JPND: Targeting epigenetic dysregulation in the brainstem in Alzheimer's Disease (EPI-AD)
Lead Research Organisation:
UNIVERSITY OF EXETER
Department Name: Institute of Biomed & Clinical Science
Abstract
Alzheimer's disease is a very complex disease, with its cause still largely unknown, although it is widely believed that both genetic and environmental factors can alter a person's risk. In 2015 more than 850,000 people will be living with dementia in the UK, with care costs in excess of £26 billion per year. Alzheimer's disease accounts for more than 60% of dementia cases and is characterised by the loss of specific brain cells, leading to increasingly severe behavioural and personality changes, loss of the sufferer's independence, ever greater care requirements and ultimately death after many unfortunate years of suffering. Curiously the disease is characterised by brain cell loss in only some areas of the brain with some regions affected very early in disease, particularly areas of the brain involved in learning and memory, whilst other regions are relatively resistant to nerve cell loss. Although much progress has been made in understanding the cellular changes that happen in the brain in Alzheimer's disease, the treatments currently available only temporarily improve symptoms and do not treat the underlying disease. This is because by the time a person starts displaying symptoms of the disease, such as forgetfulness and personality changes, the "hallmarks" of Alzheimer's disease, which include nerve cell loss, amyloid plaque deposition and tangle formation, have already started in the brain. In fact some recent studies have shown that these changes may have been in the brain for up to ten years prior to diagnosis. Four key pivotal questions must be answered before a truly effective treatment for Alzheimer's disease can be developed. First we need to understand why the disease affects certain individuals, whilst other people remain cognitively healthy, even into very old age. Second we need to understand why certain regions of the brain succumb to disease, whilst others seem to be far less susceptible. Third we need to identify new markers of disease, called "biomarkers" that are easy to measure in blood, and that are able to not just diagnose the disease early, but to also predict how quickly a person will develop symptoms. Finally, we need to identify new drug targets. This project plans to combine clinical, genetic and molecular data to better understand the causes of Alzheimer's disease.
It is known that the expression of genes and the production of proteins relies not only on a person's specific DNA code (their genome), but can also be altered by an extra level of information called the "epigenome". Epigenetic processes are essentially chemical tags that are added to the DNA, and act to turn genes on and off, without changing the DNA sequence, and can be influenced by external factors such as the environment in which cells or individuals dwell. This project will look at levels of two different chemical tags (DNA methylation and hydroxymethylation) in the brainstem of people with Alzheimer's disease to identify genes that are epigenetically altered in disease, and could thus represent novel pharmacological targets for intervention. Further, we will look at levels of the DNA methylation tag in genes in blood samples from people with mild cognitive impairment, who represent a group of individuals at risk of developing Alzheimer's disease, to enable us to identify predictive biomarkers to allow early diagnosis. Finally we will attempt to model our epigenetic changes in an advanced experimental model system for Alzheimer's disease using induced Pluripotent Stem Cells (iPSCs) derived from the blood of Alzheimer's disease patients and age-matched controls.
It is known that the expression of genes and the production of proteins relies not only on a person's specific DNA code (their genome), but can also be altered by an extra level of information called the "epigenome". Epigenetic processes are essentially chemical tags that are added to the DNA, and act to turn genes on and off, without changing the DNA sequence, and can be influenced by external factors such as the environment in which cells or individuals dwell. This project will look at levels of two different chemical tags (DNA methylation and hydroxymethylation) in the brainstem of people with Alzheimer's disease to identify genes that are epigenetically altered in disease, and could thus represent novel pharmacological targets for intervention. Further, we will look at levels of the DNA methylation tag in genes in blood samples from people with mild cognitive impairment, who represent a group of individuals at risk of developing Alzheimer's disease, to enable us to identify predictive biomarkers to allow early diagnosis. Finally we will attempt to model our epigenetic changes in an advanced experimental model system for Alzheimer's disease using induced Pluripotent Stem Cells (iPSCs) derived from the blood of Alzheimer's disease patients and age-matched controls.
Technical Summary
Alzheimer's disease (AD) is a neurodegenerative disease that affects brain integrity and functioning, resulting in progressive cognitive deterioration. Previous work indicates that epigenetic mechanisms including DNA (hydroxy)methylation represent critical factors in the pathogenesis of AD. Moreover, the early occurrence of various neuropsychological symptoms and novel neuropathological findings suggest a key role for the brainstem, particularly serotonin (5-HT)- and noradrenaline (NA)-specific neurons.
Therefore, we hypothesise that epigenetic dysregulation in the brainstem has a critical role in the early pathogenesis of AD and aim to elucidate the exact role of DNA (hydroxy)methylation within the brainstem in the development and progression of AD. Our objectives will be addressed within our cross-disciplinary network, through the use of established large human cohorts. The consortium will link the epigenetic profiles with cognitive dysfunction, AD-related neuropathology, gene variants regulating 5-HT and NA-function (Objectives I & II). For biomarker discovery, blood epigenetic signatures of aging individuals will be linked to subsequent cognitive decline, MCI-AD conversion and depression (Objective III). The putative signatures will also be compared to established (more invasive) biomarkers to determine their validity. By making use of iPSCs (Objective IV), the project will furthermore test whether i) neurons derived from iPSCs of AD patients develop an AD-characteristic molecular/epigenetic and cellular phenotype when exposed to AD brain extracts or glucocorticoids (GCs), and ii) epigenetic editing of candidate genes (from Objectives I and II) within 5-HT and NA neurons generated from iPSCs can reverse AD-specific phenotypes.
The comprehensive approach of this project will fill the vital gap in our understanding of the links between epigenetic dysregulation and the 5-HT and NA neurotransmitter systems in the pathophysiology of AD.
Therefore, we hypothesise that epigenetic dysregulation in the brainstem has a critical role in the early pathogenesis of AD and aim to elucidate the exact role of DNA (hydroxy)methylation within the brainstem in the development and progression of AD. Our objectives will be addressed within our cross-disciplinary network, through the use of established large human cohorts. The consortium will link the epigenetic profiles with cognitive dysfunction, AD-related neuropathology, gene variants regulating 5-HT and NA-function (Objectives I & II). For biomarker discovery, blood epigenetic signatures of aging individuals will be linked to subsequent cognitive decline, MCI-AD conversion and depression (Objective III). The putative signatures will also be compared to established (more invasive) biomarkers to determine their validity. By making use of iPSCs (Objective IV), the project will furthermore test whether i) neurons derived from iPSCs of AD patients develop an AD-characteristic molecular/epigenetic and cellular phenotype when exposed to AD brain extracts or glucocorticoids (GCs), and ii) epigenetic editing of candidate genes (from Objectives I and II) within 5-HT and NA neurons generated from iPSCs can reverse AD-specific phenotypes.
The comprehensive approach of this project will fill the vital gap in our understanding of the links between epigenetic dysregulation and the 5-HT and NA neurotransmitter systems in the pathophysiology of AD.
Planned Impact
In addition to scientists interested in the aetiology of AD, the results of this project have the potential to impact on a number of other beneficiaries. These include patients suffering from AD, the pharmaceutical industry, health service providers and academic groups investigating the causes of other complex disease phenotypes. In the UK more than 850,000 people are living with dementia, with care costs in excess of £26 billion per year. Due to an increasingly ageing population, the number of cases is rising dramatically, with profound socioeconomic consequences as our healthcare systems struggle to cope. AD accounts for ~60% of cases and the current treatments temporarily alleviate some symptoms but do not modify the underlying disease process. A better understanding of the underlying mechanisms driving disease onset and progression is required to enable the design of new, more effective medications. Given the dynamic and potentially-reversible nature of the epigenome, the outputs from this research could potentially identify new targets and molecular pathways for pharmacological intervention. A number of pharmaceutical companies are actively developing "epigenetic-drugs" and could rapidly take advantage of these outputs. Another output of this research is the identification of predictive blood biomarkers for AD. By the time an individual becomes symptomatic for AD, there is already considerable neuropathology, which can appear years before the clinical diagnosis. The identification of predictive signatures in the blood would enable the diagnosis of disease many years before symptoms appear, allowing "at-risk" individuals to receive treatment before pathology has occurred.
Publications
Iatrou A
(2017)
Epigenetic dysregulation of brainstem nuclei in the pathogenesis of Alzheimer's disease: looking in the correct place at the right time?
in Cellular and molecular life sciences : CMLS
Roubroeks JAY
(2017)
Epigenetics and DNA methylomic profiling in Alzheimer's disease and other neurodegenerative diseases.
in Journal of neurochemistry
Chouliaras L
(2018)
Peripheral DNA Methylation, Cognitive Decline and Brain Aging: Pilot Findings from The Whitehall II Imaging Study
in Epigenomics
Smith A
(2019)
Parallel profiling of DNA methylation and hydroxymethylation highlights neuropathology-associated epigenetic variation in Alzheimer's disease
in Clinical Epigenetics
Smith AR
(2019)
Parallel profiling of DNA methylation and hydroxymethylation highlights neuropathology-associated epigenetic variation in Alzheimer's disease.
in Clinical epigenetics
Lardenoije R
(2019)
Alzheimer's disease-associated (hydroxy)methylomic changes in the brain and blood.
in Clinical epigenetics
Pishva E
(2020)
Psychosis-associated DNA methylomic variation in Alzheimer's disease cortex.
in Neurobiology of aging
Roubroeks JAY
(2020)
An epigenome-wide association study of Alzheimer's disease blood highlights robust DNA hypermethylation in the HOXB6 gene.
in Neurobiology of aging
Imm J
(2021)
Characterization of DNA Methylomic Signatures in Induced Pluripotent Stem Cells During Neuronal Differentiation.
in Frontiers in cell and developmental biology
Smith RG
(2021)
A meta-analysis of epigenome-wide association studies in Alzheimer's disease highlights novel differentially methylated loci across cortex.
in Nature communications
Smith AR
(2021)
The histone modification H3K4me3 is altered at the ANK1 locus in Alzheimer's disease brain.
in Future science OA
Devall M
(2022)
Genome-wide characterization of mitochondrial DNA methylation in human brain.
in Frontiers in endocrinology
Description | A multi-omic approach to elucidate novel disease mechanisms and biomarkers for psychosis in Alzheimer's disease |
Amount | $1,626,428 (USD) |
Funding ID | R01 AG067015 |
Organisation | National Institutes of Health (NIH) |
Sector | Public |
Country | United States |
Start | 12/2019 |
End | 11/2023 |
Description | An integrated "omics" analysis to elucidate the role of miRNAs in Alzheimer's disease |
Amount | £49,217 (GBP) |
Funding ID | ARUK-PPG2017B-021 |
Organisation | Alzheimer's Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 07/2017 |
End | 07/2019 |
Description | Cutting-edge precision profiling of specific cell populations using a Laser Capture Microdissection (LCM) system |
Amount | £239,166 (GBP) |
Funding ID | MR/X013413/1 |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 11/2022 |
End | 03/2023 |
Description | Determining the potential utility of epigenetic modulators to treat Alzheimer's disease: A collaboration between Exeter and Oxford ARUK Network Centres and the Oxford DDI |
Amount | £98,360 (GBP) |
Funding ID | ARUK-NCG2017A-5 |
Organisation | Alzheimer's Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 03/2017 |
End | 02/2019 |
Description | Exploring the role of epigenetic mechanisms in the manifestation of Huntington's disease |
Amount | £1,051,158 (GBP) |
Funding ID | MR/Y014685/1 |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 03/2024 |
End | 02/2027 |
Description | Major project grant |
Amount | € 1,431,308 (EUR) |
Organisation | EU Joint Programme - Neurodegenerative Disease Research (JPND) |
Sector | Public |
Country | European Union (EU) |
Start | 06/2016 |
End | 06/2019 |
Description | Utilising big data and long-read sequencing approaches to understand APOE (epi)genetics in Alzheimer's disease |
Amount | £152,854 (GBP) |
Organisation | Alzheimer's Research UK |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 09/2023 |
End | 10/2027 |
Title | An online searchable tool for the AD EWAS meta-analysis data |
Description | We have generated an online searchable tool for our Alzheimer's disease (AD) epigenome-wide association study (EWAS) meta-analysis data where researchers can download summary statistics, forest plots and Mini-Manhattan plots for their regions of interest |
Type Of Material | Database/Collection of data |
Year Produced | 2020 |
Provided To Others? | Yes |
Impact | The tool has just been published and the link included in the pre-print and in the manuscript under review at Nature Communications |
URL | https://www.epigenomicslab.com/ad-meta-analysis/ |
Title | PRS-multi-trait R package |
Description | PRS-multi-trait is an R package that focuses on using generalized summary statistics, calculation and prediction of multi-trait polygenic (risk) scores (PGS) to predict the likelihood of an individual developing a particular trait or disease based on their genetic risk factors. The package includes functions for calculating PGS for individuals based on the presence of specific genetic variants that have been associated with the trait or disease in question. PRS-multi-trait is designed to be user-friendly and easy to use, with a range of functions and documentation to help users get started quickly. Whether you are a researcher or practitioner in the field of genetics and genomics, or simply interested in exploring the genetic basis of complex traits and diseases, PRS-Multi-trait can help you generate PGS models and calculate PGS for your cohort. The method is useful for a wide range of applications, including identifying individuals who may be at risk of developing complex diseases such as diabetes or Alzheimer's disease, as well as for predicting scores for more straightforward traits such as height or eye color. |
Type Of Material | Computer model/algorithm |
Year Produced | 2022 |
Provided To Others? | Yes |
Impact | Ease of analysis for other researchers |
URL | https://github.com/Rrtk2/PRS-multi-trait |
Title | Supplementary Material. The histone modification H3K4me3 is altered at the ANK1 locus in Alzheimer's disease brain. |
Description | Supplementary Material. The histone modification H3K4me3 is altered at the ANK1 locus in Alzheimer's disease brain. Background Several epigenome-wide association studies of DNA methylation have highlighted altered DNA methylation in the ANK1 gene in Alzheimer's disease brain samples. However, no study has specifically examined ANK1 histone modifications in the disease. Methods We use chromatin immunoprecipitation-qPCR to quantify tri-methylation at histone 3 lysine 4 (H3K4me3) and 27 (H3K27me3) in the ANK1 gene in entorhinal cortex from donors with high (N= 59) or low (N=29) Alzheimer's pathology. Discussion We demonstrate decreased levels of H3K4me3, a marker of active gene transcription, with no change in H3K27me3, a marker of inactive genes. H3K4me3 is negatively correlated with DNA methylation in specific regions of the ANK1 gene. Conclusions Our study suggests that the ANK1 gene shows altered epigenetic marks indicative of reduced gene activation in Alzheimer's disease. |
Type Of Material | Database/Collection of data |
Year Produced | 2021 |
Provided To Others? | Yes |
URL | https://future-science-group.figshare.com/articles/dataset/Supplementary_Material_The_histone_modifi... |
Title | Supplementary Material. The histone modification H3K4me3 is altered at the ANK1 locus in Alzheimer's disease brain. |
Description | Supplementary Material. The histone modification H3K4me3 is altered at the ANK1 locus in Alzheimer's disease brain. Background Several epigenome-wide association studies of DNA methylation have highlighted altered DNA methylation in the ANK1 gene in Alzheimer's disease brain samples. However, no study has specifically examined ANK1 histone modifications in the disease. Methods We use chromatin immunoprecipitation-qPCR to quantify tri-methylation at histone 3 lysine 4 (H3K4me3) and 27 (H3K27me3) in the ANK1 gene in entorhinal cortex from donors with high (N= 59) or low (N=29) Alzheimer's pathology. Discussion We demonstrate decreased levels of H3K4me3, a marker of active gene transcription, with no change in H3K27me3, a marker of inactive genes. H3K4me3 is negatively correlated with DNA methylation in specific regions of the ANK1 gene. Conclusions Our study suggests that the ANK1 gene shows altered epigenetic marks indicative of reduced gene activation in Alzheimer's disease. |
Type Of Material | Database/Collection of data |
Year Produced | 2021 |
Provided To Others? | Yes |
URL | https://future-science-group.figshare.com/articles/dataset/Supplementary_Material_The_histone_modifi... |
Description | Application for MSCA Doctoral Network |
Organisation | Maastricht University (UM) |
Department | Maastricht School for Mental Health and Neuroscience (MHeNS) |
Country | Netherlands |
Sector | Academic/University |
PI Contribution | After our successful collaboration through the JPND funding we have recently submitted an application for a doctoral network through the MSCA scheme (https://marie-sklodowska-curie-actions.ec.europa.eu/calls/msca-doctoral-networks-2021), which is currently under review for funding (decision April 2022). This is for 15 PhD studentships across Europe and builds on the collaboration and work in our JPND funding |
Collaborator Contribution | Our partner has led the application, and in this project (if funded) there would be 3 joing PhD studentships between the University of Exeter and Maastricht University |
Impact | N/A - awaiting funding decision |
Start Year | 2021 |
Description | Collaboration between Maastricht University and the University of Exeter |
Organisation | Maastricht University (UM) |
Department | Maastricht School for Mental Health and Neuroscience (MHeNS) |
Country | Netherlands |
Sector | Academic/University |
PI Contribution | Prof Katie Lunnon now has an honorary position at the University of Maastricht whilst similarly Dr Ehsan Pishva now has an honorary position at the University of Exeter. We are in the process of establishing exploring double PhD awards. In the meantime we have several PhD students co-supervised across the two Universities |
Collaborator Contribution | As a result of the MRC funding we are able to co-supervise students and arrange secondments for their PhDs across the two institutions |
Impact | Numerous publications (see outputs) |
Start Year | 2020 |
Description | New JPco-fuND application 2019 |
Organisation | Maastricht University (UM) |
Country | Netherlands |
Sector | Academic/University |
PI Contribution | New JPco-fuND application submitted to continue partnership |
Collaborator Contribution | We have submitted an application that will be to continue our previous JPco-fuND partnership, but moving to the next level by performing integrative multi-omic studies |
Impact | Application to JPco-fuND submitted |
Start Year | 2016 |
Title | PRS-multi-trait R package |
Description | PRS-multi-trait is an R package that focuses on using generalized summary statistics, calculation and prediction of multi-trait polygenic (risk) scores (PGS) to predict the likelihood of an individual developing a particular trait or disease based on their genetic risk factors. The package includes functions for calculating PGS for individuals based on the presence of specific genetic variants that have been associated with the trait or disease in question. PRS-multi-trait is designed to be user-friendly and easy to use, with a range of functions and documentation to help users get started quickly. Whether you are a researcher or practitioner in the field of genetics and genomics, or simply interested in exploring the genetic basis of complex traits and diseases, PRS-Multi-trait can help you generate PGS models and calculate PGS for your cohort. The method is useful for a wide range of applications, including identifying individuals who may be at risk of developing complex diseases such as diabetes or Alzheimer's disease, as well as for predicting scores for more straightforward traits such as height or eye color. |
Type Of Technology | Webtool/Application |
Year Produced | 2022 |
Impact | Ease of analysis for other researchers |
Description | 2016 MRC Prion Unit, UCL Institute of Neurology, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Professional Practitioners |
Results and Impact | Invited speaker at UCL Prion unit |
Year(s) Of Engagement Activity | 2016 |
Description | 2017 Alzheimer's Research UK National Conference, Aberdeen, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Postgraduate students |
Results and Impact | Invited speaker at Alzheimer's Research UK annual conference in Aderdeen |
Year(s) Of Engagement Activity | 2017 |
Description | 2017 Alzheimer's Society National Conference, London, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Public/other audiences |
Results and Impact | Invited speaker at Alzheimer's Society annual meeting in London |
Year(s) Of Engagement Activity | 2017 |
Description | 2017 Arch Education, Hong Kong University, Hong Kong (Invited Speaker) |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Schools |
Results and Impact | Invited speaker to discuss research and encourage students to undertake Medical sciences degree |
Year(s) Of Engagement Activity | 2017 |
Description | 2017 Bioinformatics and Genomics Group, University of Southampton, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Professional Practitioners |
Results and Impact | Invited speaker at Southampton University |
Year(s) Of Engagement Activity | 2017 |
Description | 2017 British Neuroscience Association Annual Meeting, Birmingham, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Professional Practitioners |
Results and Impact | Invited speaker at BNA meeting to discuss research |
Year(s) Of Engagement Activity | 2017 |
Description | 2017 Department of Neuroscience, University of Sheffield, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Industry/Business |
Results and Impact | Invited speaker in Sheffield and to discuss new collaborations |
Year(s) Of Engagement Activity | 2017 |
Description | 2018 Department of Clinical Sciences, University of Cambridge, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Postgraduate students |
Results and Impact | Invited speaker at Cambridge University |
Year(s) Of Engagement Activity | 2018 |
Description | 2018 School of Medicine and Psychology, Cardiff University, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Postgraduate students |
Results and Impact | Invited speaker at Cardiff University to allow discussions about new collaborations |
Year(s) Of Engagement Activity | 2018 |
Description | 2018 School of Pharmacy, University of Reading, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Postgraduate students |
Results and Impact | Invited speaker at Reading University to allow new collaborations |
Year(s) Of Engagement Activity | 2018 |
Description | 2019 British Neuropathological Society bi-annual meeting, London, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Professional Practitioners |
Results and Impact | Invited speaker at British Neuropathological Society meeting in London UK |
Year(s) Of Engagement Activity | 2019 |
Description | 2019 Lundbeck (Pharma), Copenhagen, Denmark (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Industry/Business |
Results and Impact | Invited speaker at Lunbeck in Copenhagen to discuss potential collaborations |
Year(s) Of Engagement Activity | 2019 |
Description | 2019 UK Dementia Research Institute, Imperial College London, UK (Invited Speaker) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Postgraduate students |
Results and Impact | Invited talk at UK DRI at Imperial to allow discussions about potential collaborations |
Year(s) Of Engagement Activity | 2019 |
Description | 2019 University of Pisa, Italy |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Postgraduate students |
Results and Impact | Invited seminar at the University of Pisa, Italy to discuss findings from the grant |
Year(s) Of Engagement Activity | 2019 |
Description | ADPD Conference 2019, Lisbon, Portugal |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Talk delivered at the ADPD conference in Lisbon in 2019 on findings from grant |
Year(s) Of Engagement Activity | 2019 |
Description | ARUK Annual Public Open day |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | ARUK annual open day attendance and speaking to public |
Year(s) Of Engagement Activity | 2015,2016,2017,2018 |
Description | ARUK Annual Scientific meeting |
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 | Postgraduate students |
Results and Impact | Annual scientific open day for ARUK South West Network |
Year(s) Of Engagement Activity | 2015,2016,2017,2018 |
Description | Alzheimer's Association International Conference (AAIC) 2019 LA, US (Oral Presentation) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Industry/Business |
Results and Impact | Talk at the AAIC conference on findings from this project |
Year(s) Of Engagement Activity | 2019 |
Description | Alzheimer's Research UK Annual Conference 2019, Harrogate, UK |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Industry/Business |
Results and Impact | Talk delivered at ARUK conference on results of grant funding |
Year(s) Of Engagement Activity | 2019 |
Description | Alzheimer's Research UK Annual Conference 2020, Online |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Other audiences |
Results and Impact | Poster presentation on the project at the ARUK 2020 (online) conference |
Year(s) Of Engagement Activity | 2020 |
Description | British Neuropathological Society bi-annual meeting 2019, London, UK |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Professional Practitioners |
Results and Impact | Invited talk at the Bristish Neuropathology Society meeting for Cavanagh award |
Year(s) Of Engagement Activity | 2019 |
Description | Cardiff Dementia Research Institute (DRI) 2020, Cardiff, Wales |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Postgraduate students |
Results and Impact | Invited seminar at the Cardiff DRI on findigns from this grant |
Year(s) Of Engagement Activity | 2020 |
Description | Epigenomics of Common Disease Conference 2019, Wellcome Genome Campus (Oral Presentation) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Industry/Business |
Results and Impact | Talk on data from this grant at ECD 2019 conference |
Year(s) Of Engagement Activity | 2019 |
Description | Oral presentation at International Perspectives in Dementia Conference |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Public/other audiences |
Results and Impact | Public engagement day held for those living with and caring for those with dementia in and around the Plymouth area. |
Year(s) Of Engagement Activity | 2023 |
URL | https://www.plymouth.ac.uk/news/university-hosts-dementia-conference |
Description | Pathways to Industry Workshop |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Industry/Business |
Results and Impact | After successfully bidding for event funding we held a "Pathways to Industry" workshop to bring together academics who are interested in translating their research, and working with industry. |
Year(s) Of Engagement Activity | 2023 |