dapk1.
in eLife
Owens R
(2017)
Divergent Neuroinflammatory Regulation of Microglial TREM Expression and Involvement of NF-?B.
in Frontiers in cellular neuroscience
Owens R
(2017)
Corrigendum: Divergent Neuroinflammatory Regulation of Microglial TREM Expression and Involvement of NF-?B.
in Frontiers in cellular neuroscience
Percie Du Sert N
(2017)
The IMPROVE Guidelines (Ischaemia Models: Procedural Refinements Of in Vivo Experiments).
in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
Smith C
(2020)
Biallelic mutations in NRROS cause an early onset lethal microgliopathy.
in Acta neuropathologica
Sri S
(2023)
A multi-disciplinary commentary on preclinical research to investigate vascular contributions to dementia
in Cerebral Circulation - Cognition and Behavior
Stevenson A
(2018)
Trajectories of inflammatory biomarkers over the eighth decade and their associations with immune cell profiles and epigenetic ageing
in Clinical Epigenetics
Tzioras M
(2023)
Human astrocytes and microglia show augmented ingestion of synapses in Alzheimer's disease via MFG-E8.
in Cell reports. Medicine
Vincenti JE
(2015)
Defining the Microglia Response during the Time Course of Chronic Neurodegeneration.
in Journal of virology
Description | NC3Rs Stroke Working Group, Member |
Geographic Reach | National |
Policy Influence Type | Participation in a guidance/advisory committee |
Description | NC3Rs stroke advisory group |
Geographic Reach | Multiple continents/international |
Policy Influence Type | Participation in a guidance/advisory committee |
Description | ARUK Scotland Network Junior Grant |
Amount | £2,000 (GBP) |
Organisation | Alzheimer's Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 01/2018 |
Description | ARUK Scotland Network Junior Mmber Small Grant (Szymkowiak) |
Amount | £2,000 (GBP) |
Organisation | Alzheimer's Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start |
Description | ARUK Scotland Network Small Grant |
Amount | £4,700 (GBP) |
Organisation | Alzheimer's Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 01/2018 |
Description | Dementia Research Institute Foundation Grant |
Amount | £1,000,000 (GBP) |
Organisation | UK Dementia Research Institute |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 09/2017 |
End | 08/2022 |
Description | Developing studies on CSF-Fc for brain repair after stroke |
Amount | £26,955 (GBP) |
Organisation | Chief Scientist Office |
Sector | Public |
Country | United Kingdom |
Start |
Description | ISSF3 - Development of preclinical studies on CSF-Fc to promote brain repair |
Amount | £47,704 (GBP) |
Organisation | Wellcome Trust |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start |
Description | Leducq Foundation ECR award (to Stefan Szymkowiak) |
Amount | $10,000 (USD) |
Organisation | The Leducq Foundation |
Sector | Charity/Non Profit |
Country | France |
Start |
Description | MRC Confidence in Concept |
Amount | £123,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 02/2018 |
End | 01/2019 |
Description | MRC Confidence in Concept - CSF1-Fc to enhance brain repair and functional recovery after stroke: a preclinical proof-of-concept study |
Amount | £123,303 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 02/2018 |
End | 03/2019 |
Description | MRC project grant |
Amount | £1,316,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 02/2018 |
End | 01/2021 |
Description | MRF Equipment funding competition |
Amount | £75,570 (GBP) |
Funding ID | C0495 |
Organisation | Medical Research Council (MRC) |
Department | Medical Research Foundation |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 06/2014 |
End | 02/2015 |
Description | Moray Endowment Fund |
Amount | £1,842 (GBP) |
Organisation | University of Edinburgh |
Sector | Academic/University |
Country | United Kingdom |
Start | 10/2016 |
Description | Neuro-Inflammation after Cerebral Haemorrhage in Edinburgh (NICHE) |
Amount | £449,482 (GBP) |
Funding ID | TSAPPA2017/01 |
Organisation | Stroke Association |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 04/2018 |
End | 04/2023 |
Description | Project grant |
Amount | £27,774 (GBP) |
Organisation | Brain Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start |
Description | Small Scale Project Grant |
Amount | £5,760 (GBP) |
Organisation | University of Edinburgh |
Department | The Roslin Institute |
Sector | Academic/University |
Country | United Kingdom |
Start |
Description | Stroke-IMPaCT (Stroke - Immume mediated pathways and cognitive trajectory) |
Amount | $6,000,000 (USD) |
Organisation | The Leducq Foundation |
Sector | Charity/Non Profit |
Country | France |
Start | 01/2020 |
End | 12/2025 |
Description | Wellcome Trust ISSF3 - Priming the development of an interdisciplinary Edinburgh centre of excellence in pig neuroimmune research |
Amount | £56,772 (GBP) |
Organisation | Wellcome Trust |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start |
Title | Mouse microglial isolation method |
Description | Refined method to enable efficient and high-quality extraction of adult mouse microglia for downstream phenotyping and ex vivo applications |
Type Of Material | Biological samples |
Year Produced | 2018 |
Provided To Others? | Yes |
Impact | Citations and direct enquiries indicating uptake of technique by other groups in their research |
URL | https://link.springer.com/protocol/10.1007%2F978-1-4939-7837-3_7 |
Title | MCAO spleen datasets |
Description | Spleen microarray datasets from experimental stroke study |
Type Of Material | Database/Collection of data |
Year Produced | 2015 |
Provided To Others? | Yes |
Impact | Not known |
URL | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE70841 |
Title | Microglia datasets |
Description | Microarray datasets |
Type Of Material | Database/Collection of data |
Year Produced | 2015 |
Provided To Others? | Yes |
Impact | Datasets have been used by other groups and their re-analysis of data included in publications |
URL | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE62420 |
Title | Transcriptome dataset on resolution of acute brain inflammation |
Description | Transcriptome dataset on resolution of acute brain inflammation generated from an in vivo mouse model of intracerebral inflammation |
Type Of Material | Database/Collection of data |
Year Produced | 2019 |
Provided To Others? | Yes |
Impact | Enquiries from other researchers to access and extract data for their studies |
URL | https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE122815 |
Description | Alector collaboration |
Organisation | Alector |
Country | United States |
Sector | Private |
PI Contribution | Project design, technical expertise |
Collaborator Contribution | Reagent provision, project design, analytical expertise |
Impact | N/A |
Start Year | 2020 |
Description | Alicia Garcia collaboration |
Organisation | Complutense University of Madrid |
Country | Spain |
Sector | Academic/University |
PI Contribution | Sharing of data, training of student, provision of technical and analytical expertise, provision of reagents under MTA, proposals for future research |
Collaborator Contribution | Student placement, sharing of data, provision of technical and analytical expertise, conducting experimental work using reagents provided by us |
Impact | MTA and CDA |
Start Year | 2015 |
Description | Andrea Caporali lab collaboration |
Organisation | University of Edinburgh |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Project design, planning, data analysis |
Collaborator Contribution | Project design, planning, data analysis |
Impact | Grant submission |
Start Year | 2018 |
Description | Andrew Greenhalgh lab collaboration |
Organisation | University of Bordeaux |
Country | France |
Sector | Academic/University |
PI Contribution | Sharing of knowledge and technical expertise |
Collaborator Contribution | Sharing of knowledge and technical expertise |
Impact | Grant submissions |
Start Year | 2017 |
Description | Bruce Whitelaw lab collaboration |
Organisation | University of Edinburgh |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Conducting experimental work, sharing of data, provision of technical and analytical expertise |
Collaborator Contribution | Provision of technical and analytical expertise, creation of materials, sharing of data |
Impact | Funding application |
Start Year | 2015 |
Description | Colin Farquharson lab collaboration |
Organisation | University of Edinburgh |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Sharing of data, provision of technical and analytical expertise |
Collaborator Contribution | Sharing of data, provision of technical and analytical expertise |
Impact | No outcomes yet |
Start Year | 2016 |
Description | Craig Smith collaboration |
Organisation | University of Manchester |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Sharing of data, conducting experimental work using samples supplied by collaborator, provision of technical and analytical expertise |
Collaborator Contribution | Sharing of data, provision of biological samples, provision of clinical expertise |
Impact | Publication Funding application submitted |
Start Year | 2012 |
Description | DDF partnership |
Organisation | Dementia Discovery Fund |
Country | United Kingdom |
Sector | Private |
PI Contribution | Project design, planning, management, data analysis |
Collaborator Contribution | Project guidance, funding |
Impact | Platform development |
Start Year | 2018 |
Description | David Hume lab collaboration |
Organisation | University of Edinburgh |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Sharing of data, provision of technical and analytical expertise, conducting experimental work |
Collaborator Contribution | Sharing of data, provision of technical and analytical expertise, conducting experimental work |
Impact | Publication Funding applications submitted MTA and CDA with other collaborators involved in studies |
Start Year | 2012 |
Description | Giles Hardingham lab collaboration |
Organisation | University of Edinburgh |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Sharing of knowledge and technical expertise, input to project design, experimental work and analysis |
Collaborator Contribution | Sharing of knowledge and technical expertise, input to project design, experimental work and analysis |
Impact | Publication doi: 10.7554/eLife.17161 |
Start Year | 2017 |
Description | Kristian Doyle collaboration |
Organisation | University of Arizona |
Country | United States |
Sector | Academic/University |
PI Contribution | Project design, sample provision, analytical expertise |
Collaborator Contribution | Project design, sample provision, analytical expertise |
Impact | n/a |
Start Year | 2020 |
Description | Lawrence Moon collaboration |
Organisation | King's College London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Led study design, conception and preparation of funding proposal |
Collaborator Contribution | Input to study design, funding proposal |
Impact | Awarded Brain Research UK project grant |
Start Year | 2019 |
Description | MRC Mouse Network |
Organisation | MRC Harwell |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Proposed genes to prioritise for phenotyping |
Collaborator Contribution | Generation of knockout mouse line and phenotyping |
Impact | Generation of mouse line |
Start Year | 2013 |
Description | Rustam Al Shahi Salman lab collaboration |
Organisation | University of Edinburgh |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Project and experimental design |
Collaborator Contribution | Project and experimental design |
Impact | Stroke Association project grant awarded |
Start Year | 2017 |
Description | Sam David lab collaboration |
Organisation | McGill University |
Country | Canada |
Sector | Academic/University |
PI Contribution | Sharing of data from our studies and provision of reagents under MTA |
Collaborator Contribution | Sharing of data and conducting studies using reagents provided by us |
Impact | MTA and CDA put in place to enable formal collaboration and sharing of data and reagents |
Start Year | 2016 |
Description | Stuart Allan collaboration |
Organisation | University of Manchester |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Project design, funding, management, analysis |
Collaborator Contribution | Project design, funding, management, analysis |
Impact | Publications: PMID: 31700615, PMID: 29325217, PMID: 28422126, PMID: 25367678 |
Start Year | 2010 |
Description | Stuart Allan lab collaboration |
Organisation | University of Manchester |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Sharing of knowledge and technical expertise, input to project design, experimental work and analysis |
Collaborator Contribution | Sharing of knowledge and technical expertise, input to project design, experimental work and analysis |
Impact | Publications, MRC grant awarded |
Start Year | 2017 |
Description | Stuart Allan lab collaboration |
Organisation | University of Manchester |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Sharing of data, provision of technical and analytical expertise, proposing ideas for future studies |
Collaborator Contribution | Sharing of data, provision of technical and analytical expertise, proposing ideas for future studies |
Impact | Publications Funding applications |
Start Year | 2010 |
Description | McGill talk 2016 |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Talk presented as part of a symposium led to discussions and identifying common areas for collaboration with hosts - collaboration with Sam David lab initiated from this. |
Year(s) Of Engagement Activity | 2016 |
Description | Neuroinflammation Keystone Symposium (New Mexico) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Presentations and discussion at international conference enabled wider recognition of our work and has resulted in new collaborations |
Year(s) Of Engagement Activity | 2015 |
Description | Roslin Open Day |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Public/other audiences |
Results and Impact | Institute Open Day to engage general public in our projects and broader research activities in the Institute. Visitors reported interest in learning about our work and why animals are necessary for some aspects of mediacl research |
Year(s) Of Engagement Activity | 2014,2015,2016 |
Description | Symposium organiser/chair at BNA Festival of Neuroscience |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Organised and chaired a symposium at BNA conference - led to revised opinions on topic under discussion among presenters and audience |
Year(s) Of Engagement Activity | 2015 |
Description | Trinity College talk 2017 |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Talk presented as part of a symposium enable dissemination of recent findings to a new audience. Discussion among fellow attendees also led to proposals for a joint consortium funding application |
Year(s) Of Engagement Activity | 2017 |
Description | UK Preclinical Stroke Symposium (Glasgow) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Professional Practitioners |
Results and Impact | Oral presentations and discussion that enable dissemination of our data and led to revised opinions on the involvement of immune processes in stroke among the audience |
Year(s) Of Engagement Activity | 2015 |