Defining the role of ciliary BBS proteins in neuroplasticity
Lead Research Organisation:
University College London
Department Name: Institute of Child Health
Abstract
Neuronal plasticity is among the most important areas of modern neuroscience research and one of the best existing cellular models for learning and memory. The hippocampus is a brain structure important for learning and the storage of memories. It has been shown that there is an area in hippocampus where new neurons are born even during adult life. New neurons integrate into existing networks and are important for developing new skills and memory. It has also recently emerged that memories and learning skills are "stored" in dendritic spines, mushroom like protrusions on the dendrites of nerve cells. Dendritic spines are very "plastic", that is, they change significantly in shape, volume, and number over a short time course. Because spines mostly comprise an actin cytoskeleton, they are dynamic, with the majority of spines able to change their shape within seconds to minutes following actin remodelling. New experiences and learning lead to the formation of new spines. It has been observed that malformed spines or reduced spine number can be associated with learning disabilities.
Recently, an exciting link between cilia/ciliary proteins and adult neurogenesis has emerged. Cilia are hair-like projections from the cell membrane. They are found on almost all eukaryotic cells. In the last decade it has been shown normal human functions such as ability to see, hear, smell, breathe, excrete, reproduce critically depend on correct ciliary function. It has been also shown that cilia are important for normal brain functions such as learning and memory. Normal cilia function depends on integrity of many proteins including BBS.
We have generated preliminary data indicating that there is a reduction in formation of adult new born neurons as well as reduction in dendritic spine number and density in Bbs mice model. These mice lack a functional BBS protein and therefore recapitulates the main features of human BBS and thus, will provide Here we propose to investigate how mutation in a single BBS protein might lead to the changes in neuroplasticity. We hypothesise that the absence of a fully functioning Bbs protein affects the formation of dendritic spines thus reducing the hippocampal capacity for information storage and effective learning.
Recently, an exciting link between cilia/ciliary proteins and adult neurogenesis has emerged. Cilia are hair-like projections from the cell membrane. They are found on almost all eukaryotic cells. In the last decade it has been shown normal human functions such as ability to see, hear, smell, breathe, excrete, reproduce critically depend on correct ciliary function. It has been also shown that cilia are important for normal brain functions such as learning and memory. Normal cilia function depends on integrity of many proteins including BBS.
We have generated preliminary data indicating that there is a reduction in formation of adult new born neurons as well as reduction in dendritic spine number and density in Bbs mice model. These mice lack a functional BBS protein and therefore recapitulates the main features of human BBS and thus, will provide Here we propose to investigate how mutation in a single BBS protein might lead to the changes in neuroplasticity. We hypothesise that the absence of a fully functioning Bbs protein affects the formation of dendritic spines thus reducing the hippocampal capacity for information storage and effective learning.
Technical Summary
Neuronal plasticity is among the most important areas of modern neuroscience research and one of the best existing cellular models for learning and memory. Dynamic changes in axon and dendritic growth, integration of adult new-born neurons into existing networks, synaptogenesis, and dendritic spine formation are just some examples of the molecular and cellular underpinnings of neuronal plasticity.
Recently, an exciting link between cilia and adult neurogenesis has emerged. Loss of cilia in adult progenitor cells leads to significant decrease of proliferation in hippocampal amplifying progenitors. Moreover, loss of ciliary protein Arl13b causes aberrant polarity of radial progenitors leading to the disruption of neuron organisation in cortex.
Cilia are microtubule-based, centriole-derived projections from the apical cell membrane. In the last decade it has been identified that normal human functions such as ability to see, hear, smell, breathe, excrete, reproduce and learn/remember critically depend on correct ciliary function.
Bardet-Biedl syndrome, BBS, proteins play an important role in cilia function being a core facilitators of ciliogenesis and cilia receptor trafficking. We, and others have previously shown that the BBS4 protein is involved in microtubular stabilisation suggesting involvement of BBS proteins in the regulation of the cytoskeleton and protein trafficking. In spite a well-defined role in ciliagenesis, the role of BBS proteins in neurogenesis and dendritic spine formation has not been investigated. In our preliminary experiments we have determined that Bbs4 and Bbs5 null mice have significantly reduced neurogenesis and dendritic spine formation in the dentate gyrus suggesting that there is an overall reduction in neuronal plasticity. Here we propose to investigate the molecular mechanisms of BBS proteins involvement in adult neurogenesis and synaptogenesis.
Recently, an exciting link between cilia and adult neurogenesis has emerged. Loss of cilia in adult progenitor cells leads to significant decrease of proliferation in hippocampal amplifying progenitors. Moreover, loss of ciliary protein Arl13b causes aberrant polarity of radial progenitors leading to the disruption of neuron organisation in cortex.
Cilia are microtubule-based, centriole-derived projections from the apical cell membrane. In the last decade it has been identified that normal human functions such as ability to see, hear, smell, breathe, excrete, reproduce and learn/remember critically depend on correct ciliary function.
Bardet-Biedl syndrome, BBS, proteins play an important role in cilia function being a core facilitators of ciliogenesis and cilia receptor trafficking. We, and others have previously shown that the BBS4 protein is involved in microtubular stabilisation suggesting involvement of BBS proteins in the regulation of the cytoskeleton and protein trafficking. In spite a well-defined role in ciliagenesis, the role of BBS proteins in neurogenesis and dendritic spine formation has not been investigated. In our preliminary experiments we have determined that Bbs4 and Bbs5 null mice have significantly reduced neurogenesis and dendritic spine formation in the dentate gyrus suggesting that there is an overall reduction in neuronal plasticity. Here we propose to investigate the molecular mechanisms of BBS proteins involvement in adult neurogenesis and synaptogenesis.
Planned Impact
The proposed research will likely have immediate and long term impact on academic communities and clinical researchers. Even though it is not our primary goal to investigate a Bardet-Biedl syndrome patients neurophysiology, this study will have an impact on BBS patients, their clinicians, and the National Health and Social services
Academic community:
Although the proposed research project is multi-disciplinary in nature, we predict that the greatest impact for researchers will be in the cilia and neuro-biology fields. Cilia is a organell which is recognised to be vital for many normal human functions such as hearing, vision, taste, reproduction and learning and memory. The evidence of cilia profound significance lies in the fact that defects in cilia lead to a broad range of organ specific disorders: situs inversus, polycystic kidneys, retinal degeneration, obesity etc. However, little is known as to how defects in cilia function affect learning, memory and even psychiatric disease. This project will help to evaluate the potential link between neuronal plasticity and its impact on learning, memory and behaviour. Bbs mice might provide an excellent tool for the neurobiological studies of neuronal plasticity.
Bardet-Biedl patients and their clinicians
In this study we propose to investigate the role of BBS proteins in neuroplasticity. BBS proteins when mutated, cause Bardet-Biedl syndrome (BBS) which is a highly debilitating autosomal-recessive genetic disorder in which patients present with early-onset blindness, polydactyly, renal disease, obesity, diabetes and cognitive impairment. There is no cure. In addition to learning disabilities, the neuropsychiatric component of BBS comprises behavioural difficulties such as disinhibition, an inability to recognise social cues, obsessive-compulsive tendencies, anxiety and depression, autism and even psychosis. Most adult patients experience short-term memory deficits but relatively well-preserved long term memory.
For the clinicians, the knowledge of the underlying aetiology of the cognitive impairment in BBS patients is critical for how clinicians regard the intellectual development of these patients who currently have no strategy for improvement. For example, early recognition of the disorder by GPs, mid-wives or health visitors, and subsequent correct diagnosis by paediatricians and clinical geneticists is vital if affected children are to be given the appropriate and timely therapy.
National Health Service and Social Services
Approximately 500 patients attend the NHS nationally commissioned clinical service (led by P. Beales). Each BBS patient requires input from multiple services including ophthalmology, nephrology, urology, dietetics, endocrinology, clinical genetics, psychology and neurology. The BBS specialised service provides a one-stop shop clinic visit delivered by four NHS trusts; Birmingham Children's Hospital, Queen Elizabeth Hospital (Birmingham), Guys Hospital and Great Ormond Street Hospital (London). Genetic testing for each patient is also provided through this service. BBS patients require lifelong monitoring of their disease and treatment of organ-specific problems which is partly delivered through this service.
An important observation from the service is that learning disabilities and memory deficits are much less pronounced in the early years than during adolescence and adulthood indicating that these are not likely due to defects in embryonic development but decline with age. By investigating the role of BBS proteins in learning and memory, we could potentially develop early intervention programmes and targeted educational approaches for BBS syndrome patients.
Academic community:
Although the proposed research project is multi-disciplinary in nature, we predict that the greatest impact for researchers will be in the cilia and neuro-biology fields. Cilia is a organell which is recognised to be vital for many normal human functions such as hearing, vision, taste, reproduction and learning and memory. The evidence of cilia profound significance lies in the fact that defects in cilia lead to a broad range of organ specific disorders: situs inversus, polycystic kidneys, retinal degeneration, obesity etc. However, little is known as to how defects in cilia function affect learning, memory and even psychiatric disease. This project will help to evaluate the potential link between neuronal plasticity and its impact on learning, memory and behaviour. Bbs mice might provide an excellent tool for the neurobiological studies of neuronal plasticity.
Bardet-Biedl patients and their clinicians
In this study we propose to investigate the role of BBS proteins in neuroplasticity. BBS proteins when mutated, cause Bardet-Biedl syndrome (BBS) which is a highly debilitating autosomal-recessive genetic disorder in which patients present with early-onset blindness, polydactyly, renal disease, obesity, diabetes and cognitive impairment. There is no cure. In addition to learning disabilities, the neuropsychiatric component of BBS comprises behavioural difficulties such as disinhibition, an inability to recognise social cues, obsessive-compulsive tendencies, anxiety and depression, autism and even psychosis. Most adult patients experience short-term memory deficits but relatively well-preserved long term memory.
For the clinicians, the knowledge of the underlying aetiology of the cognitive impairment in BBS patients is critical for how clinicians regard the intellectual development of these patients who currently have no strategy for improvement. For example, early recognition of the disorder by GPs, mid-wives or health visitors, and subsequent correct diagnosis by paediatricians and clinical geneticists is vital if affected children are to be given the appropriate and timely therapy.
National Health Service and Social Services
Approximately 500 patients attend the NHS nationally commissioned clinical service (led by P. Beales). Each BBS patient requires input from multiple services including ophthalmology, nephrology, urology, dietetics, endocrinology, clinical genetics, psychology and neurology. The BBS specialised service provides a one-stop shop clinic visit delivered by four NHS trusts; Birmingham Children's Hospital, Queen Elizabeth Hospital (Birmingham), Guys Hospital and Great Ormond Street Hospital (London). Genetic testing for each patient is also provided through this service. BBS patients require lifelong monitoring of their disease and treatment of organ-specific problems which is partly delivered through this service.
An important observation from the service is that learning disabilities and memory deficits are much less pronounced in the early years than during adolescence and adulthood indicating that these are not likely due to defects in embryonic development but decline with age. By investigating the role of BBS proteins in learning and memory, we could potentially develop early intervention programmes and targeted educational approaches for BBS syndrome patients.
Organisations
- University College London (Lead Research Organisation)
- Eberhard Karls University of Tübingen (Collaboration)
- QUEEN MARY UNIVERSITY OF LONDON (Collaboration)
- University College London (Collaboration)
- Heidelberg University (Collaboration)
- Heptares Therapeutics Ltd (Collaboration)
- Pasteur Institute, Paris (Collaboration)
- KING'S COLLEGE LONDON (Collaboration)
Publications
Oud MM
(2017)
Mutations in EXTL3 Cause Neuro-immuno-skeletal Dysplasia Syndrome.
in American journal of human genetics
Savastano CP
(2017)
Impact of rare variants in ARHGAP29 to the etiology of oral clefts: role of loss-of-function vs missense variants.
in Clinical genetics
Thompson CL
(2017)
Chondrocyte expansion is associated with loss of primary cilia and disrupted hedgehog signalling.
in European cells & materials
Melhem M
(2017)
Novel G6B gene variant causes familial autosomal recessive thrombocytopenia and anemia.
in European journal of haematology
Williams HJ
(2016)
The use of whole-exome sequencing to disentangle complex phenotypes.
in European journal of human genetics : EJHG
Antony D
(2017)
Exome sequencing for the differential diagnosis of ciliary chondrodysplasias: Example of a WDR35 mutation case and review of the literature.
in European journal of medical genetics
Thompson CL
(2021)
Polycystin-2 Is Required for Chondrocyte Mechanotransduction and Traffics to the Primary Cilium in Response to Mechanical Stimulation.
in International journal of molecular sciences
Kammermeier J
(2017)
Phenotypic and Genotypic Characterisation of Inflammatory Bowel Disease Presenting Before the Age of 2 years.
in Journal of Crohn's & colitis
Forsythe E
(2017)
Risk Factors for Severe Renal Disease in Bardet-Biedl Syndrome.
in Journal of the American Society of Nephrology : JASN
Bakey Z
(2023)
IFT74 variants cause skeletal ciliopathy and motile cilia defects in mice and humans.
in medRxiv : the preprint server for health sciences
Description | Outputs from this award have impacted clinical management of NHSE patients (outlined in clinical management submission) as far as intellectual disabilities are concerned. This has led to novel cognitive assessments implemented in clinic for paediatric patients with a view to managing their educational needs given we now know that outcomes are plastic. |
First Year Of Impact | 2022 |
Sector | Healthcare |
Description | Amendment to Clinical Management and Practice |
Geographic Reach | National |
Policy Influence Type | Influenced training of practitioners or researchers |
Description | Newborn Sequencing Programme - Genomics England committee and workshop |
Geographic Reach | National |
Policy Influence Type | Implementation circular/rapid advice/letter to e.g. Ministry of Health |
Description | Apollo Therapeutics Fund |
Amount | £900,000 (GBP) |
Organisation | Apollo Therapeutics |
Sector | Private |
Country | United Kingdom |
Start | 01/2017 |
End | 08/2018 |
Description | NIHR Senior Investigator |
Amount | £45,000 (GBP) |
Funding ID | NIHR200282 |
Organisation | National Institute for Health Research |
Sector | Public |
Country | United Kingdom |
Start | 05/2019 |
End | 05/2022 |
Description | Newlife Foundation Project Grant |
Amount | £119,000 (GBP) |
Organisation | Newlife the Charity for Disabled Children |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 12/2016 |
End | 11/2017 |
Title | Development of reagents and resources for studying Bardet-Biedl syndrome |
Description | We have generated gene modified cells, GPCR libraries, MRI assays, physical exercise protocols, applied RNASeq techniques and Proteomics to the study of Bardet-Biedl syndrome. We have implemented CRISPR gene editing in cells to model disease, established ELISA assays, new Immmunohistochemistry tools, developed FACS sorting methods for studying ciliopathies and new cloning strategies. |
Type Of Material | Technology assay or reagent |
Year Produced | 2015 |
Provided To Others? | Yes |
Impact | Part of this resource was published in JOVE. |
Title | UK Registry of Bardet-Biedl Syndrome |
Description | Clinical and genetic data is routinely collected from over 600 patients with Bardet-Biedl Syndrome who attend the NHSE highly specialised service clinics. These have been compiled in RedCap and held on compliant safe haven UCL servers. The information is deidentified but only accessible through relevant application. |
Type Of Material | Database/Collection of data |
Year Produced | 2022 |
Provided To Others? | Yes |
Impact | This is the largest collection of clinical and genetics information compiled on patients with Bardet-Biedl Syndrome worldwide. It has already provided insights in to the natural history of disease and genotype-phenotype correlations. These will aid in development of better diagnostics, prognoses and therapeutics. |
Description | Characterisation of neuroplasticity in the brain of Bardet-Biedl Syndrome mice |
Organisation | University College London |
Department | London Centre for Nanotechnology |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We have worked closely with Dr Christoph Schmied -Hieber, Prof Michael Hausser and Prof Patricia Salinas to develop a unqiue program of research aimed at understanding the role of neurplasticity in the brain. We have provided mouse mutants (e.g. Bbs5, Bbs4) and reagents to this collaboration. |
Collaborator Contribution | Dr Christoph Schmied -Hieber, Prof Michael Hausser and Prof Patricia Salinas have provided both intellectual expertise and resources/skills (neurophysiology) toward the characterisation of BBS mouse mutants. |
Impact | This is multidisciplinary whereby Prof Salinas has providing training in aspect of neuronal cell culture. Dr Christoph Schmied -Hieber did electrophysiology experiments on brain sections. Prof Hausser has provided valuable insights and advice into the study design and data analysis. |
Start Year | 2015 |
Description | Collaboration with Christoph Schmidt-Hieber, Institut Pasteur, Paris |
Organisation | Pasteur Institute, Paris |
Country | France |
Sector | Charity/Non Profit |
PI Contribution | We have made key neuroplasticity discoveries in ciliopathies using neuronal cultures |
Collaborator Contribution | Christoph has been working with on neuroplasticity by undertaking electrophysiological studies in neuronal cultures |
Impact | None yet. Paper in preparation |
Start Year | 2017 |
Description | EMMAC |
Organisation | Eberhard Karls University of Tübingen |
Department | Institute for Ophthalmic Research |
Country | Germany |
Sector | Academic/University |
PI Contribution | We are leading on a new Wellcome Trust Collaborative grant to define systematically the role and function of missense mutations in disease (ciliopathies). We will provide cell modelling capability and CRISPR generated patient mutations to this study. |
Collaborator Contribution | Marius Ueffing and Karsten Boldt will provide proteomics expertise by modelling protein interactions in which key missense mutations have been introduced to determine the effects on protein complex perturbation in cells and organisms. |
Impact | This multidisciplinary project has only just begun and will last 5 years. No outputs have yet been registered. |
Start Year | 2018 |
Description | EMMAC |
Organisation | Heidelberg University |
Country | Germany |
Sector | Academic/University |
PI Contribution | We are leading on a new Wellcome Trust Collaborative grant to define systematically the role and function of missense mutations in disease (ciliopathies). We will provide cell modelling capability and CRISPR generated patient mutations to this study. |
Collaborator Contribution | Marius Ueffing and Karsten Boldt will provide proteomics expertise by modelling protein interactions in which key missense mutations have been introduced to determine the effects on protein complex perturbation in cells and organisms. |
Impact | This multidisciplinary project has only just begun and will last 5 years. No outputs have yet been registered. |
Start Year | 2018 |
Description | EMMAC |
Organisation | King's College London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We are leading on a new Wellcome Trust Collaborative grant to define systematically the role and function of missense mutations in disease (ciliopathies). We will provide cell modelling capability and CRISPR generated patient mutations to this study. |
Collaborator Contribution | Marius Ueffing and Karsten Boldt will provide proteomics expertise by modelling protein interactions in which key missense mutations have been introduced to determine the effects on protein complex perturbation in cells and organisms. |
Impact | This multidisciplinary project has only just begun and will last 5 years. No outputs have yet been registered. |
Start Year | 2018 |
Description | EMMAC |
Organisation | Queen Mary University of London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We are leading on a new Wellcome Trust Collaborative grant to define systematically the role and function of missense mutations in disease (ciliopathies). We will provide cell modelling capability and CRISPR generated patient mutations to this study. |
Collaborator Contribution | Marius Ueffing and Karsten Boldt will provide proteomics expertise by modelling protein interactions in which key missense mutations have been introduced to determine the effects on protein complex perturbation in cells and organisms. |
Impact | This multidisciplinary project has only just begun and will last 5 years. No outputs have yet been registered. |
Start Year | 2018 |
Description | Elucidating the role of GPCRs in ciliopathy neurocognitive phenotypes |
Organisation | Heptares Therapeutics Ltd |
Country | United Kingdom |
Sector | Private |
PI Contribution | We are providing staff, resources and expertise in Bardet-Biedl syndrome experimental modelling. |
Collaborator Contribution | Heptares will provide funding for a PhD studenship beginning in May 2017 for 3 years. They will also provide expertise in GPCR biology, compounds and an industrial placement for the student. |
Impact | We are currently agreeing an MTA and collaboration agreement between UCL and Heptares. There are no outcomes yet to report. |
Start Year | 2016 |
Title | A study of the value of exercise intervention on hippocampal volume and function in children with Bardet-Biedl syndrome |
Description | We are perfoming a pilot trial of 20 children under 16 years with Bardet-Biedl syndrome. Each child is randomly assigned to the intervention/non-intervention arm whereupon each child receives a brain MRI at day 1. Half the group go onto undertake a prescribed routine of exercises supervised by a trainer at their local gym for sixth months. On completion each child (both arms) is rescanned and analysed for changes in hippocampal, volume, blood flow, memory and cognitive changes. |
Type | Diagnostic Tool - Imaging |
Current Stage Of Development | Initial development |
Year Development Stage Completed | 2017 |
Development Status | Actively seeking support |
Clinical Trial? | Yes |
Impact | The study ia ongoing and no results have been analysed yet. |
Description | Bardet-Biedl Syndrome UK Annual Family Conference 2016 |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Patients, carers and/or patient groups |
Results and Impact | Over 200 delegates made up of Bardet-Biedl syndrome patients, their relatives and friends as well as healthcare professionals and scientists, attended the residential weekend. Beales chairs and presents a round of the latest medical and scientific advance relating to Bardet-Biedl syndrome patients. There is always a patient perspective and involved public debate. New and old patients alike value this occasion for its information content and social engagement. |
Year(s) Of Engagement Activity | Pre-2006,2006,2007,2008,2009,2010,2011,2012,2013,2014,2015,2016,2017 |
URL | http://www.lmbbs.org |
Description | CILIA2016 Amsterdam |
Form Of Engagement Activity | Participation in an activity, workshop or similar |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Patients, carers and/or patient groups |
Results and Impact | Organisation and support for the premier international conference of Cilia and disease held biennially. Beales chaired opening scientific session and assisted in patient facing activity and panel debate. |
Year(s) Of Engagement Activity | 2016 |
URL | http://events.embo.org/16-cilia/ |
Description | Gordon conference |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Gordon Conference (Dendrites: Molecules, Structure and Function) 26.03.17-31.04.17 |
Year(s) Of Engagement Activity | 2017 |
Description | Key Note Lecture: Cilia and Ciliopathies; 10 years on - at EMBO Cilia 2022 in Cologne, Germany (4th October 2022) |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Other audiences |
Results and Impact | Over 400 delegates attended in person (more than 100 online) this biennial international Cilia2022 conference in Cologne from 4-7th October 2022. The audience was made up of scientists, medics, patients and patient advisory groups and inductry representatives. The first day was devoted to ciliopathy patients and their organisations. The latest research was reported in talks and posters (300). There were also a number of early career power breakfast workshops reviewing everything from the latest cilia biology research to career advice. |
Year(s) Of Engagement Activity | 2022 |
URL | https://www.cilia2022.de |
Description | Opening talk at BBSUK family conference in Northampton, UK in September 10th, 2022 |
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 | This opening lecture at the annual patient conference provided an overview of the latest research/clinical advances with a focus on gene therapy for Bardet-Biedl syndrome. It was attended in hybrid format by over 200 patients, relatives, healthcare and education proessionals and industry reps. |
Year(s) Of Engagement Activity | 2022 |
URL | https://bbsuk.org.uk/news-events/bbs-uk-conference/ |
Description | Patient Support Group Patient Conference |
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 | 120 families attended the annual support group weekend conference of BBSUK in Northampton where they listened to a programme of talks on patient care and research. Later they participated in workshops providing further interaction with researchers and medical workers. Patients have been willing to take part in further studies and surveys. The support scoiety has also received further financial support from bodies such as the lottery to support these PPEs. |
Year(s) Of Engagement Activity | Pre-2006,2006,2007,2008,2009,2010,2011,2012,2013,2014,2015,2016 |
URL | http://www.lmbbs.org.uk |
Description | Presentations/abstracts at Volga Neuroscience conference 2016 |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Presented early stage research findings in the form of a poster and discussion groups. |
Year(s) Of Engagement Activity | 2016 |