Dissecting molecular mechanisms of Parkinson's disease
Lead Research Organisation:
University College London
Department Name: Institute of Neurology
Abstract
Parkinson's disease is devastating neurodegenerative disorder, that remains incurable due to our lack of understanding about its cause at a molecular level. Understanding the molecular origins of human diseases requires accurate characterisation of the underlying processes. However, PD is complex and multifactorial, and it is therefore challenging to choose which molecular events to study, and indeed which molecular events are causative. Notably, 90% of Parkinson's disease cases are sporadic, whilst 5-10% are familial due to an identified mutation. Autosomal dominant and autosomal recessive forms of PD share many common pathological and clinical features with the sporadic PD, albeit with some variation. Importantly in this group of familial PD, the causative gene and protein is known and therefore provides a robust starting point for understanding potential molecular causative events in PD. Taken further, the large genome wide association studies in PD have highlighted that genetic risk to sporadic PD is caused by aberration in pathways that broadly map to those raised by the mendelian forms of PD: namely the abnormal aggregation of proteins, abnormal function of mitochondria, abnormal clearance mechanisms by lysosomes, and inflammation. Thus, the outcomes from both mendelian genetics and common variation converge, and therefore may be used to rationalise the basis for determining causation in both familial and sporadic PD.
I propose a framework within which selected human familial forms of PD (mitochondrial-PD, lysosomal-PD, and proteinopathy-PD) are used to in first to understand key molecular causative events at the onset of disease. Informed by the human genetics, this will focus first, in theme 1, on specific pathways to disease, in particular, how and why protein aggregation occurs inside cells, and then how the aggregation affects cellular function, and organellar function with mitochondria and lysosomes. In order to achieve this aim, we will apply sophisticated methods derived from physical chemistry and biophysics that allow us to visualize each protein aggregate as it is formed, and therefore understand the size and structure of the aggregates at unprecedented resolution. The application of novel biophysical methodology to track the intracellular aggregation process of alpha-synuclein in iPSC derived models of PD should reveal the structure of the toxic species of alpha-synuclein, and determine how it interacts with, and disrupts specific cellular processes such as mitochondrial function. In theme 2, we ask whether different cell types in the human brain play an important role in Parkinson's disease pathogenesis. Glial cells play crucial roles in neuronal function, and alterations in glial cells are known to occur in PD and induce inflammation in the brain. Utilising iPSC derived neurons and astrocytes, we will investigate how glial cells may be activated during PD, and how alterations in astrocyte function affect neurons. In theme 3, we will utilize the information from the mendelian forms of PD to generate a framework of data. This framework will then be used to interrogate the mechanisms that underlie a large group of cells derived from patients with sporadic PD. Specifically it will reveal whether the sporadic PD population is heterogeneous in its molecular aetiology, whether the genetic and molecular drivers of any individual with PD clusters closely to the mendelian forms. As a consequence, it will ultimately determine whether patients with sporadic disease can be subdivided according to their molecular causes. If the sporadic PD population in composed of forms of PD that are 'mitochondrial' or 'lysosomal' for example, then this would raise the possibility that therapies in fact need to be designed to address the molecular basis of an individual's form of PD, in this way laying the foundation for developing personalised medicine approaches in PD.
I propose a framework within which selected human familial forms of PD (mitochondrial-PD, lysosomal-PD, and proteinopathy-PD) are used to in first to understand key molecular causative events at the onset of disease. Informed by the human genetics, this will focus first, in theme 1, on specific pathways to disease, in particular, how and why protein aggregation occurs inside cells, and then how the aggregation affects cellular function, and organellar function with mitochondria and lysosomes. In order to achieve this aim, we will apply sophisticated methods derived from physical chemistry and biophysics that allow us to visualize each protein aggregate as it is formed, and therefore understand the size and structure of the aggregates at unprecedented resolution. The application of novel biophysical methodology to track the intracellular aggregation process of alpha-synuclein in iPSC derived models of PD should reveal the structure of the toxic species of alpha-synuclein, and determine how it interacts with, and disrupts specific cellular processes such as mitochondrial function. In theme 2, we ask whether different cell types in the human brain play an important role in Parkinson's disease pathogenesis. Glial cells play crucial roles in neuronal function, and alterations in glial cells are known to occur in PD and induce inflammation in the brain. Utilising iPSC derived neurons and astrocytes, we will investigate how glial cells may be activated during PD, and how alterations in astrocyte function affect neurons. In theme 3, we will utilize the information from the mendelian forms of PD to generate a framework of data. This framework will then be used to interrogate the mechanisms that underlie a large group of cells derived from patients with sporadic PD. Specifically it will reveal whether the sporadic PD population is heterogeneous in its molecular aetiology, whether the genetic and molecular drivers of any individual with PD clusters closely to the mendelian forms. As a consequence, it will ultimately determine whether patients with sporadic disease can be subdivided according to their molecular causes. If the sporadic PD population in composed of forms of PD that are 'mitochondrial' or 'lysosomal' for example, then this would raise the possibility that therapies in fact need to be designed to address the molecular basis of an individual's form of PD, in this way laying the foundation for developing personalised medicine approaches in PD.
Technical Summary
Parkinson's disease (PD) is a common neurodegenerative disease that remains defined by pathological hallmarks of end-stage disease, neuronal loss and protein aggregation. The aim of this research program is to understand the earliest molecular events that drive pathogenesis. Powerful clues to pathogenesis are provided by mendelian genes that cause familial PD, and genetic loci that confer risk to sporadic PD. Importantly, both approaches highlight selective convergent processes to be causal in PD, namely protein aggregation, mitochondrial homeostasis, lysosomal biology and inflammation. This provides the rationale for the overall approach of this program: monogenic forms of PD can be harnessed to delineate causative mechanisms in human neurons and astrocytes, and these mechanisms will be relevant in the sporadic PD population.
This proposal first addresses when and where protein oligomerization occurs in human neurons, and how oligomerisation is modulated by mitochondrial function, or lysosomal function. Second, we address what is the earliest mitochondrial defect in PD, and the underlying mitochondrial mechanisms that lead to neuronal loss. Single molecule and single cell methods in human iPSC derived monogenic models are used to characterize protein aggregation and mitochondrial function at high resolution, determine their intersection, and causality in monogenic PD. Third, we investigate whether PD specific astrogliopathy is due to reactive astrocytosis and inflammation, or intrinsic molecular changes in astrocytes causing loss of neuronal homeostasis. Co-culture paradigms of astrocytes and neurons are combined with imaging and transcriptomics to dissect the role of astrocytic biology and inflammation in PD. Fourth, the proposal defines a pipeline to harness information from monogenic PD to validate its relevance in sporadic PD, with the ultimate aim of critically refining our classification of the molecular origins of sporadic disease.
This proposal first addresses when and where protein oligomerization occurs in human neurons, and how oligomerisation is modulated by mitochondrial function, or lysosomal function. Second, we address what is the earliest mitochondrial defect in PD, and the underlying mitochondrial mechanisms that lead to neuronal loss. Single molecule and single cell methods in human iPSC derived monogenic models are used to characterize protein aggregation and mitochondrial function at high resolution, determine their intersection, and causality in monogenic PD. Third, we investigate whether PD specific astrogliopathy is due to reactive astrocytosis and inflammation, or intrinsic molecular changes in astrocytes causing loss of neuronal homeostasis. Co-culture paradigms of astrocytes and neurons are combined with imaging and transcriptomics to dissect the role of astrocytic biology and inflammation in PD. Fourth, the proposal defines a pipeline to harness information from monogenic PD to validate its relevance in sporadic PD, with the ultimate aim of critically refining our classification of the molecular origins of sporadic disease.
Planned Impact
Parkinson's disease (PD) is the most common movement disorder caused by neurodegeneration, affecting 1-2% of people over the age of 65, with an estimated number of over 1.2 million people affected in Europe. This condition represents a very significant burden on our healthcare systems, as it is estimated that care for these patients costs 14 billion Euro per year in Europe. Treatment is currently purely symptomatic and there is an urgent need to develop disease-modifying therapies, as well as biomarkers capable of tracking its risk of onset and stage of progression. Perhaps the biggest challenge to addressing this need is the lack of understanding about the causes of PD. This program of work meets this need in the following ways: it utilizes familial forms of PD in which the initiating cause, or mutation is known, to identify key molecular events that can cause PD in human cells; it establishes the most important cell type that drives PD in the human brain; finally, it integrates this information to generate a network of molecular events that likely overlap or interact to cause PD in the sporadic (non-genetic) forms of disease. At this stage, it aims to classify sporadic PD cases on their molecular and cellular behavior in relation to the familial forms, allowing researchers to define different individuals with PD as having a different molecular subtype that drives their particular disease. If such stratification is possible then this opens the door to the possibility of designing specific treatments for specific individuals with PD.
This program of work therefore has a broad impact, and may bring about health, economic and societal benefits, that are outlined below.
(1) Discovery of new pathways in familial and sporadic PD will translate into new biomarkers and new druggable targets. This will have an important influence on biomarker development, drug discovery, drug development and ultimately to bringing drugs to market. Importantly as the discovery work, and the validation is performed in human models, this may overcome the current barriers to translational success. The impact goal is to drive rapid translation of molecular discoveries into realistic drug targets. Engagement with key pharmaceutical and biotech companies interested in drug development and commercialisation of diagnostic tests and biomarkers will be necessary to deliver this impact goal.
(2) Discovery of the molecular etiology of PD, and of new potential drug therapies will significantly impact the lives of patients with Parkinson's disease, patients with other alpha-synucleinopathies whose molecular pathogenesis is likely shared with Parkinson's disease (eg dementia with Lewy Body Disease, Multiple system atrophy), patients with other neurodegenerative diseases and their carers. The impact goal is to inform patients and their carers, to engage them in the research process, to recruit to trials, and to improve patient management and treatments. The target population for this impact is patients with PD and DLBD, patients with other neurodegenerative disorders, and patient charities, specifically Parkinson's UK and Cure Parkinson's Trust in the UK, and the Michael J Fox Foundation and the Safra Foundation globally.
(3) Scientific discovery will impact certain members of the public, and in particular, I am keen to see the impact of work reach, and inspire people of diverse backgrounds to recognize science as an equitable, accessible and exciting career, in particular school students and young people underrepresented in careers in STEM, and biomedical researchers who are underrepresented in senior roles. The impact goal is to enable, facilitate and inspire careers in biomedicine in underrepresented groups, through the promotion of equality and diversity in science.
This program of work therefore has a broad impact, and may bring about health, economic and societal benefits, that are outlined below.
(1) Discovery of new pathways in familial and sporadic PD will translate into new biomarkers and new druggable targets. This will have an important influence on biomarker development, drug discovery, drug development and ultimately to bringing drugs to market. Importantly as the discovery work, and the validation is performed in human models, this may overcome the current barriers to translational success. The impact goal is to drive rapid translation of molecular discoveries into realistic drug targets. Engagement with key pharmaceutical and biotech companies interested in drug development and commercialisation of diagnostic tests and biomarkers will be necessary to deliver this impact goal.
(2) Discovery of the molecular etiology of PD, and of new potential drug therapies will significantly impact the lives of patients with Parkinson's disease, patients with other alpha-synucleinopathies whose molecular pathogenesis is likely shared with Parkinson's disease (eg dementia with Lewy Body Disease, Multiple system atrophy), patients with other neurodegenerative diseases and their carers. The impact goal is to inform patients and their carers, to engage them in the research process, to recruit to trials, and to improve patient management and treatments. The target population for this impact is patients with PD and DLBD, patients with other neurodegenerative disorders, and patient charities, specifically Parkinson's UK and Cure Parkinson's Trust in the UK, and the Michael J Fox Foundation and the Safra Foundation globally.
(3) Scientific discovery will impact certain members of the public, and in particular, I am keen to see the impact of work reach, and inspire people of diverse backgrounds to recognize science as an equitable, accessible and exciting career, in particular school students and young people underrepresented in careers in STEM, and biomedical researchers who are underrepresented in senior roles. The impact goal is to enable, facilitate and inspire careers in biomedicine in underrepresented groups, through the promotion of equality and diversity in science.
Publications
Angelova PR
(2020)
Alpha synuclein aggregation drives ferroptosis: an interplay of iron, calcium and lipid peroxidation.
in Cell death and differentiation
Athauda D
(2022)
The Impact of Type 2 Diabetes in Parkinson's Disease.
in Movement disorders : official journal of the Movement Disorder Society
Athauda D
(2021)
The impact of Type 2 diabetes in Parkinson's disease
Choi M
(2020)
Tracking Oligomerization of Alpha-Synuclein Demonstrates Pivotal Role of Mitochondria in Seeding
in Biophysical Journal
Choi ML
(2022)
Pathological structural conversion of a-synuclein at the mitochondria induces neuronal toxicity.
in Nature neuroscience
D'Sa K
(2023)
Prediction of mechanistic subtypes of Parkinson's using patient-derived stem cell models.
in Nature machine intelligence
Description | Appointed Assistant Research Director |
Geographic Reach | Local/Municipal/Regional |
Policy Influence Type | Contribution to new or improved professional practice |
Impact | We have defined better practices for managing human stem cells, for experimentation, and for handling of human data |
Description | Defining mechanisms in neurons and oligodendrocytes that drive progression in Parkinson's |
Amount | £589,000 (GBP) |
Organisation | Michael J Fox Foundation |
Sector | Charity/Non Profit |
Country | United States |
Start | 02/2023 |
End | 02/2025 |
Description | Dissecting molecular mechanisms in Parkinson's disease |
Amount | £1,900,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 01/2020 |
End | 01/2025 |
Description | EJS ACT-PD |
Amount | £1,375,000 (GBP) |
Organisation | Edmond J. Safra Philanthropic Foundation |
Sector | Charity/Non Profit |
Country | Switzerland |
Start | 01/2021 |
End | 01/2024 |
Description | Harnessing human iPSC technology to understand and stratify idiopathic Parkinson's disease |
Amount | £298,000 (GBP) |
Organisation | Merck |
Sector | Private |
Country | Germany |
Start | 12/2020 |
End | 12/2023 |
Description | Lysosome Enhancement in synucleinopathies |
Amount | £384,000 (GBP) |
Organisation | Eisai Ltd |
Sector | Private |
Country | Japan |
Start | 03/2020 |
End | 04/2022 |
Description | Mapping the PD brain: oligomer driven functional genomics |
Amount | $7,700,000 (USD) |
Organisation | Aligning Sciences Across Parkinson's |
Sector | Charity/Non Profit |
Country | United States |
Start | 01/2021 |
End | 01/2025 |
Description | Multiscale modelling of progression in Parkinson's disease |
Amount | £1,200,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 12/2022 |
End | 12/2025 |
Description | Understanding the cellular basis of Parkinson's disease dementia |
Amount | £281,071 (GBP) |
Organisation | Parkinson's UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 02/2023 |
End | 02/2025 |
Title | A new protocol to derive dopaminergic neurons from iPSCs |
Description | We have worked on developing a method to generate enriched cultures of midbrain neurons that are functionally active, from iPSCs in control and patients with PD causing mutations. This method forms the basis of the platform for all other mechanistic data and therapeutic studies. We will publish this method in due course, but have presented it to internal conferences. |
Type Of Material | Model of mechanisms or symptoms - human |
Year Produced | 2020 |
Provided To Others? | No |
Impact | This method is fast, reliable and much less expensive than current methods used in the literature. Therefore we expect it to have significant impact if adopted. |
Title | CAP-1: amyloid precipitation from bio fluids |
Description | We developed a molecule in collaboration with synthetic and physical chemists, that can purify small protein assemblies from human biofluuids, and perform mass spec to understand their identity. We published our findings in Nature Chemistry 2022. |
Type Of Material | Technology assay or reagent |
Year Produced | 2022 |
Provided To Others? | Yes |
Impact | This tool may represent a new way of identifying aggregates in human CSF, and ultimately help understand the natural history of the disease. |
Title | Machine Learning and Cellular phenotyping |
Description | I initiated a new collaboration with an AI organisation (Faculty.AI) and my laboratory underwent a training course in python coding, followed by an 8 week fellowship program in training in ML algorithms. We have developed an image analysis pipeline and a disease classifier that can predict disease state in human iPSC derived neurons. |
Type Of Material | Improvements to research infrastructure |
Year Produced | 2021 |
Provided To Others? | No |
Impact | This method is in development, but we expect to publish our first classifier this year. This classifier provides information on disease mechanisms. |
Title | Analysis of single cell and deep bulk data from astrocytes |
Description | We generated single cell sequencing and bulk RNA sequencing data from stem cell derived astrocytes and analysed it to understand how astrocytes respond to proteinpathy |
Type Of Material | Data analysis technique |
Year Produced | 2023 |
Provided To Others? | No |
Impact | This led to the identification of a new pathway in Parkinson's - RNA editing |
Title | Establishing deep proteomics of cell models |
Description | We are generating proteomic analyses in iPSC models and postmortem brain, and using these analyses and public datasets to search for the isoforms of SNCA that we identified from the long read data |
Type Of Material | Data analysis technique |
Year Produced | 2024 |
Provided To Others? | No |
Impact | We anticipate this methodology being important in the coming year |
Title | Long read sequencing of SNCA in iPSC derived models |
Description | We utilised the iPSC derived models of Parkinson's to generate long read sequencing for the SNCA gene. We also utilised the ASO treatments to modulate transcript use in these systems. We will make this data available once validated. |
Type Of Material | Data analysis technique |
Year Produced | 2022 |
Provided To Others? | No |
Impact | We identified novel transcripts of SNCA in the brain and model systems. ASO treatment alters transcript use. These analyses may reveal important and relevant transcripts in disease. |
Title | Machine learning classifiers of disease |
Description | We generated a series of classifiers that can predict the chemical subtype of genotype of Parkinson's using images from stem cell derived neurone stained for different intracellular organelles. |
Type Of Material | Computer model/algorithm |
Year Produced | 2023 |
Provided To Others? | Yes |
Impact | -This work is in the top 5% of all research outputs scored by Altmetric. This work was written about by 150 news outlets, including the Daily Mail, The Evening Standard, The Independent (https://www.independent.co.uk/tech/scientists-francis-crick-institute-sonia-gandhi-london-symptoms-b2390970.html), and The National. |
Title | Single nuclear RNA seq and ATAC seq data in postmortem human brain |
Description | As part of the ASAP funding, we generated multiome data on 110 postmortem brain samples in early Parkinson's and controls. We are using this dataset to establish the critical cell types and states involved in disease, and will use this information to aid the spatial transcriptomics approach in brain tissue |
Type Of Material | Data analysis technique |
Year Produced | 2023 |
Provided To Others? | No |
Impact | This dataset is due to be released in 2024 |
Description | ASAP partnership - aligning science against Parkinson's disease |
Organisation | Francis Crick Institute |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | This new partnership pursues a research program called 'MapPD'. My laboratory will ensure the acquisition and analysis of postmortem brain tissue and human iPSC lines to understand the factors that promote oligomerisation of alpha-synuclein in the brain. |
Collaborator Contribution | University of Cambridge - the Department of Chemistry have developed the single molecule and super resolution imaging methods to detect oligomers in tissue and cells UCL - provide the bioinformatics and statistical genomics expertise to interrogate the datasets |
Impact | Mulitdiscplinary - the PIs are physical chemists, theoretical physicists, cell biologists, bioinformaticians and geneticists |
Start Year | 2020 |
Description | ASAP partnership - aligning science against Parkinson's disease |
Organisation | University College London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | This new partnership pursues a research program called 'MapPD'. My laboratory will ensure the acquisition and analysis of postmortem brain tissue and human iPSC lines to understand the factors that promote oligomerisation of alpha-synuclein in the brain. |
Collaborator Contribution | University of Cambridge - the Department of Chemistry have developed the single molecule and super resolution imaging methods to detect oligomers in tissue and cells UCL - provide the bioinformatics and statistical genomics expertise to interrogate the datasets |
Impact | Mulitdiscplinary - the PIs are physical chemists, theoretical physicists, cell biologists, bioinformaticians and geneticists |
Start Year | 2020 |
Description | ASAP partnership - aligning science against Parkinson's disease |
Organisation | University of Cambridge |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | This new partnership pursues a research program called 'MapPD'. My laboratory will ensure the acquisition and analysis of postmortem brain tissue and human iPSC lines to understand the factors that promote oligomerisation of alpha-synuclein in the brain. |
Collaborator Contribution | University of Cambridge - the Department of Chemistry have developed the single molecule and super resolution imaging methods to detect oligomers in tissue and cells UCL - provide the bioinformatics and statistical genomics expertise to interrogate the datasets |
Impact | Mulitdiscplinary - the PIs are physical chemists, theoretical physicists, cell biologists, bioinformaticians and geneticists |
Start Year | 2020 |
Description | Collaboration with MRC PPU (Alessi group) in Dundee |
Organisation | University of Dundee |
Department | MRC Protein Phosphorylation and Ubiquitylation Unit |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We established a collaboration with the Alessi group that has enabled proteomic datasets to be generated on our cell models and brain tissue samples |
Collaborator Contribution | Our partners have performed the proteomics analyses and we have provided the sample sets |
Impact | Manuscripts: Protein aggregation and calcium dysregulation are hallmarks of familial Parkinson's disease in midbrain dopaminergic neurons. Virdi GS, Choi ML, Evans JR, Yao Z, Athauda D, Strohbuecker S, Nirujogi RS, Wernick AI, Pelegrina-Hidalgo N, Leighton C, Saleeb RS, Kopach O, Alrashidi H, Melandri D, Perez-Lloret J, Angelova PR, Sylantyev S, Eaton S, Heales S, Rusakov DA, Alessi DR, Kunath T, Horrocks MH, Abramov AY, Patani R, Gandhi S. NPJ Parkinsons Dis. 2022 Nov 24;8(1):162. doi: 10.1038/s41531-022-00423-7. PMID: 36424392 |
Start Year | 2022 |
Description | Industry Collaboration - Eisai |
Organisation | Eisai Ltd |
Department | Eisai Europe Ltd |
Country | United Kingdom |
Sector | Private |
PI Contribution | This is a collaborative project across three laboratories and Eisai to study lysosomal targets in synucleinopathies for drug discovery |
Collaborator Contribution | My involvement is to provide the iPSC derived neuronal models of Parkinson's, that have been deeply characterised. |
Impact | Collaboration includes protein biochemistry (Bartels lab) and lysosomal biology (Stefan lab) and industry. |
Start Year | 2020 |
Description | Industry Collaboration - Eisai |
Organisation | University College London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | This is a collaborative project across three laboratories and Eisai to study lysosomal targets in synucleinopathies for drug discovery |
Collaborator Contribution | My involvement is to provide the iPSC derived neuronal models of Parkinson's, that have been deeply characterised. |
Impact | Collaboration includes protein biochemistry (Bartels lab) and lysosomal biology (Stefan lab) and industry. |
Start Year | 2020 |
Description | Industry Collaboration - MSD |
Organisation | MSD Europe |
Country | Belgium |
Sector | Private |
PI Contribution | I received a grant from Crick-MSD scheme to utilise single cell and bulk RNA sequencing approaches in iPSC derived models of Parkinson's disease. |
Collaborator Contribution | Funding for the generation of models and sequencing data. |
Impact | This is a collaboration between industrial partner and academic lab. |
Start Year | 2021 |
Description | Crick Insight Event: Was Science Ever Apolitical? |
Form Of Engagement Activity | A formal working group, expert panel or dialogue |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Postgraduate students |
Results and Impact | Was Science Ever Apolitical? A Q & A panel discussion with Crick researchers and Science Journalist, Angela Saini to discuss her books, particularly Superior, and links to current events with Black Lives Matter(BLM) and COVID. Hosted by: The Francis Crick Institute with EDI committee and Athena Swan. Date: 12th October 12 - 1:45pm Panel: Pontus Skoglund, Group leader of the Ancient Genomics Laboratory, Sonia Gandhi, Group leader of the Neurodegeneration Biology Lab, MRC Senior Clinical Fellow, Consultant Neurologist |
Year(s) Of Engagement Activity | 2020 |
Description | International Symposium for Movement Disorders |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Supporters |
Results and Impact | I organised a UCL QS Movement Disorders Centre symposium with international and national speakers. This was attended by 200 people face to face, and the audience included all stakeholders - charity, research funders, industry, researchers, and students. |
Year(s) Of Engagement Activity | 2022 |
Description | Organised national conference for Parkinson's UK |
Form Of Engagement Activity | A formal working group, expert panel or dialogue |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Postgraduate students |
Results and Impact | I was on the organising committee for Parkinson's UK annual conference, held virtually I chaired two sessions |
Year(s) Of Engagement Activity | 2020 |
Description | Organising ACT-PD launch event |
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 | I organised the launch event for a new trial initiative - this brought together several key team members, and established the program with setting up seven working groups. |
Year(s) Of Engagement Activity | 2021 |
Description | PPI activity for the UCL Movement Disorders Centre |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Patients, carers and/or patient groups |
Results and Impact | Monday (9/11/2020) for people with Parkinson's. Attendance of 230 people joining in! The webinar included a talk about clinical research, the impact of Covid-19 and a Q&A session |
Year(s) Of Engagement Activity | 2020 |
Description | Participation in patient webinar |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Patients, carers and/or patient groups |
Results and Impact | I participated in a webinar for patients: Why is there no cure for Parkinson's?', organised as part of PAR-CON, Parkinson's UK. This reached an audience of 1K people. |
Year(s) Of Engagement Activity | 2021 |