The NET-PDD study: defining the roles of NEuroinflammation and Tau aggregation in Parkinson's Disease Dementia

Lead Research Organisation: University of Cambridge
Department Name: Clinical Neurosciences

Abstract

Parkinson's disease (PD) causes problems with walking and movement, but around half of patients will also develop dementia within the first 10 years of their disease course. The primary goal of this study is to better understand the earliest changes in the brain that lead to memory problems and dementia in PD. These early changes would be the best targets for new treatments to prevent or slow dementia, and may be relevant not just to PD dementia but to other forms of dementia (including Alzheimer's disease), because a number of these conditions share similar features when brains are examined after death. In most conditions involving dementia, it is difficult to study the earliest brain changes before symptoms emerge, but this is possible in PD because the dementia comes later than the movement problems. In addition, my previous work has identified a method of determining whether an individual with early PD is at high risk or low risk of going on to develop a dementia within the next few years (based on performance on thinking tests and genetic variation). This means that we can look specifically at what brain changes are occurring in high dementia risk patients before the dementia actually becomes apparent.

My previous research has contributed to the theory that 2 processes - build-up of a protein called tau, and inflammation within the brain - might be particularly important in the development of PD dementia. The main aim of this study is to investigate this theory by comparing markers of these processes in 2 groups of patients: a group at high dementia risk, and a group at low dementia risk (20 per group). Healthy volunteers of similar age will also be included for comparison. Inflammation and tau deposits will be measured using a special type of brain scanning (PET imaging), as well as in the fluid that bathes the brain and spinal cord (cerebrospinal fluid), and in the blood. Participants will undergo PET scanning at the beginning of the study, as well as a lumbar puncture to collect a cerebrospinal fluid sample, a blood test, and clinical and memory assessments. They will be seen again at 18 months to assess changes in their clinical condition and memory, and have a blood test. Scans, lumbar punctures and blood tests will then be repeated at 3 years to look at how measures of inflammation and build-up of tau protein have changed, and how they relate to the development of memory problems and dementia. As well as measuring markers of inflammation and tau on the scans and in the fluid samples, immune cells will be extracted from blood and used in experiments in the laboratory to look at how they respond to tau and other key proteins. Finally, the most promising of the inflammation and tau-related markers identified in cerebrospinal fluid and blood will be measured in a separate large group of approximately 200 patients and 100 healthy individuals to confirm their value in tracking progression to dementia.

The research will specifically address these key questions:
1. Are inflammation and tau deposition important early events in the brain as Parkinson's dementia is developing?
2. Can we measure small clumps ('oligomers') of tau and other related proteins (such as alpha synuclein) in the spinal fluid and blood of Parkinson's patients at high risk of dementia, and is this a useful tool to help predict and track development of dementia?
3. Do these abnormal clumps of tau protein drive an inflammatory response in patients' immune cells?

Answering these questions will bring us much closer to developing new treatments to prevent or slow the onset of the dementia which has such devastating consequences for patients with PD. It will also allow us to work out which combination of the tools we are studying (brain imaging, blood and spinal fluid tests) is most useful for tracking progression to dementia and the effect of treatments on this over time, which will be critical for future clinical trials of these treatments.

Technical Summary

BACKGROUND
Dementia affects half of Parkinson's disease patients within 10 years of diagnosis with a major impact on quality of life. Whilst cortical a-synuclein pathology has been linked to PD dementia (PDD), other factors are implicated. I hypothesize that PDD is driven by oligomeric forms of tau as well as a-synuclein, which provoke a neuroinflammatory response through activation of microglial Toll-like receptors (TLRs), in turn catalyzing the disease process.
AIMS
1. to establish that neuroinflammation and tau aggregation are critical early events in PDD;
2. to demonstrate that oligomers of tau and a-synuclein are quantifiable in CSF and blood and are reliable biomarkers of PDD risk;
3. to show that these oligomers play a critical role in driving an inflammatory response in PD through activation of TLRs.
METHODS
I will compare 2 groups with newly-diagnosed PD, at 'high risk' (n=20) or 'low risk' (n=20) of dementia, and age-matched controls (n=40). Participants will undergo PET scans, lumbar puncture and blood sampling at baseline and 3 years, with interim clinical assessment. Specifically:
1. [11C]PK11195 and [18F]AV1451 PET will be used to measure microglial activation and tau deposition in the brain respectively;
2. CSF and serum samples will be analyzed for inflammatory cytokines, a-synuclein and tau using multiplex immunoassays;
3. novel methods will be used to quantify oligomers in CSF and blood including single molecule fluorescence spectroscopy and proximity ligation assays;
4. the inflammatory response of participant monocytes to tau and a-synuclein oligomers will be measured in vitro, with and without TLR inhibition.
Candidate CSF and blood biomarkers will be validated in an independent cohort (200 PD, 100 controls).
IMPORTANCE
This will provide definitive evidence to support clinical trials of immunotherapeutic and anti tau-aggregation therapies to delay the onset of dementia in PD, and establish optimal biomarkers for these trials.

Planned Impact

The following groups will gain benefit from this research.

1. Patients and carers
Parkinson's disease (PD) affects around 2% of those over 65, with the number of UK cases predicted to rise to 162,000 by 2020 (Parkinson's UK). My own work has shown that 50% of these individuals will develop dementia within 10 years of diagnosis, for which no effective treatment is available. Dementia has a devastating effect on quality of life of patients, their families and their carers. The impact on these individuals who are at risk of PD dementia, and on those who will care for them, will be twofold:
i. It will provide an opportunity to acquire understanding of this research and take an active role in providing feedback to shape both this study and our future work. This is an immediate benefit facilitated through the involvement of patients and carers in discussion forums at our 6-monthly open days at the John Van Geest Centre for Brain Repair. In addition, our PD-Patient and Public Involvement (PD-PPI) panel will take an active advisory role on both the conduct of the study and the dissemination of research findings to the public, as outlined in more detail in the 'Pathways to Impact' statement.
ii. In the longer term (within 5 years of project completion), this work has the potential to facilitate clinical trials of therapies targeting neuroinflammation and/or tau aggregation to prevent or slow the development of dementia in PD. If the findings are positive, the study will both confirm the relevance of inflammation and tau as therapeutic targets, and establish the utility of imaging/CSF/blood-based markers of these 2 processes as biomarkers for tracking response to therapy. This will benefit the PD community, but may also benefit those with other dementias such as Alzheimer's disease in which neuroinflammation and tau may play a common pathogenic role.

2. Drug discovery organizations
This work will benefit such organizations (both non-commercial and commercial) within the timespan of the project by providing definitive evidence for (or against) a critical contribution of tau aggregation and/or neuroinflammation in the early stages of PD dementia which will guide development of new therapies. Specific examples include the ARUK Drug Discovery Institute which seeks to develop anti-tau therapies for dementia, and Medimmune, a Cambridge-based subsidiary of Astra Zeneca which seeks to develop immunotherapies for neurological disease.

3. Pharmaceutical industry
The work will benefit commercial organisations (within 5 years of project completion) by informing clinical trial design and optimizing the likelihood of positive trial outcomes through:
i. establishing a strategy for identifying individuals with early evidence of neuroinflammation and tau aggregation so that enriched cohorts can be selected for trials;
ii. identifying the optimal imaging/CSF/blood markers of inflammation and tau aggregation for tracking disease progression and response to therapy over time.

4. National Health Service and Social Care
Through its capacity to accelerate the development of new treatment options to prevent dementia, this research is in line with the key priorities of the government as outlined in the Prime Minister's Challenge on Dementia 2020 and supported by the NIHR's expanding dementia research programme and the establishment of a national Dementia Research Institute. PD dementia is an untreatable problem affecting around 39000 individuals in the UK and has major socioeconomic implications. It is a significant risk factor for hospital admissions and for nursing home placement. Indeed costs of care in PD are estimated to be over 3 times greater for those with dementia than those without. This research will help accelerate progress along therapeutic pathways to slow PD progression and delay the onset of dementia, thus ultimately resulting in significant savings for the NHS and social care within an estimated 10-20 years.

Publications

10 25 50
 
Description Characterising the soluble toxic protein aggregates in Parkinson's disease
Amount £277,423 (GBP)
Funding ID G-1901 
Organisation Parkinson's UK 
Sector Charity/Non Profit
Country United Kingdom
Start 09/2019 
End 10/2022
 
Description GASTROINTESTINAL DYSFUNCTION IN PARKINSON'S DISEASE: INTERACTIONS BETWEEN THE GUT, IMMUNE MARKERS AND DISEASE PROGRESSION
Amount £46,605 (GBP)
Funding ID 19/24 
Organisation The Evelyn Trust 
Sector Charity/Non Profit
Country United Kingdom
Start 09/2019 
End 09/2022
 
Description Immunophenotyping sub-study of Azathioprine immunosuppression and disease modification in Parkinson's disease (AZA-PD): a randomised double-blind placebo-controlled phase II trial.
Amount £202,507 (GBP)
Funding ID CW011 
Organisation Cure Parkinson's Trust 
Sector Charity/Non Profit
Country United Kingdom
Start 02/2020 
End 01/2023
 
Description Inflammation Biomarkers for Parkinson's disease
Amount $146,899 (USD)
Organisation Michael J Fox Foundation 
Sector Charity/Non Profit
Country United States
Start 03/2018 
End 04/2020
 
Description Investigating the immune basis of Parkinson's disease
Amount £103,911 (GBP)
Funding ID 2251337 
Organisation Medical Research Council (MRC) 
Sector Public
Country United Kingdom
Start 08/2019 
End 03/2023
 
Description Pump priming grant - Evaluation of Candesartan as an inhibitor of Toll-like receptor mediated inflammation in Parkinson's disease using patient-derived monocytes
Amount £45,205 (GBP)
Organisation National Institute for Health Research 
Sector Public
Country United Kingdom
Start 12/2020 
End 03/2021
 
Description Activation of transposable elements as a trigger of neuroinflammation in Parkinson's disease 
Organisation Cold Spring Harbor Laboratory (CSHL)
Country United States 
Sector Charity/Non Profit 
PI Contribution This collaboration is part of the ASAP Collaborative Research Network on neuro-immune interactions in Parkinson's disease. I am part of Team Jakobsson. My group will evaluate neuroinflammatory change in post-mortem brains from our Parkinson's disease cohorts and contribute relevant tissue samples for single cell analysis of transposable element (TE) expression and inflammation in the Jakobsson lab.
Collaborator Contribution TEs are viral-like mobile genetic elements that comprise nearly 50% of the human genome. This study aims to determine whether transposable elements are active in tissues from patients with Parkinson's disease and whether this activity can induce inflammation in the nervous system. Our collaborators will look for evidence of transposable element activity using single-cell RNA sequencing of tissues from people with Parkinson's disease. This particular experiment will allow us to determine whether patient cells that show more transposable element activity also show increased signs of inflammation. Neurons, astrocytes and microglia will also be studied in vitro to test whether manipulations that induce transposable element activity in these cells also cause an immune response that would result in inflammation. This would suggest that blocking transposon activity could block inflammation. Read Full Proposal
Impact This is a multidisciplinary collaboration involving Clinical Neurosciences, Neuropathology, Stem Cell Biology, Genomics, and Molecular Neurogenetics.
Start Year 2021
 
Description Activation of transposable elements as a trigger of neuroinflammation in Parkinson's disease 
Organisation Lund University
Country Sweden 
Sector Academic/University 
PI Contribution This collaboration is part of the ASAP Collaborative Research Network on neuro-immune interactions in Parkinson's disease. I am part of Team Jakobsson. My group will evaluate neuroinflammatory change in post-mortem brains from our Parkinson's disease cohorts and contribute relevant tissue samples for single cell analysis of transposable element (TE) expression and inflammation in the Jakobsson lab.
Collaborator Contribution TEs are viral-like mobile genetic elements that comprise nearly 50% of the human genome. This study aims to determine whether transposable elements are active in tissues from patients with Parkinson's disease and whether this activity can induce inflammation in the nervous system. Our collaborators will look for evidence of transposable element activity using single-cell RNA sequencing of tissues from people with Parkinson's disease. This particular experiment will allow us to determine whether patient cells that show more transposable element activity also show increased signs of inflammation. Neurons, astrocytes and microglia will also be studied in vitro to test whether manipulations that induce transposable element activity in these cells also cause an immune response that would result in inflammation. This would suggest that blocking transposon activity could block inflammation. Read Full Proposal
Impact This is a multidisciplinary collaboration involving Clinical Neurosciences, Neuropathology, Stem Cell Biology, Genomics, and Molecular Neurogenetics.
Start Year 2021
 
Description Activation of transposable elements as a trigger of neuroinflammation in Parkinson's disease 
Organisation University of Copenhagen
Country Denmark 
Sector Academic/University 
PI Contribution This collaboration is part of the ASAP Collaborative Research Network on neuro-immune interactions in Parkinson's disease. I am part of Team Jakobsson. My group will evaluate neuroinflammatory change in post-mortem brains from our Parkinson's disease cohorts and contribute relevant tissue samples for single cell analysis of transposable element (TE) expression and inflammation in the Jakobsson lab.
Collaborator Contribution TEs are viral-like mobile genetic elements that comprise nearly 50% of the human genome. This study aims to determine whether transposable elements are active in tissues from patients with Parkinson's disease and whether this activity can induce inflammation in the nervous system. Our collaborators will look for evidence of transposable element activity using single-cell RNA sequencing of tissues from people with Parkinson's disease. This particular experiment will allow us to determine whether patient cells that show more transposable element activity also show increased signs of inflammation. Neurons, astrocytes and microglia will also be studied in vitro to test whether manipulations that induce transposable element activity in these cells also cause an immune response that would result in inflammation. This would suggest that blocking transposon activity could block inflammation. Read Full Proposal
Impact This is a multidisciplinary collaboration involving Clinical Neurosciences, Neuropathology, Stem Cell Biology, Genomics, and Molecular Neurogenetics.
Start Year 2021
 
Description Characterising soluble protein aggregates in Parkinson's disease (with department of Chemistry) 
Organisation University of Cambridge
Department Department of Chemistry
Country United Kingdom 
Sector Academic/University 
PI Contribution We are sharing blood, cerebrospinal fluid and post-mortem brain tissue samples collected from research participants with Parkinson's disease and healthy controls with Prof David Klenerman's group in the department of Chemistry. We are working together to investigate the characteristics of small protein aggregates in these samples and assess how the number, size and function of aggregates is related to disease state. We are also investigating the interactions of these protein aggregates with immune cells derived from patients and the role of Toll-like receptors in mediating this interaction.
Collaborator Contribution Professor Klenerman's team are developing novel ultra-sensitive methods to image small soluble protein aggregates which come from 'soaked brain' samples. They are also developing similar methods to look at small protein aggregates in the biological samples collecting from our research participants during life, and they are assessing whether and how these aggregates induce inflammation and damage to nerve cells in vitro.
Impact New research grant - Characterizing the soluble toxic protein aggregates in Parkinson's disease, Parkinson's UK, Jan 2020-2023. Publication - Lobanova E, Whiten D, Ruggeri FS, Taylor C, Kouli A, Xia Z, Emin D, Zhang YP, Lam JYL, Williams-Gray CH, Klenerman D. Imaging protein aggregates in the serum and cerebrospinal fluid in Parkinson's disease. Brain. 2021 Aug 19:awab306. doi: 10.1093/brain/awab306. This is a multidisciplinary collaboration involving Clinical Neurosciences and Chemistry.
Start Year 2018
 
Description Discovery study 
Organisation University of Oxford
Department Nuffield Department of Clinical Neurosciences
Country United Kingdom 
Sector Academic/University 
PI Contribution This is a multicentre longitudinal cohort study of patients with Parkinson's disease, and individuals with REM Sleep Behaviour Disorder (which is associated with a high risk of conversion to Parkinson's disease). I am a co-investigator on the study. My team are responsible for collecting clinical research data longitudinally in REM Sleep Behaviour Disorder cases from the East Anglia region, as well as blood and cerebrospinal fluid samples. The key aim of the study is to identify the pathological pathways which are of most relevance in the earliest stages of Parkinson's disease. My team will focus on immune activation, which we will assess though immunophenotyping and measurement of inflammatory markers in blood and CSF.
Collaborator Contribution Professor Michele Hu, University of Oxford is the chief investigator and runs the lead site. University of Oxford is the sponsor.
Impact No outputs to report yet.
Start Year 2020
 
Description Immunosenescence in Parkinson's disease 
Organisation Newcastle University
Country United Kingdom 
Sector Academic/University 
PI Contribution We have collected clinical data and blood samples from cohorts with Parkinson's disease and age-matched healthy controls, and measured blood markers of immune activation and senescence. We have shared blood cell samples from these cohorts with our collaborators in Newcastle for measurement of senescence markers. We have also shared our clinical and immune marker data.
Collaborator Contribution Our collaborators have measured markers of cell senescence in the samples that we have shared. Collaboratively, we have analysed relationships between markers of immune activation, cellular senescence and clinical disease progression.
Impact Publication - Martin-Ruiz C, Williams-Gray CH, Yarnall AJ, et al. Senescence and Inflammatory Markers for Predicting Clinical Progression in Parkinson's Disease: The ICICLE-PD Study. J Parkinsons Dis. 2020;10(1):193-206. doi:10.3233/JPD-191724. Publication - Kouli, A., Jensen, M., Papastavrou, V. et al. T lymphocyte senescence is attenuated in Parkinson's disease. J Neuroinflammation. 2021; 18: 228. doi: 10.1186/s12974-021-02287-9. New research grant - Inflammation Biomarkers for Parkinson's disease, Michael J Fox Foundation, 2018-2020. This is a multidisciplinary collaboration involving Clinical Neurosciences in Cambridge and Ageing Research in Newcastle.
Start Year 2018
 
Description Dementia Research Institute/Parkinson's UK workshop 
Form Of Engagement Activity Participation in an activity, workshop or similar
Part Of Official Scheme? No
Geographic Reach National
Primary Audience Other audiences
Results and Impact Workshop hosted by the Dementia Research Institute and Parkinson's UK to discuss the latest research developments in Parkinson's disease in the UK and the direction of future research. The aim was to help the DRI to prioritise areas for future research support.
Year(s) Of Engagement Activity 2019
 
Description EU Marie Curie Syndegen Network workshop 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Postgraduate students
Results and Impact I delivered a virtual talk on my research into the role of the immune system in Parkinson's disease at a workshop for PhD students involved in an EU Neurogeneration Network. A number of interesting questions were raised on the interaction between immune changes and neurodegneration.
Year(s) Of Engagement Activity 2021
 
Description External speaker - Sheffield department of neurology postgraduate meeting 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Professional Practitioners
Results and Impact Delivered a talk to the Sheffield Clinical Neurosciences department entitled 'What Drives the Heteroegeneity of Parkinson's Disease?'
The talk included a summary of the work of my research group on the role of the immune system in mediating clinical variability of outcomes in Parkinson's , and the implications of this for developing new immune-based therapies for this condition.
The talk provoked an interesting discussion, and the visit led to the development of a new collaboration with colleagues in Sheffield around a project to investigate immune activation in a zebrafish model of Parkinson's disease.
Year(s) Of Engagement Activity 2018
 
Description GSK Immunology Network Seminar 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Industry/Business
Results and Impact I delivered a talk entitled "What drives heterogeneity in Parkinson's disease: is the immune system a critical player?" as part of the GSK Immunology Network Seminar Series, and participated in a roundtable discussion with GSK immunologists following the talk. The GSK Immunology Network is an initiative which fosters collaboration with external academics with relevant immunological expertise. This was a useful opportunity to make contacts with scientists working in related research areas in GSK, and may lead to future collaborations.
Year(s) Of Engagement Activity 2021
 
Description International Congress of Parkinson's Disease and Movement Disorders 2019 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Professional Practitioners
Results and Impact Caroline Williams-Gray delivered a presentation at the International Congress of Parkinson's Disease and Movement Disorders in Nice, France in September 2019. She presented her work on cognitive dysfunction in Parkinson's disease to research peers and students, as well as clinicians and other health care professionals. This led to an increase in international recognition for her research group and facilitated networking with other investigators which may lead to new future collaborations.
Year(s) Of Engagement Activity 2019
 
Description Krembil Knowledge Gaps in Parkinson's Disease Symposium 
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 Caroline Williams-Gray participated in a symposium with an international panel of academic and industry experts, discussing the challenges of developing disease modifying therapies for Parkinson's disease. This was held in Toronto in April 2019. The presentations and discussion focused on the issue of whether we should be concentrating on common pathogenic mechanisms in clinically heterogeneous Parkinson's population, or focusing on more targeted approaches in smaller subgroups of patients, distinguished by well-defined molecular characteristics. This led to publication of a manuscript summarising the discussions at the symposium and conclusions reached - Espay AJ, Kalia LV, Gan-Or Z, Williams-Gray CH, Bedard PL, Rowe SM, Morgante F, Fasano A, Stecher B, Kauffman MA, Farrer MJ, Coffey CS, Schwarzschild MA, Sherer T, Postuma RB, Strafella AP, Singleton AB, Barker RA, Kieburtz K, Olanow CW, Lozano A, Kordower JH, Cedarbaum JM, Brundin P, Standaert DG, Lang AE. Disease modification and biomarker development in Parkinson disease: Revision or reconstruction? Neurology. 2020.
Year(s) Of Engagement Activity 2019
 
Description Parkinson's 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 Patients, carers and/or patient groups
Results and Impact My research team has participated in annual Open Days for patients with Parkinson's disease and their carers, held at the John Van Geest Centre for Brain Repair, University of Cambridge. During these events, we deliver both oral and poster presentations on our current research in Parkinson's and its associated dementia, and the role of the immune system in this.
The intended purpose of these events is to disseminate information about our research to patients and the public for educational reasons, to gain their feedback on our work, and to stimulate further interest in participation in our research.
Year(s) Of Engagement Activity 2017,2018,2019
 
Description Parkinson's UK Annual Research Conference 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach National
Primary Audience Professional Practitioners
Results and Impact I delivered a talk at the virtual Parkinson's UK research conference entitled "The immune system as a therapeutic target in Parkinson's disease."
Year(s) Of Engagement Activity 2020
URL https://www.parkinsons.org.uk/events/online-research-conference-2020
 
Description Parkinson's disease newsletter 
Form Of Engagement Activity A magazine, newsletter or online publication
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Study participants or study members
Results and Impact Our annual Parkinson's disease newsletter provides an update on the progress of all our current Parkinson's research projects. Each year, our newsletter is distributed to over 500 individuals with Parkinson's disease on our research database. The primary purpose of the newsletter is to disseminate information about our research to individuals who are currently participating in our research, or have done so in the past.
Year(s) Of Engagement Activity 2018,2019,2020
 
Description Parkinson's research newsletter 
Form Of Engagement Activity A magazine, newsletter or online publication
Part Of Official Scheme? No
Geographic Reach Regional
Primary Audience Patients, carers and/or patient groups
Results and Impact My group produces an annual newsletter reporting the research activities of our group over the past 12 months. Our latest newsletter was circulated to over 600 patients with Parkinson's disease and research participants from our local region.
Year(s) Of Engagement Activity 2020,2021
URL http://www.thebarkerwilliamsgraylab.co.uk/parkinsons-disease-newsletter/
 
Description Poster presentation (Antonina Kouli) at the Society for Neuroscience Meeting, San Diego, November 2018 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Postgraduate students
Results and Impact Antonina Kouli, a PhD student in my research group, presented her work as a poster at the Society for Neuroscience 2018 meeting in San Diego. (Kouli A, Kuan WL, Wijeyekoon RS, Scott KM, He X, Barker RA, Williams-Gray CH; 'The efficacy of Toll-like receptor 2 & 4 inhibitors in human monocytes and in a novel rat model of Parkinson's disease'.)
The SfN meeting is attended by approximately 30,000 neuroscience researchers, thus presenting our work here gave us an excellent opportunity to promote our research amongst our peers internationally. Antonina had the opportunity to discuss the project with international experts working in closely related fields, and she received a large amount of useful feedback which is helping us to develop the project further.
Year(s) Of Engagement Activity 2018
URL https://www.sfn.org/Meetings/Neuroscience-2018/Abstracts/Neuroscience-2018-Abstracts
 
Description Presentation at annual departmental away day (Antonina Kouli) 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Postgraduate students
Results and Impact Antonina Kouli, postdoctoral research assistant in the Williams-Gray group, delivered a talk at the annual away day of the University of Cambridge Department of Clinical Neurosciences, entitled "What drives progression to dementia in Parkinson's disease? Is inflammation a key player?". This led to useful feedback from our research peers, and to the planning of new research collaborations.
Year(s) Of Engagement Activity 2019
 
Description Presentations at Parkinson's UK branch meetings (Marta Camacho) 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach Local
Primary Audience Patients, carers and/or patient groups
Results and Impact Marta Camacho, PhD student in the Williams-Gray group, delivered talks at 2 Parkinson's UK local branch meetings (Hertford, and Cromer) during 2019. She presented and discussed our current research with patients and carers.
The main purpose of this was to disseminate our research findings to patients and the public. Attendees reported an improved understanding of current research efforts in Parkinson's. The events also led to requests about participation in our future research.
Year(s) Of Engagement Activity 2019
 
Description World Parkinson Congress 2019 
Form Of Engagement Activity A talk or presentation
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Professional Practitioners
Results and Impact Caroline Williams-Gray delivered a talk at the World Parkinson Congress in Kyoto in June 2019, discussing her work on cognitive impairment in Parkinson's disease. Following the talk, she hosted a round table discussion on the same topic. The event was attended by patients with Parkinson's and their carers as well as researchers, clinicians, other health care professionals.This event led to an increase in international recognition for Dr Williams-Gray and her research group; and patients and healthcare professionals reported increased understanding of the topic following the event.
Year(s) Of Engagement Activity 2019
 
Description World Parkinson's Congress Blog 
Form Of Engagement Activity Engagement focused website, blog or social media channel
Part Of Official Scheme? No
Geographic Reach International
Primary Audience Media (as a channel to the public)
Results and Impact I wrote a blog for the World Parkinson's Congress entitled "Can we treat Parkinson's disease by suppressing the immune system?" This was written in an accessible format for patients and carers, as well as researchers. The blog discussed work from my group supporting the hypothesis that peripheral immune activation contributes to disease progression in Parkinson's, and outlined our plans for a clinical trial of an immunosuppressant drug for PD. I received positive feedback from patients who found the blog informative, and requests for further information about participation in our research.
Year(s) Of Engagement Activity 2020
URL https://www.worldpdcongress.org/home/2020/12/7/can-we-treat-parkinsons-disease-by-suppressing-the-im...