Opportunities

This page is designed to help researchers and people looking for research opportunities find each other. We want to make it easier for people to make MND their area of focus and hope that the advancements that come out of these projects will make a positive difference to the MND community.

If you have a vacancy or are looking for a specific opportunity please contact us.

Opportunities in New Zealand

Small Project Grant | Neurological Foundation of NZ

Project Grants are the main avenue by which the Neurological Foundation sponsors research. Applicants can be scientifically or medically qualified, and the research can be clinical or biomedical.

Neurological Foundation Small Project Grants offer up to $15,000. Funds are usually for pilot or feasibility studies or a piece of equipment.

The application must be made on the Foundation’s form, and with the approval sent to the Foundation before the closing dates of April 1 and September 1 to douglas.ormrod@neurological.org.nz.

Note: Only one resubmission of a declined Small Project application will be considered. See advice to applicants for more details.

Click here for more detail

 

Project Grant | Neurological Foundation of NZ

Project Grants are the main avenue by which the Neurological Foundation sponsors research. Applicants are usually salaried by their institutions and a grant will typically cover salaries for technicians, scientists or nurses, plus working expenses. There are two rounds each year and the NF funds approximately 15 project grants annually.

Eligibility

Applicants can be scientifically or medically qualified, and the research can be clinical or biomedical.

Duration

Projects can be from one to three year’s duration.

How to Apply

The application must be made on the Foundation’s form, and include the Referee Nominations, Confidentiality, Ethical and Administrative Agreements (Sections 8 through 11), as well as the Excel budget sheet. It needs to be sent to the Foundation before the closing dates of April 1 and September 1 to douglas.ormrod@neurological.org.nz.

Note: Only one resubmission of a declined Project application will be considered. See advice to applicants for more details.

Click here for more detail

 

Senior Postdoctoral Fellowship | Neurological Foundation of NZ

The Senior Postdoctoral Fellowships provide two years of personal support for outstanding researchers while they establish themselves as independent investigators at an institution in New Zealand.

Eligibility

Candidates for the Senior Postdoctoral Fellowship will have submitted or been awarded a PhD within the eight years prior to the application closing date.  If a successful applicant is based overseas at the time of award, a single airfare to return to New Zealand will be included in the grant.

Duration

2 years

How to Apply

The closing dates for the Senior Postdoctoral Fellowship are 1 April and 1 September each year. The application must be made on the Foundation’s form and should be electronically submitted to the Research Manager before the closing dates. For further information see the Advice to Applicants document.

Click here for more detail

 

First Postdoctoral Fellowship | Neurological Foundation of NZ

The First Postdoctoral Fellowships provide two years of personal support for outstanding early career researchers so that they can complete their first post-doctoral fellowship under the close mentorship of an academic with a continuing position at an institution in New Zealand.

How to Apply

The closing dates are 1 April and 1 September each year. The application must be made on the Foundation’s form and should be electronically submitted to the Research Manager before the closing dates. For further information see the Advice to Applicants document.

Click here for more detail

 

O'Brien Clinical Fellowship | Neurological Foundation of NZ

This Fellowship will be awarded to a New Zealand registered non-medical health professional who is committed to a clinical research career with a major focus on treatment or care of those affected by brain disease or injury, including end of life care. It is intended to enhance their research skills and experience and thus contribute to improved patient outcomes in New Zealand.

Eligibility

Fellowship with be available to, but not limited to: Clinical Nurses, Clinical Psychologists, Clinical Trials Managers, Dieticians, Exercise Physiologists, Health Psychologists, Medical Laboratory Technologists, Medical Physicists, Neurophysiologists, Neuropsychologists, Occupational Therapists, Pharmacists, Physiotherapists, Radiographers, Research Nurses, Social Workers, Speech Language Therapists. Those unsure about eligibility should contact the Neurological Foundation Research Manager douglas.ormrod@neurological.org.nz.

How to Apply

The closing dates for this fellowship are 1 April and 1 September each year. The application must be made on the Foundation’s form and should be electronically submitted to the Research Manager before the closing dates. For further information see the Advice to Applicants document.

Click here for more detail

 

Conference and Training Course Grants | Neurological Foundation of NZ

These grants are intended to support international keynote speakers and early career researchers at neurology and neuroscience conferences in New Zealand, or facilitate early career researcher participation in advanced training courses in New Zealand or Australia.

What can be funded?

  • Support for early career researcher participation in conferences and advanced training courses, such as
    • Subsidised registration
    • Subsidised travel
    • Subsidised childcare
    • Prizes for conference presentations by early career researchers
  • Support for international keynote speaker participation, such as
    • Airfares
    • Domestic transfers
    • Accommodation

Maximum Value

$20,000

How to Apply

The closing dates are 1 April and 1 September each year.

  • Complete your application on the current version of the Conference Grant application form, available on the Foundation’s website
  • Submit your application form as a PDF, with supporting documents as separate PDFs, by the closing date
  • Supporting documentation:
    • Application data collection form, available on the Foundation’s website
    • Quotes for any keynote speaker travel and accommodation
  • Applicants will be advised of the outcome early in July or December
  • Successful applicants will be informed of the conditions of the grant and asked for their formal acceptance of the funding contract.
  • If you have any queries or doubts, please contact the Foundation’s Research Manager for advice. research@neurological.org.nz

Click here for more detail

 

Postgraduate Student Project - Building a Brain Machine Interface for song production | University of Auckland

Project Code: 10387354
University: Auckland
Faculty: Faculty of Medical and Health Sciences
Department: Anatomy
Main Supervisor: Dr M Fabiana Kubke
Application open date: 02 Oct 2017
Application deadline:
Enrolment information: NZ Citizens, NZ Permanent Residents, International

Introduction

Brain machine interfaces are used to extract the neural code associated with a behaviour, and use that code to drive a robotic device. In the context of human health, it allows people with motor disabilities to have their brains ‘talk’ directly to a device, such as a prosthetic arm.

What we are looking for in a successful applicant

The project involves understanding the models of auditory-vocal learning and vocal production, understanding how vocal motor commands are coded in ‘motor cortex’, how these can be analysed through machine learning algorithms, and animal behaviour analysis. Students with a background in biology, neuroscience, mathematics, engineering or bioengineering are encouraged to apply.

Objective

We are currently trying to exploit this technology to study how auditory and somatosensory information contribute to the production of speech. We are using a song bird as an animal model because the neural substrates and the process of learning song are similar to those of humans. To separate the processes that are involved in the ‘intention’ to sing from the act of singing itself, we are training birds to learn how to ‘sing’ (through a brain machine interface) using an audio speaker rather than through their vocal apparatus.

Information on how to enroll and apply 

Contact the project supervisor

Postgraduate Student Project - Neural Engineering | University of Auckland

Project Code: 1003
University: Auckland
Faculty: Faculty of Engineering
Department: Engineering Science
Main Supervisor: Associate Professor Charles Peter Unsworth
Application open date: 14 April 2014
Application deadline: 13 Feb 2022
Enrolment information: NZ Citizens, NZ Permanent Residents, International

Introduction

Our research is focussed on understanding the basic science of communication in the brain by combining both the fields of Cell Patterning  and ‘Multi-Electrode-Arrays’(MEAs) which are concerned with arrangement, control and stimulation/recording of cells on silicon chip. By applying novel laser cell steering and laser ablative microsurgery to highly organise and prune cell networks to a high fidelity. This has enabled our group to create a transformative chip technology allowing for the construction of precise large-scale regular grid networks of human neurons or astrocytes on chip, which are individually addressable, electrically and photonically, at the cellular level, such that communication can be mapped accurately from the single-cell level to large network scales. This platform technology will allow for the mapping of signal propagation in real neural networks from the single cell level through to large network scales. The novelty is that we organise the neural cells into regular grid arrays so that communication can be more effectively and repeatably studied.  We then apply nonlinear signal processing strategies such as Artificial Neural Networks and Machine Learning techniques, Wavelets and Chaos theory to extract/analyse/predict from the multi-channel data obtained from the chip work. We then build mathematical and computational models from the multi-channel data on chip. The technology would help provide insights into debilitating human neuropathologies such as epilepsy, stroke and hypoxic ischemia and provide a silicon chip platform technology to facilitate broader neuroscientific discovery

What we are looking for in a successful applicant

We are looking for a keen student.  Necessary skills for the above research objectives  are shown below:

1) Patterning neural cells on silicon chips – Although not necessary experience in cell culture and biomaterials would be an advantage

2) Development of substrate technology and controlling microelectronics – electronics and microelectronics necessary. Although not necessary experience in nanotechnology, biomaterials would be an advantage.

3) Development of new biomaterials & nanotubes for cell patterning – Although not necessary experience in nanotechnology, biomaterials would be an advantage.

4) Development of novel electrode designs on chip – electronics and microelectronics necessary. Although not necessary experience in nanotechnology, biomaterials would be an advantage.

Objective

Depending ion the project developed by the supervisor and student, the generic project objectives will fall into one of several categories outlined below.

1) Patterning neural cells on silicon chips

2) Development of substrate technology and controlling microelectronics

3) Development of new biomaterials & nanotubes for cell patterning

4) Development of novel electrode designs on chip

Click here to learn more

 

Funding Opportunity - Identify and Evaluate Potential Risk Factors for ALS | Agency for Toxic Substances and Disease Registry (ATSDR)

The Agency for Toxic Substances and Disease Registry (ATSDR) is pleased to announce publication of research grant Notice of Funding Opportunity RFA-TS-20-001 Identify and Evaluate Potential Risk Factors for Amyotrophic Lateral Sclerosis.

ATSDR is soliciting investigator initiated research that will further the understanding of potential risk factors for ALS, while supporting the ATSDR National ALS Registry’s mission. The National ALS Registry’s goals are to estimate the number of new ALS cases each year, estimate the number of people who have ALS at a specific point in time, better understand who gets ALS, and identify what contributing factors, including environmental, may affect ALS. ATSDR is seeking investigator-initiated research that will identify and evaluate risk factors contributing to ALS, with preferred focus in this Notice of Funding Opportunity on factors related to military service, contact sports, traumatic brain injury, neuroinflammation and infectious agents.

ATSDR is especially interested in innovative research applications that propose to conduct an epidemiological investigation using the ATSDR National ALS Registry and/or using a third party ALS registry on risk factors related to military service, contact sports, traumatic brain injury, neuroinflammation and infectious agents. Examples of ALS registry research previously funded by ATSDR can be found at https://www.cdc.gov/als/ALSExternalResearchfundedbyRegistry.html.

 

Deadline

Applications are due to CDC/ATSDR by March 4, 2020 at 5:00PM EST.

RFA-TS-20-001 may be viewed, and applications submitted, at: https://www.grants.gov/web/grants/view-opportunity.html?oppId=322433.

Eligibility

Eligibility for RFA-TS-20-001 is open to both United States and Foreign Organization applicant institutions, as specified in RFA-TS-20-001. Applicants are encouraged to carefully review all RFA-TS-20-001 Eligibility requirements and contact Dr. Marcienne Wright (lxv8@cdc.gov) with questions regarding eligibility.   

Click here for more details

International Opportunities

MSc by Research Programme: ADP-ribosylation in the aging nervous system | University of Dundee

Project Description

ADP-ribosylation is a fundamental posttranslational modification where ADP-ribose is linked on to target proteins by ADP-ribose transferases and removed by the ADP-ribose hydrolases. Emerging data implicate ADP-ribosylation in maintaining the health of the nervous system; mutations in the genes that encode the enzymes that reverse ADP-ribosylation cause neurodegenerative disease in humans and pharmacological inhibition of the ADP-ribose transferases is therapeutically beneficial in various cellular and animal models of human neurodegenerative diseases such as stroke, Parkinson’s disease and motor neuron disease (reviewed in 1). This suggests that ADP-ribosylation regulates key proteins involved in brain aging, however what these proteins are and how they are regulated by ADP-ribosylation is unknown. To elucidate the proteins and underlying mechanisms that regulate brain aging, the student will use an interdisciplinary approach that combines genetics of the fruit fly with molecular and cellular approaches to determine the role of nuclear ADP-ribosylation in the aging and diseased nervous system of the fly (AIM1) and in human iPSC-derived neurons (AIM2). At the end of this project the student will have identified novel aspects of ADP-ribosylation in the normal and diseased nervous system.

This course allows you to work alongside our world renowned experts from the School of Life Sciences and gain a ’real research’ experience. You will have the opportunity to select a research project from a variety of thematic areas of research.

You will be part of our collaborative working environment and have access to outstanding shared facilities such as microscopy and proteomics. Throughout your year, you will develop an advanced level of knowledge on your topic of interest as well as the ability to perform independent research in the topic area. Alongside basic science training in experimental design, data handling and research ethics, we will help you to develop skills in critical assessment and communication. This will be supported by workshops in scientific writing, presentation skills, ethics, laboratory safety, statistics, public engagement and optional applied bioinformatics.

The period of study is one year full-time or two years part-time research, which includes two months to write up the thesis.

Deadline

July 16, 2020

Please apply via the UCAS postgraduate application form: https://digital.ucas.com/courses/details?coursePrimaryId=c735d826-42b6-ca1f-50db-2a3ac6f68718

Click here for more details.

PhD Project: Metabolic dysfunction in MND/ALS | University of Queensland, Australia

Project Description

Motor Neuron Disease/Amyotrophic Lateral Sclerosis (MND/ALS) is a neurodegenerative disease that is characterised by the degeneration of both upper and lower alpha motor neurons. The irreversible loss of neurons in the brain and spinal cord results in progressive skeletal muscle paralysis and death within 2-5 years of diagnosis. There is no known cure for the disease, and treatments are of limited benefit. In the absence of a cure for MND/ALS, there is a pressing need to lessen the severity of symptoms associated with, and to slow the progression of disease, whilst enhancing quality of life.

While the fundamental mechanisms that underlie the development of MND/ALS remains unknown, recent studies suggest that defective regulation of energy homeostasis may exacerbate the degenerative process throughout the course of disease. In the last 7 years, our team has made novel observations of metabolic dysfunction and altered metabolic flexibility in mouse models of MND, and paradigm-shifting discoveries that for the first time, highlight the impact of increased energy use (hypermetabolism) in patients with MND on disease progression and prognosis. In this time, our team have also successfully generated induced pluripotent stem cell (iPSC)-derived motor neurons (including CRISPR-Cas9 TDP-43 iPSCs with isogenic controls), and to our knowledge the only directly reprogrammed motor neurons from MMD patients in Australia.

All PhD projects fall under a broader research program that investigates how altered glucose and fatty acid metabolism contributes to the progression of MND/ALS. Projects span the clinical and basic research settings, and involve working with patients living with MND, or mouse and human-derived models of MND. Projects focus on identifying the mechanisms that cause metabolic dysfunction in MND, and identifying treatments to alleviate metabolic perturbations.

Contact Dr Shyuan Ngo for more information

Click here for more details.

PhD Project: Longitudinal study on the relationship of the gut microbiome to disease progression in the UK MND population | University of Sheffield

Project Description

Motor neurone disease (MND) is a devastating neurodegenerative condition characterised by progressive deterioration of motor functions until death normally results from respiratory failure. There is no cure for MND, so treatment is focussed on management of associated symptoms such as depression, hyper-salivation and pain resulting from stiffness/cramping. Patient survival is often quoted as being on average 2-3 years post-diagnosis, but there is huge variation in individual outcomes. Whilst genomic studies have revealed a number of mutations associated with the condition, the reasons for such widely varying prognostic outcomes are still poorly understood.

Microbiomics is the study of the collective genomes of microscopic organisms living within and upon individuals, and the roles these inhabitants play in the biology of the host. Recently, actions of microbes have been implicated in modifying a number of conditions, including neurodegenerative diseases such as Parkinson’s and Alzheimer’s. To date, little work has been done investigating the impact of the microbiome on MND.

The aim of this project is to characterise the microbiomes of newly-diagnosed MND patients, and investigate any link between the microbial groups represented and rate of disease progression. With the help of a well-established clinical research team, the objectives are:
– identify any global differences that exist between controls, confirmed MND and disease controls
– within the MND group, investigate any microbiome differences between slow and fast progressors
– if appropriate, infer functional significance of any differences and attempt to find evidence in support of these hypotheses

This PhD project provides an excellent opportunity to undertake groundbreaking research in a fast-developing area of science. The successful candidate will benefit from working within a highly successful research group in a world leading centre for research into neurodegenerative diseases.

How to Apply

Interested candidates should in the first instance contact (Prof Chris McDermott, c.j.mcdermott@sheffield.ac.uk)

Please complete a University Postgraduate Research Application form available here: www.shef.ac.uk/postgraduate/research/apply

Deadline

Applications will be reviewed until a suitable candidate is appointed. 

Eligibility

Candidates must have a first or upper second class honors degree or significant research experience. Either experience in a molecular biology laboratory or of bioinformatics analysis of large genomic datasets is essential. Candidates must be fluent in written and spoken English.

Funding

This project is open to self-funded students only.

Click here for more details.

Non-Clinical Research Fellowship | MND Association

The MND Association is proud to announce our newly launched non-clinical fellowships in MND. These fellowships will aim to foster and nurture post-doctoral researchers into the MND research leaders of tomorrow.

The fellowships will be awarded at two levels, depending on the experience of the applicant: Junior Non-Clinical fellowships or Senior Non-Clinical fellowships.

Deadline

The deadline date for receipt of summary applications is 1 May 2020This round will open on 6 March 2020

Please read our GuidelinesTerms and Conditions and our Guide to Completing the Online Summary Application Form. It is also recommended that you read the MND Association Research Strategy and Research Governance Overview

Duration

Grants will be offered for up to three or four years duration.

  • Junior Non-Clinical – awards will be offered for 2 – 3 years
  • Senior Non-Clinical – awards will be offered for 3 – 4 years

Eligibility

Fellowship awards may only be held at an institute in the UK and Ireland. At the time of application the prospective fellow may be based elsewhere

  • Junior Non-Clinical – applicants must have 2 – 5 years post-doctoral experience at the time of commencement of the award. Exceptional final year PhD students may apply but should consult the Association prior to submitting a summary application.
  • Senior Non-Clinical – applicants must have 4 – 10 years post-doctoral experience at the time of commencement of the award.

Assessment and Budget

Please see our guidelines for more information on assessment criteria and budget information.

Click here for more details.

PhD Project: TDP-43 The Key protein for finding a cure for Motor Neurone Disease | University of Liverpool

Project Description

Motor neurone disease is a progressive, fatal neurological disorder with no known cure. It is characterised by selective loss of motor neurons in the spinal cord and cortex. Over 90% of MND (ALS) cases, both sporadic and familial, feature TDP-43-positive inclusions in the cytoplasm of affected neurons. Most MND patients die within 3-10 years due to respiratory failure. Understanding the molecular mechanism of MND and finding a therapeutic solution to remedy the disease-causing properties is our goal. 

TAR DNA binding protein-43 (TDP-43), has multiple functions in transcriptional repression, pre-mRNA splicing and translational regulation. Its ability to bind UG-rich RNA is very important for normal localisation of TDP-43 in the nucleoplasm. Cytoplasmic mis-localisation and elevated half-life are characteristics of mutant TDP-43. ALS-associated TDP-43 mutations in the central nucleic acid binding RRM domains lead to increased thermal stability and elevated half-life in a TDP-43 disease cell model. Full length TDP-43 has been purified at Liverpool recently enabling SAXS measurements that hold promise for structure determination of full-length TDP-43. This is a major breakthrough in understanding the molecular mechanism of MND and finding a therapeutic solution to remedy the disease-causing properties of this critical protein. 

The student will build on this success in a multidisciplinary programme using molecular biology, protein chemistry, bioinformatics, protein crystallography and Small angle X-ray scattering. Required ’wet-lab’ facilities for the project (e.g. cloning, expression and purification of proteins) are available at our institution. Additionally, UoL has a combined SAXS/MX facility on a super bright in-house X-ray generator FR-E+ and a crystallization robot. 

Deadline

Applications will be reviewed until a suitable candidate is appointed. 

Eligibility

Candidates must have, or expect to gain, a first or strong upper second class degree (or equivalent) in a relevant discipline. 

Funding

The project is open to both UK and International students with their own funding/scholarship. Potential applicants are encouraged to contact the Principal Supervisor directly to discuss their application and the project. 

Assistance will be given to those who are applying to international funding schemes. 
The successful applicant will be expected to provide the funding for tuition fees and living expenses as well as research costs of £3000 per year. 
A tuition fee bursary may be available for well qualified and motivated applicants with a First class degree. 

Click here for more details.

PhD Project: SOD1 The Key protein for finding a cure for familial Motor Neurone Disease | University of Liverpool

Project Description

Motor neurone disease is a progressive, fatal neurological disorder with no known cure. It is characterised by selective loss of motor neurons in the spinal cord and cortex. Over 90% of MND (ALS) cases, both sporadic and familial, feature TDP-43-positive inclusions in the cytoplasm of affected neurons. Most MND patients die within 3-10 years due to respiratory failure. Understanding the molecular mechanism of MND and finding a therapeutic solution to remedy the disease-causing properties is our goal. 

Cu/Zn binding superoxide dismutase is a homo-dimeric protein with an intra-subunit disulphide bond. This protein is responsible for converting harmful free superoxide radicals to hydrogen peroxide and oxygen in the body. Extensive structural studies have established that disease-causing mutations in SOD1 reduce the ability of protein to fold, bind metal cofactors and form the disulphide bond. As a result, mutant SOD1 is prone to misfolding and aggregation. Global efforts to correct this ‘gain-of-function’ have led to identification of a variety of ‘ligand-binding pockets’ that are suitable for drug development. Ebselen, an organoselenium compound with strong antioxidant activity, has been shown to rescue SOD1 from aggregation, especially in the A4V mutant. This discovery is the starting point for guiding discovery of the next generation of compounds aimed at stabilizing SOD1 mutants. 

The student will build on this success in a multidisciplinary programme using molecular biology, protein chemistry, protein crystallography and human cell line assays. Required ’wet-lab’ facilities for the project (e.g. cloning, expression and purification of proteins) are available at our institution. Additionally, UoL has a combined SAXS/MX facility on a super bright in-house X-ray generator FR-E+ and a crystallization robot. 

Deadline

Applications will be reviewed until a suitable candidate is appointed. 

Eligibility

Candidates must have, or expect to gain, a first or strong upper second class degree (or equivalent) in a relevant discipline. 

Funding

The project is open to both UK and International students with their own funding/scholarship. Potential applicants are encouraged to contact the Principal Supervisor directly to discuss their application and the project. 

Assistance will be given to those who are applying to international funding schemes. 

The successful applicant will be expected to provide the funding for tuition fees and living expenses as well as research costs of £3000 per year. 

A tuition fee bursary may be available for well qualified and motivated applicants with First class degree. 

Click here for more details.

PhD Project: Understanding the Electric Field in Electrical Stimulation for biomedical application | University of Reading

Project Description

Functional electrical stimulation (FES) is a treatment that applies small electrical charges to a muscle that has become paralysed or weakened, due to damage in your brain or spinal cord. The electrical charge stimulates the muscle to make its usual movement. FES is a technique can help with swallowing, hand and arm function, and even breathing problems for pulmonary disease patients and for stroke patients. It has a number of potential future therapies uses to retrain voluntary motor functions such as grasping, reaching and walking. 

FES can be applied in a number of ways: transcutaneous, using electrodes which are placed on the skin; percutaneous, with electrodes inserted; through the skin to make direct contact with the motor nerves; or sub-cutaneous, where the stimulator is implanted and electrodes are attached either to the motor nerves directly, or to the nerve roots at the point where they emerge from the base of the spine. This method stimulates mainly the nerve fibres innervating of the muscle. 
Current amplitude and duration of the pulsewidth describe the intensity (charge) which determines if a specific neuron is recruited. With low intensity pulses large low-threshold neurons and neurons close to the electrodes will be recruited at first. Smaller neurons with higher threshold and neurons located further away from the electrodes will be recruited with increasing charge per pulse. An electrical field is generated between the electrodes however very little is known of how the electric field propagate in term of magnitude and direction. 

This PhD study will aim to answer this question by developing a model from the Maxwell equations and finite element methods of the electric field through the material (Skin and Muscle). A characterisation is needed to understand the level of penetration with respect to the electrodes sizes and polarity separation. An application will be to determine what configuration of transcutaneous stimulation electrodes gives a focal electrical field similar to the one obtained with epidural electrode stimulation. 

Deadline

Applications will be reviewed until a suitable candidate is appointed. 

Eligibility

Bachelors or Masters Degree (at least 2.1 or equivalent) with Mathematics, Numerical Methods and Electromagnetism as major subjects. Experience in modelling and programming in Matlab/Simulink techniques is highly desirable

Funding

There is no funding attached to this project. 

Click here for more details.

PhD Project: Interactome visualisation of ALS using virtual reality | Ulster University

Project Description

Visualising high dimensional data is challenging and a significant constraint is the need to render in 2D for the screen or page. With the arrival of virtual reality (VR) and augmented reality (AR) comes the opportunity to explore and share biomedical data in new ways. VR/AR can extend 2D analyses intuitively to higher dimensions, providing richer interaction with data. Critically, they also provide us with new ways to explore the topological structure of data, particularly valuable for network graphs of arcs and vertices. 2D renders of network graphs are inherently ambiguous due to the crossing of arcs, something that grows polynomially with graph size, making large graphs unintelligible. 3D rendering eliminates this problem completely.

Network graphs are routinely used to depict the Interactome: the networks of interactions that drive physiological function. We will develop the first VR tools to facilitate 3D rendering, navigation and manipulation of the pathways of cell, gene, protein and small molecule interactions that drive the interactome. The tools will be enable the interactome to be embedded in other renderings, such as the spatial structure of cells, tissues, organs or organisms and can be reused across diseases. As an exemplar, the tools will be first applied to disrupted cellular processes in the motor neuron disorder, Amyotrophic Lateral Sclerosis (ALS). By cross-relating the structure of the human molecular interaction network against genomic data, we have previously identified clusters of interacting genes with newly identified mutations that we believe are involved in the development of ALS. 3-D modelling will greatly help us to understand their role in disease development.

Pathways of the interactome are routinely described using the Systems Biology Graphical Notation (SBGN), an open, community-driven 2D mapping standard [1] adopted by many software tools [2]. We propose to develop it for 3D visualisation. SBGN3D will exploit the Google Cardboard framework [3], facilitating visualisation using cheap viewers and phone apps, or as interactive models embedded in 2D digital content.

Aim 1: Translation of SBGN from 2D to 3D
* Develop 3D glyphs corresponding to 2D glyphs.
* Define compartment structure and text orientation.
* Extend current SBGN file formats to SBGN3D.
Aim 2: Development of SBGN3D viewer in Google Cardboard
* Develop import/export libraries for SBGN3D files.
* Build navigation interface for controlling SBGN3D maps.
* Export interface as phone app.
Aim 3: ALS application.
* Curate new ALS interactome maps to SBGN3D.
* Identify topological structure of ALS interactome.
* Export ALS SBGN3D maps to public repositories for reuse.

This project will yield:-
* The first schema for 3D mapping of the pathways of the interactome.
* The first toolset for viewing 3D pathway structures in VR environments.
* A richer understanding of ALS interactome topology VR schema/tools are the first step to AR modelling, the goal of follow up work.

Supervisors
* Dr Steven Watterson
• Prof Damien Coyle
• Dr William Duddy

Deadline

7 February 2020

Eligibility

Desirable Criteria
If the University receives a large number of applicants for the project, the following desirable criteria may be applied to shortlist applicants for interview.
• Demonstrable programming skills and mathematical ability.
• Familiarity with biomedical science is desirable, but not essential.
• Completion of Masters at a level equivalent to commendation or distinction at Ulster is desirable, but not essential.
• A background in computer science, mathematics, physics, bioinformatics, biomedical science, stratified/personalised medicine, biomedical engineering, or another quantitative science.

Essential criteria
• To hold, or expect to achieve by 15 August, an Upper Second Class Honours (2:1) Degree or equivalent from a UK institution (or overseas award deemed to be equivalent via UK NARIC) in a related or cognate field.
• Sound understanding of subject area as evidenced by a comprehensive research proposal

Funding

The University offers awards to support PhD study and applications are invited from UK, EU and overseas applicants. View Website for details of funding.

Click here for more details.

PhD Project: The potential of elevating Epac2 to modulate glial activation and promote motor neuron regeneration in ALS | Aberdeen University

Project Description

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterised by the selective degeneration and death of motor neurons. Despite several decades of intensive research it remains incurable, and its underlying disease mechanisms are still poorly understood. Medical treatment is mostly limited to alleviation of symptoms and palliative care. It is clear that novel approaches are required to confer effective treatments to this debilitating disease. In addition to motor neuron involvement, recent evidence suggests that there is a complex interplay between motor neurons and neighbouring non-neuronal cells in ALS, such as astrocytes, which have been shown to be critically involved in the survival and demise of motor neurons. Recent work from Dr Huang’s lab has shown that elevation of the second messenger Epac2 not only promotes cortical neuron outgrowth in vitro and enhances axonal regrowth in an ex vivo model of spinal cord injury, but also attenuates in vitro and ex vivo astrocyte activation. Hence, the proposed project will explore the potential of Epac2 activation to modulate astrocyte activation and thereby promote motor neuron survival as a novel approach to treating ALS.

The project will exploit state-of-the-art human cell co-culture techniques, with human induced pluripotent stem cells (iPSCs) from ALS patients, astrocytes from human bone marrow-derived mesenchymal stem cells (MSCs), microfluidic chip culture systems which allow the tripartite divided co-culture of motor neurons, muscle cells and astrocytes, pharmacological and genetic elevation of Epac2, and flow cytometry.

Dr Huang has an internationally recognised track record in studying neuroprotection for traumatic spinal cord injury and peripheral nerve injury (Brain 2007,130:3004-19; Exp Neurol 2013,239:13-27; J Neurosci 2012,32:563-71), as well as in using novel biomaterials and molecules to promote spinal cord repair (Biomaterials 2012,33:59-71; Scientific Reports 2017,7:1-10; J Neurosci 2019,39:8330-46). Dr Bewick is a world-leading expert in neuromuscular research, with >30 years’ experience. His interests centre on understanding how appropriate nerve-muscle connections are established and maintained, both in motor and sensory systems, and has published significantly in this area (Science, 255:200-203; Neuron, 9:805-813; J Neurosci, 23:9340-9348; PNAS, 107:13515-13519; Inter J Mol Sci, 19:1936; Nature Comm, 7:1-15; J Anatomy, 227:194-213; Phil Trans R Soc B, 373:20170327).

Deadline

Friday, March 13, 2020

APPLICATION PROCEDURE:
This project is advertised in relation to the research areas of MEDICAL SCIENCES. Formal applications can be completed online: https://www.abdn.ac.uk/pgap/login.php. You should apply for Degree of Doctor of Philosophy in Medical Sciences, to ensure that your application is passed to the correct person for processing.

NOTE CLEARLY THE NAME OF THE SUPERVISOR AND EXACT PROJECT TITLE ON THE APPLICATION FORM. Applicants are limited to applying for a maximum of 3 applications for funded projects. Any further applications received will be automatically withdrawn.

Eligibility

Candidates should have (or expect to achieve) a minimum of a First Class Honours degree in a relevant subject. Applicants with a minimum of a 2:1 Honours degree may be considered provided they have a Distinction at Masters level.

Funding

This project is funded by a University of Aberdeen Elphinstone Scholarship. An Elphinstone Scholarship covers the cost of tuition fees only, whether home, EU or overseas.

For details of fees: View Website

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PhD Project: Characterisation of the biological processes affected by a new ALS gene, CCNF, in motor neuron proteostasis | Macquarie University

Project Description

This project will investigate the signalling pathways and biological processes affected by a new ALS/FTD gene discovered by our researchers at the Macquarie University Motor Neurone Disease (MND) Centre. Mutations in this new ALS/FTD gene, CCNF, which encodes the protein Cyclin F, is involved in maintaining cellular health by tagging unwanted proteins (ubiquitylation) for breakdown and recycling within the cell. Mutant versions of Cyclin F, found in some ALS patients, are defective in that they lack the necessary features needed to regulate proper function, which ultimately leads to improper function, accumulation of proteins, and effects on downstream signalling pathways and biological processes. This project will use quantitative proteomics to identify changes to the phosphoproteome and ubiquitome, and validate these biological changes in primary neurons and/or iPS-derived motor neurons.

Hypothesis 1: Only six substrates of cyclin F have been characterised to date, all of which are involved with cell cycle processes. We predict that cyclin F in neurons (post-mitotic) plays a vastly different role in maintaining proteostasis.

Hypothesis 2: We predict that wild-type cyclin F and ALS-causing mutant cyclin F bind to different protein substrates to direct them for degradation by the ubiquitin-proteasome system.

Hypothesis 3: The different forms of cyclin F cause target common and unique signalling pathways and biological processes downstream, and these targets will be relevant to the biology of motor neurons.

 

Aim 1: Establish inducible stable neuronal cell lines expressing cyclin F and examine neuronal markers for dividing and differentiated status.

Aim 2: Identify protein interacting partners of cyclin F from neuronal cells by immunprecipitation and liquid chromatography mass spectrometry distinguishing between binding partner and substrate.

Aim 3: Characterise the phosphoproteome and ubiquitome affected by the different forms of cyclin F to identify common and unique signalling pathways. These pathways will be further validated in primary neurons and/or iPS-derived motor neurons using standard biochemistry techniques.

Enquires

Professor Roger Chung, roger.chung@mq.edu.au

Dr Marco Morsch, marco.morsch@mq.edu.au

Dr Albert Lee, albert.lee@mq.edu.au

Dr Bingyang Shi, bingyang.shi@mq.edu.au

Click here for more details.

PhD Project: Does the transfer of ALS protein aggregates between motor neurons trigger neurodegeneration? | Macquarie University

Project Description

Accumulation of proteins into insoluble aggregates in neurons and glia is now recognized as a common pathological hallmark of many neurodegenerative diseases (e.g. in Alzheimer’s, and Parkinson’s disease). In Amyotrophic Lateral Sclerosis (ALS), the intracellular accumulation of proteins in neurons is also well established. Importantly, clinical evidence indicates the transmissibility or spread of these aggregates in patients from a focal onset to other regions over time. This spread of aggregation is beginning to substantiate but is entirely limited to studies using cultured nerve cells (in-vitro studies).

This project will investigate this potential pathogenic mechanism using an animal model (in-vivo). Our team has established comprehensive preliminary data that establishes the release, survival and spread of aggregated ALS-proteins from neurons into other cells in the zebrafish spinal cord. We will use an innovative series of experiments to selectively trigger the death of a single neuron containing these aggregates and investigate their fate after being   released, and if they are incorporated into neighbouring cells.

Hypothesis

This project will investigate the hypothesis that ALS proteins have propagating characteristics, such that insoluble aggregates can transfer between cells and seed aggregation and degeneration in non-affected cells.

Aim 1: Observe the fate of TDP-43 and SOD1 released from a single dying motor neuron and the impact upon the viability of surrounding motor neurons.

Aim 2: Assess aggregation of ALS proteins released from dying motor neurons in vivo

Aim 3: Histological verification of the intercellular transfer of ALS proteins

Outcome

We predict that we will be able to track ALS aggregates and visualize their disintegration or survival in the living organism. This will provide important insights into the pathogenic mechanisms underlying ALS-mediated neurodegeneration

Enquires

Professor Roger Chung, roger.chung@mq.edu.au

Dr Marco Morsch, marco.morsch@mq.edu.au

Dr Albert Lee, albert.lee@mq.edu.au

Dr Bingyang Shi, bingyang.shi@mq.edu.au

Click here for more details.

PhD Project: Investigating the regulatory and functional roles of Cyclin F in the development of ALS | Macquarie University

Project Description

This project will investigate the cellular and functional roles of a new ALS/FTD gene discovered by researchers at the Macquarie University Motor Neurone Disease (MND) Centre. Mutations in this new ALS/FTD gene, CCNF, which encodes the protein Cyclin F, is involved in maintaining cellular health by tagging unwanted proteins (ubiquitylation) for breakdown and recycling within the cell. Mutant versions of Cyclin F, found in some ALS patients, are defective in that they lack the necessary features needed to regulate proper function, which ultimately leads to impaired ubiquitylation and accumulation of proteins. This project will systemically investigate the regulatory and functional role of each mapped phosphorylation site of Cyclin F focusing on those that have been mapped to ALS mutations, and determine whether upstream kinases can be modulated to promote survival responses in ALS cell models. Moreover, this project will investigate the role Cyclin F phosphorylation on its nuclear and cytoplasmic translocation and degradation.

Hypothesis 1: Cyclin F contains >80 predicted phosphorylation sites some of which are hypothesised to be involved in nuclear/cytoplasmic shuttling.

Hypothesis 2: What is the effect of mutations to cyclin F to its E3 ligase activity? And consequently how does this affect the ubiquitylation of substrates and formation of protein inclusions

Hypothesis 3: Does cyclin F (and its ALS mutants) influence upstream kinases through a feedback

Aim 1: Determine whether phosphorylation plays a role in nuclear/cytoplasmic shuttling through dephosphorylation treatments and artificial cyclin F constructs.

Aim 2: Measure the E3 ligase activity using our customised ELISA and other biochemical techniques and determine to effect does mutated versions of cyclin F influence protein inclusion formation.

Aim 3: Generate phosphomimetic versions of cyclin F and monitor the effect of upstream kinase activity that are predicted to phosphorylate cyclin F.

Enquires

Professor Roger Chung, roger.chung@mq.edu.au

Dr Marco Morsch, marco.morsch@mq.edu.au

Dr Albert Lee, albert.lee@mq.edu.au

Dr Bingyang Shi, bingyang.shi@mq.edu.au

Click here for more details.

PhD Project: Why are neurons selectively vulnerable in MND? Optogentic approaches to understand the role of oxidative stress in ALS | Macquarie University

Project Description

Motor neurons are selectively vulnerable to oxidative stress in comparison to other neurons, and mutations in the anti-oxidant enzyme SOD1 are associated with 20% of all inherited cases of ALS. We have generated experimental zebrafish models that allow us to selectively induce oxidative stress within a single spinal motor neuron, in the presence or absence of co-expression of ALS genes (SOD1, TDP-43).

The aim of this project is to investigate how sub-lethal and lethal levels of oxidative stress, delivered specifically to motor neuron subpopulations, contribute to the etiology of ALS. Our newly designed transgenic zebrafish allow us to induce different levels of oxidative stress in single spinal motor neurons and to visualize real-time responses of both the individually stressed neurons and surrounding cells such as neurons, microglia and astrocytes.

Our approach will determine the cellular mechanisms of stress induced motor neuron degeneration using a range of different techniques, including molecular biology, transgenic zebrafish lines, optogenetic techniques and confocal live-imaging protocols.

Hypothesis

This project will demonstrate if oxidative stress is a primary instigator of the disease (e.g. if motor neurons in ALS patients are more vulnerable to oxidative stress than healthy motor neurons), and if oxidative stress can trigger secondary neurodegeneration in surrounding MNs.

Aims

1.Compare the susceptibility of individual spinal motor neurons expressing either ALS-wildtype or ALS-mutant genes to experimentally induced oxidative stress

2.  Investigate the effect of oxidative stress induced degeneration of a single spinal MN upon surrounding motor neurons that express either ALS-wildtype or ALS-mutant genes

Outcome

This approach will provide compelling in vivo evidence that oxidative stress could be involved in the propagation of neurodegeneration in ALS, and will provide critical insights into potential therapeutic interventions that could halt the progression of neurodegeneration in ALS.

Enquires

Professor Roger Chung, roger.chung@mq.edu.au

Dr Marco Morsch, marco.morsch@mq.edu.au

Dr Albert Lee, albert.lee@mq.edu.au

Dr Bingyang Shi, bingyang.shi@mq.edu.au

Click here for more details.

PhD Project: New approaches to plasma biomarker studies in MND | Macquarie University

Project Description

There is an urgent need to identify a series of biomarkers that can be used to improve the speed of diagnosis, and predict more accurately prognosis and other clinical parameters in MND.  This project will utilize a new proteomic technology to identify potential protein biomarkers in plasma samples from MND patients. This will include identification of maps of proteins that can be used to distinguish between different clinical parameters, and evaluation of specific proteins biomarkers.  We predict that these biomarkers may be useful in future for improving diagnostic and prognostic clinical evaluations.  These protein biomarkers may identify also novel biological processes associated with disease pathogenesis, and this may lead to new insight into the causes of MND.

Importantly, this biomarker study will be undertaken using samples from two unique patient cohorts; i) identical twins with disease discordance (one with disease, the other without), and ii) multi-generational families with disease discordance.  This allows us to screen for disease-associated biomarkers with reduced variation across samples (ie: less genetic variation).  Identified biomarkers will subsequently be validated in a cohort of sporadic MND patients.  This provides a systematic approach towards identifying robust biomarkers of disease in MND.

Hypothesis

We hypothesize that low-abundance plasma biomarkers are present that will be informative of disease pathogenesis.  We will use a new proteomic technique to screen for the presence of robust protein biomarkers that can be used in future for early diagnosis of MND and for tracking the prognosis of patients. New biomarkers may also add to our understanding of disease pathology and thereby could possibly highlight new avenues for research towards future therapies.

Aims

1. Unbiased proteomic profiling of plasma from cohorts of familial MND patients displaying disease discordance.

2. Validation of potential proteomic biomarkers in a cohort of sporadic MND patients.

Outcome

We ultimately expect that a “toolbox” of biomarker parameters will be required to adequately address the clinical requirements for improved measures for diagnosis, prognosis and evaluation of disease progression and response to current and future therapeutic strategies.  The proteomic biomarkers identified through this project may become an important component of such a future “toolbox”, together with other existing biomarkers such as clinical examinations, genetic testing, electrophysiological recording and neuroimaging.  Such a biomarker toolbox is likely to be critical in improving the design of future clinical trials, as stratification of patients into subgroups and more sensitive predictors of disease progression and severity are essential for improving recruitment and analysis in clinical trials.

Enquires

Professor Roger Chung, roger.chung@mq.edu.au

Dr Marco Morsch, marco.morsch@mq.edu.au

Dr Albert Lee, albert.lee@mq.edu.au

Dr Bingyang Shi, bingyang.shi@mq.edu.au

Click here for more details.

PhD Project: Identifying regulators of the molecular pathologies associated with motor neuron disease and frontotemporal dementia | University of Queensland

Project Description

he associated PhD project aims to identify genes and proteins regulating cellular and molecular processes involved in motor neuron disease (MND) and frontotemporal dementia (FTD). Our laboratory specialises in understanding mechanisms of cellular stress, protein aggregation, and neuronal degeneration in the central nervous system of people living with MND and FTD. We are also focused on identifying and validating novel therapeutic strategies for these diseases by conducting preclinical testing in vivo. You will join an ambitious, inclusive, and collaborative group at the Queensland Brain Institute with access to world-class facilities and support to build your research career (https://walkerneurolab.org/).

There will be many opportunities to learn advanced techniques including, lentivirus production, CRISPR knockout and activation, in vivo preclinical testing of therapeutic strategies, high-end microscopy, and next generation sequencing. The PhD project is not prescriptive and will be developed in conjunction with the selected student depending on their research interests and their existing research skills.

Eligibility

First class Honours or Masters with an intensive research component in cell biology, biochemistry, and neuroscience is required.

*The successful candidate must commence by Research Quarter 4, 2020. You should apply at least 3 months prior to the research quarter commencement date. International applicants may need to apply much earlier for visa reasons. 

Contacts

Dr Rebecca San Gil

r.sangil@uq.edu.au

and

Dr Adam Walker

adam.walker@uq.edu.au

 

Click here for more details.

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