The regulation of axon degeneration by SARM1
Lead Research Organisation:
University of Cambridge
Department Name: Clinical Neurosciences
Abstract
The aim of this Industrial Partnership is to understand a preventable and widely-occurring mechanism of axon degeneration, known as Wallerian degeneration, underpinning a rapidly increasing interest in drug development. When activated by nerve injury, blocking Wallerian degeneration can rescue axons for several weeks. When activated by disrupting one specific protein, we recently showed that blocking it rescues axons indefinitely. Animal and cell culture studies indicate the Wallerian degeneration mechanism contributes widely to disease so it has become an important goal in the Pharmaceutical industry. Together with our industrial partner, AstraZeneca, we will focus on crucial step in the pathway generating new basic knowledge that will support future drug development.
Axons are the long fibres that connect one nerve cell with another, relaying electrical information around our nervous system. They are essential for many normal body functions, not only those we typically associate with nervous system such as thinking, memory, pain and movement, but also for vision, hearing, gut function, bladder control and breathing. In short, without fully functional axons there is no normal life.
Unfortunately, axons are the most vulnerable parts of our nerve cells. Many of them are very long, up to one meter compared to typical cellular dimensions of a fraction of a millimeter. Other axons are highly branched, posing a significant challenge for the far smaller cell body to support it. Like any remote structure dependent on central support, axons die first when things go wrong, for example in ageing, injury and disease.
Our research opened up an entirely new field in understanding why axons degenerate and how we can prevent it. We identified the first gene known to preserve injured axons and showed that it also protects axons that are compromised in other ways without physical injury. Stemming from this finding, disruption of other genes has been found to block Wallerian degeneration too. This project focusses on one of them, SARM1, a protein required for axons to undergo Wallerian degeneration. In some circumstances, blocking SARM1 confers lifelong rescue of axons.
SARM1 has become an area of considerable interest to the Pharma industry, including to our industrial partner AstraZeneca, following identification of an enzyme activity associated with it. In order to maximise the chance of success, it is vital to understand SARM1 function more than we currently do. In particular, we need
to understand how it is regulated and the molecular consequences of its activation that lead to axon death. Our group has already made significant progress by identifying steps in the Wallerian degeneration mechanism that precede SARM1 activation. Here we present new hypotheses regarding these next steps together with strategies to test them.
These studies should identify new strategies to block SARM1 activation and rescue axons from degeneration. Thus, our industrial partner AstraZeneca is co-sponsoring this proposal and will contribute significant additional expertise in molecular neuroscience, chemistry and mass spectrometry. Together with our long-term collaborators Giuseppe Orsomando and colleagues, experts in NAD metabolism, we make a highly effective team able to drive this important topic forward and underpin future drug development.
Axons are the long fibres that connect one nerve cell with another, relaying electrical information around our nervous system. They are essential for many normal body functions, not only those we typically associate with nervous system such as thinking, memory, pain and movement, but also for vision, hearing, gut function, bladder control and breathing. In short, without fully functional axons there is no normal life.
Unfortunately, axons are the most vulnerable parts of our nerve cells. Many of them are very long, up to one meter compared to typical cellular dimensions of a fraction of a millimeter. Other axons are highly branched, posing a significant challenge for the far smaller cell body to support it. Like any remote structure dependent on central support, axons die first when things go wrong, for example in ageing, injury and disease.
Our research opened up an entirely new field in understanding why axons degenerate and how we can prevent it. We identified the first gene known to preserve injured axons and showed that it also protects axons that are compromised in other ways without physical injury. Stemming from this finding, disruption of other genes has been found to block Wallerian degeneration too. This project focusses on one of them, SARM1, a protein required for axons to undergo Wallerian degeneration. In some circumstances, blocking SARM1 confers lifelong rescue of axons.
SARM1 has become an area of considerable interest to the Pharma industry, including to our industrial partner AstraZeneca, following identification of an enzyme activity associated with it. In order to maximise the chance of success, it is vital to understand SARM1 function more than we currently do. In particular, we need
to understand how it is regulated and the molecular consequences of its activation that lead to axon death. Our group has already made significant progress by identifying steps in the Wallerian degeneration mechanism that precede SARM1 activation. Here we present new hypotheses regarding these next steps together with strategies to test them.
These studies should identify new strategies to block SARM1 activation and rescue axons from degeneration. Thus, our industrial partner AstraZeneca is co-sponsoring this proposal and will contribute significant additional expertise in molecular neuroscience, chemistry and mass spectrometry. Together with our long-term collaborators Giuseppe Orsomando and colleagues, experts in NAD metabolism, we make a highly effective team able to drive this important topic forward and underpin future drug development.
Technical Summary
This Industrial Partnership proposal is a three-way collaboration between experts in axon degeneration (Coleman, Cambridge), NAD metabolism (Orsomando, Ancona) and drug discovery (Wang, AstroZeneca). We seek to understand the mechanism of activation of the SARM1 protein, a closely-regulated NAD degrading enzyme required for axons to degenerate in many circumstances. Deletion of the SARM1 gene blocks the Wallerian degeneration of axons distal to an injury for several weeks. In axons specifically lacking the NAD synthesising enzyme NMNAT2 it confers a lifelong rescue of their survival and function.
This striking, indefinite rescue of axons has led to significant interest in targeting SARM1 for drug development in axonal disorders such as peripheral neuropathies, Parkinson's disease, multiple sclerosis, glaucoma and others. However, several fundamental aspects of SARM1 function remain unclear, most notably how it is regulated, how it causes axon degeneration and its subcellular location. We will use unique resources and expertise available to our three collaborating laboratories to address these questions, thereby underpinning future drug development strategies.
We will test the hypothesis that one or more activators of SARM1 accumulate/s in the axoplasm of NMNAT2-/-;SARM1-/- double mutant mice, a healthy strain in which Wallerian degeneration has been first constitutively activated by removing NMNAT2 and then prevented from completing by also removing SARM1. We will test the hypothesis that SARM1 causes axon death not by NAD depletion but by signalling for calcium mobilisation through the products of its NADase activity. Finally, we will identify the subcellular location where SARM1 resides by colocalisation and cosegregation studies and test whether this changes during axon degeneration.
This striking, indefinite rescue of axons has led to significant interest in targeting SARM1 for drug development in axonal disorders such as peripheral neuropathies, Parkinson's disease, multiple sclerosis, glaucoma and others. However, several fundamental aspects of SARM1 function remain unclear, most notably how it is regulated, how it causes axon degeneration and its subcellular location. We will use unique resources and expertise available to our three collaborating laboratories to address these questions, thereby underpinning future drug development strategies.
We will test the hypothesis that one or more activators of SARM1 accumulate/s in the axoplasm of NMNAT2-/-;SARM1-/- double mutant mice, a healthy strain in which Wallerian degeneration has been first constitutively activated by removing NMNAT2 and then prevented from completing by also removing SARM1. We will test the hypothesis that SARM1 causes axon death not by NAD depletion but by signalling for calcium mobilisation through the products of its NADase activity. Finally, we will identify the subcellular location where SARM1 resides by colocalisation and cosegregation studies and test whether this changes during axon degeneration.
Planned Impact
The actual and potential non-academic beneficiaries of this project will be:
(1) Our industrial partner, AstraZeneca, who will gain from intellectual and practical collaboration particularly in the field of Wallerian degeneration and longer-term with the potential to license and develop new intellectual outputs from this project taking it towards drug discovery. However, it is highly likely that our discussions will be even more wide-ranging as the project goes forward and other areas of potential interaction emerge. This will be an extremely important collaboration for both sides of this partnership.
(2) Other Pharma/biotech companies targeting axon degeneration disorders. We will of course pay full regard to the commercial sensitivities of our industrial partner and adhere to the agreement that we make. Nevertheless, in the general field of axon degeneration the increased understanding we will gain from this research, including after any period for patenting and publication, will be of significant interest to the wider Pharma and biotech community. We are aware of a significant number of companies who are targeting the Wallerian degeneration pathway who will closely watch this research.
(3) Patients with axonal disorders. There is no treatment for axon degeneration in neurodegenerative disease, nor indeed in ageing or metabolic disorders such as diabetes. This work has significant potential for later translation into drug discovery with applications particularly in chemotherapy-induced peripheral neuropathy, multiple sclerosis, stroke and other acute or relapsing/remitting conditions where even temporary axon protection is useful. As the human genetics of axonal disorders becomes clearer, it is likely that the few cases of NMNAT2 mutation we are already aware of (papers in preparation) will grow and these individuals could benefit significantly from blocking SARM1 activity, considering the lifelong rescue of axons we found in mice (Gilley et al, Cell Rep 2017).
(4) Lay public interested in nervous system function and dysfunction. In our public engagement activities we find a strong interest in the nervous system among the lay public. While there is only a limited amount that individuals can do about the health of their nervous system, understanding what goes wrong can at least help some patients to come to terms with it, and motivates some healthy individuals to ensure they avoid a lifestyle that places strains on axon survival (e.g., excessive alcohol consumption, obesity, drug abuse).
(1) Our industrial partner, AstraZeneca, who will gain from intellectual and practical collaboration particularly in the field of Wallerian degeneration and longer-term with the potential to license and develop new intellectual outputs from this project taking it towards drug discovery. However, it is highly likely that our discussions will be even more wide-ranging as the project goes forward and other areas of potential interaction emerge. This will be an extremely important collaboration for both sides of this partnership.
(2) Other Pharma/biotech companies targeting axon degeneration disorders. We will of course pay full regard to the commercial sensitivities of our industrial partner and adhere to the agreement that we make. Nevertheless, in the general field of axon degeneration the increased understanding we will gain from this research, including after any period for patenting and publication, will be of significant interest to the wider Pharma and biotech community. We are aware of a significant number of companies who are targeting the Wallerian degeneration pathway who will closely watch this research.
(3) Patients with axonal disorders. There is no treatment for axon degeneration in neurodegenerative disease, nor indeed in ageing or metabolic disorders such as diabetes. This work has significant potential for later translation into drug discovery with applications particularly in chemotherapy-induced peripheral neuropathy, multiple sclerosis, stroke and other acute or relapsing/remitting conditions where even temporary axon protection is useful. As the human genetics of axonal disorders becomes clearer, it is likely that the few cases of NMNAT2 mutation we are already aware of (papers in preparation) will grow and these individuals could benefit significantly from blocking SARM1 activity, considering the lifelong rescue of axons we found in mice (Gilley et al, Cell Rep 2017).
(4) Lay public interested in nervous system function and dysfunction. In our public engagement activities we find a strong interest in the nervous system among the lay public. While there is only a limited amount that individuals can do about the health of their nervous system, understanding what goes wrong can at least help some patients to come to terms with it, and motivates some healthy individuals to ensure they avoid a lifestyle that places strains on axon survival (e.g., excessive alcohol consumption, obesity, drug abuse).
Publications
Ademi M
(2022)
Natural variants of human SARM1 cause both intrinsic and dominant loss-of-function influencing axon survival
in Scientific Reports
Arthur-Farraj P
(2021)
Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.
in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
Coleman M
(2020)
Programmed axon degeneration: from mouse to mechanism to medicine.
Coleman MP
(2022)
Axon Biology in ALS: Mechanisms of Axon Degeneration and Prospects for Therapy.
in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
Coleman MP
(2020)
Programmed axon degeneration: from mouse to mechanism to medicine.
in Nature reviews. Neuroscience
Gilley J
(2020)
Microinjection of Superior Cervical Ganglion Neurons for Studying Axon Degeneration.
in Methods in molecular biology (Clifton, N.J.)
Gould SA
(2021)
Sarm1 haploinsufficiency or low expression levels after antisense oligonucleotides delay programmed axon degeneration.
in Cell reports
Hopkins EL
(2021)
A Novel NAD Signaling Mechanism in Axon Degeneration and its Relationship to Innate Immunity.
in Frontiers in molecular biosciences
Horsefield S
(2019)
NAD+ cleavage activity by animal and plant TIR domains in cell death pathways.
Horsefield S
(2019)
NAD+ cleavage activity by animal and plant TIR domains in cell death pathways.
in Science (New York, N.Y.)
Llobet Rosell A
(2022)
The NAD+ precursor NMN activates dSarm to trigger axon degeneration in Drosophila.
Llobet Rosell A
(2022)
The NAD+ precursor NMN activates dSarm to trigger axon degeneration in Drosophila.
in eLife
Llobet Rosell A
(2022)
The NAD+ precursor NMN activates dSarm to trigger axon degeneration in Drosophila.
Description | NMN and VMN are activators of SARM1 NAD and NADP inhibit SARM1 There are natural LoF and GoF mutations in SARM1 in the human population Evidence of compensatory mechanisms for NMNAT2 LoF and SARM1 GoF NMN, NAD and NADP all regulate SARM1 within the physiological range Base exchange by SARM1 can be dominant over NADase activity |
Exploitation Route | We aim to build on these findings in a new funding application to generate more specific/potent inhibitors of SARM1 and to understand the compensatory mechanisms that may reveal new drug targets. |
Sectors | Education Pharmaceuticals and Medical Biotechnology |
Description | Association of SARM1 gene variants with neurological disease |
Amount | $999,081 (USD) |
Organisation | Bristol-Myers Squibb |
Sector | Private |
Country | United States |
Start | 01/2024 |
End | 01/2027 |
Description | BBSRC CASE studentship with AstraZeneca |
Amount | £100,000 (GBP) |
Organisation | Biotechnology and Biological Sciences Research Council (BBSRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2020 |
End | 09/2024 |
Description | Cambridge MRC DTP Industrial CASE (iCASE) Studentship |
Amount | £120,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2023 |
End | 09/2027 |
Description | Compensatory effects preventing SARM1-dependent neuron and axon death |
Amount | $75,000 (USD) |
Organisation | Johns Hopkins University |
Department | The Robert Packard Center for ALS Research at Johns Hopkins |
Sector | Charity/Non Profit |
Country | United States |
Start | 02/2024 |
End | 01/2025 |
Description | DTP-MR PhD studentship |
Amount | £104,388 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2023 |
End | 09/2027 |
Description | Establishing causative roles for SARM1 coding and expression level variants in ALS |
Amount | $400,000 (USD) |
Organisation | The ALS Association |
Sector | Charity/Non Profit |
Country | United States |
Start | 03/2022 |
End | 02/2024 |
Description | Genetic and environmental risk factors that combine with SARM1 in ALS |
Amount | £138,658 (GBP) |
Funding ID | Coleman 2326-792 |
Organisation | Motor Neurone Disease Association (MND) |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 02/2024 |
End | 07/2027 |
Description | Programmed axon death: a preventable axon degeneration mechanism in some ALS patients |
Amount | $50,000 (USD) |
Organisation | Johns Hopkins University |
Department | The Robert Packard Center for ALS Research at Johns Hopkins |
Sector | Charity/Non Profit |
Country | United States |
Start | 02/2021 |
End | 01/2022 |
Description | Programmed axon death: a preventable axon degeneration mechanism in some ALS patients |
Amount | $50,000 (USD) |
Organisation | Johns Hopkins University |
Department | The Robert Packard Center for ALS Research at Johns Hopkins |
Sector | Charity/Non Profit |
Country | United States |
Start | 02/2022 |
End | 07/2023 |
Description | Using human genetics to identify neurodegenerative disorders likely to be alleviated by blocking SARM1 |
Amount | £105,688 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2023 |
End | 09/2027 |
Description | Wellcome Collaborative Award in Science: Preventable axon degeneration in human disease |
Amount | £3,500,000 (GBP) |
Funding ID | 220906/Z/20/Z |
Organisation | Wellcome Trust |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 03/2021 |
End | 03/2026 |
Description | Prof Ahmet Hoke sabbatical |
Organisation | Johns Hopkins University |
Department | School of Medicine Johns Hopkins |
Country | United States |
Sector | Academic/University |
PI Contribution | The Coleman Lab is hosting Professor Ahmet Hoke for a sabbatical visit allowing new collaboration between our teams. In particular, for example, his contribution will be invaluable to the work of one of our PhD students. |
Collaborator Contribution | Johns Hopkins School of Medicine is contributing through Professor Hoke's participation in our research. |
Impact | Sabbatical was terminated early due to pandemic lockdown. |
Start Year | 2020 |
Description | OPCD Seminar - Oxford |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Professional Practitioners |
Results and Impact | Talk titled: Mechanisms of axon degeneration in injury and disease, held at Nuffield Department of Clinical Neurosciences. Level 6, West Wing, John Radcliffe Hospital, Oxford OX3 9DU on September 12th 2019 |
Year(s) Of Engagement Activity | 2019 |
Description | Packard Center PI meeting |
Form Of Engagement Activity | A formal working group, expert panel or dialogue |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | This meeting brings together principal investigators from organisations around the world for discussion and knowledge-sharing. |
Year(s) Of Engagement Activity | 2020,2021 |
Description | Presentation at Peripheral Nerve Society Annual Meeting (Miami) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | A presentation at the Peripheral Nerve Society Annual Meeting in Miami. Findings and conclusions were shared with a wide audience. The presentation prompted questions and discussion afterwards. |
Year(s) Of Engagement Activity | 2022 |
Description | Presentation at the 2nd Workshop of the Neurobiology of Pain and Inflammation Program |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Professional Practitioners |
Results and Impact | I presented a talk at the 2nd Workshop of the Neurobiology of Pain and Inflammation Program, Instituto de Neurociencias UMH-CSIC San Juan de Alicante, Spain. The talk sparked discussion and the dissemination of knowledge, as well as generating possible collaborations. |
Year(s) Of Engagement Activity | 2023 |
Description | Presentation for Cambridge Opthalmological Symposium |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Presentation at the Cambridge Opthalmological Syposium sparked discussion and ideas for further collaboration and research. |
Year(s) Of Engagement Activity | 2022 |
Description | Robert Packard Center for ALS 22nd Research Symposium |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Presentation at the Robert Packard Center for ALS 22nd Research Symposium in Baltimore. This shared research findings and generated a great deal of further discussion and new ideas for future collaborations. |
Year(s) Of Engagement Activity | 2022 |
Description | Robert Packard Center for ALS 23rd Research Symposium |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | A talk at this conference, to share research aims and findings with an international audience. Discussion followed, regarding new ideas for research and sharing of knowledge. Engagement also made future funding more likely. |
Year(s) Of Engagement Activity | 2023 |
Description | Seminar at Cardiff University Dementia Research Institute |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Postgraduate students |
Results and Impact | I gave a seminar at Cardiff University Dementia Research Institute at the invitation of Owen Peters. |
Year(s) Of Engagement Activity | 2020 |
Description | Seminar at Harvard University |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Postgraduate students |
Results and Impact | I presented a seminar at Harvard University at the invitation of Roz Segal. |
Year(s) Of Engagement Activity | 2019 |
Description | Seminar for Cambridge Neuroscience Virtual Interdisciplinary Seminar Series |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Postgraduate students |
Results and Impact | Seminar presentation as part of the Cambridge Neuroscience Virtual Interdisciplinary Seminar Series. Information and findings were shared, which prompted questions and discussion afterwards. |
Year(s) Of Engagement Activity | 2023 |
Description | Seminar for Cardiff University |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Other audiences |
Results and Impact | Approximately 70 people attended this seminar on 'Programmed axon death: from animal models into human disease'. The talk generated questions and discussion. Research findings were disseminated, and new ideas for potential areas of research generated. |
Year(s) Of Engagement Activity | 2023 |
Description | Suna Kirac Conference, Istanbul |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | I attended and presented at this conference at the invitation of Bob Brown and Nazli Basak. There was an audience of between 100 and 150 people. |
Year(s) Of Engagement Activity | 2019 |
Description | Talk at Axon Biology webinar run by ALS Finding A Cure (ALSFAC) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | This webinar was focused on Translational Opportunities for Targeting Axonal Degeneration in ALS. There has been substantial progress in delineating new concepts in the molecular biology of axon development, degeneration and regeneration. In parallel there have been exciting advances in understanding the molecular pathophysiology of ALS. The intention for this meeting was to discern how these two areas intersect and thereby define new ways to understand ALS pathophysiology. Thought leaders in the field of axonal biology and ALS, along with new investigators, held extensive discussions to identify new research priorities and projects. |
Year(s) Of Engagement Activity | 2020 |
Description | Virtual seminar (Indiana University) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | I gave a seminar at the invitation of Hui-Chen Lu, Director and Gill Chair for Linda and Jack Gill Center of Neuroscience, and met with various staff members for discussions, as well as joining their lab meeting. Outcomes were shared learning and ideas. |
Year(s) Of Engagement Activity | 2020 |
Description | Virtual seminar (Presidency University, Kolkata) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | I gave a virtual seminar on 'Programmed axon death and its roles in human disease' and held various discussions as a result. |
Year(s) Of Engagement Activity | 2020 |
Description | Virtual seminar (University of Melbourne) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | I gave a virtual seminar on 'Programmed axon death and its roles in human disease' at the invitation of Professor Keith Martin and engaged in several discussions afterwards, leading to sharing of information, ideas and plans for future research. |
Year(s) Of Engagement Activity | 2020 |
Description | Virtual seminar at Peking University, Beijing |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Policymakers/politicians |
Results and Impact | I gave a virtual seminar and engaged in discussions afterwards with others working in fields related to my own, leading to sharing of information and ideas. |
Year(s) Of Engagement Activity | 2020 |
Description | Virtual seminar for Montreal Neurological Institute (Killam Research Seminar) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | I gave a virtual Killam Research Seminar at Montreal Neurological Institute, at the invitation of Dr Alyson Fournier. Discussions were held around the seminar, leading to sharing of new plans for research. |
Year(s) Of Engagement Activity | 2020 |
Description | Webinar presentation |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Presentation at Peripheral Nerve Society Toxic Neuropathy Consortium webinar 'Programmed Axon Degeneration in Human Disease and on Models of CIPN' (presenter with Ahmet Hoke). Research findings were shared and potential for clinical applications were discussed. |
Year(s) Of Engagement Activity | 2021 |