2017 HOPE Selwyn Scholarships
The cornerstone funding from the Selwyn Foundation plus additional grants from Family Trusts have enabled us to extend our grants to a record number of ten scholarships:
Philip Sanders – The University of Auckland
Measuring Plasticity and Ageing through Multisensory Integration
A decline in sensory abilities (such as loss of hearing and sight) usually accompanies ageing. The brain receives input signals from various sensory modalities (e.g. sight, sound, touch) and combines these into a single percept through processes collectively known as multisensory integration (MSI). People become more dependent on these processes as they age and the information from individual modalities degrades.
Cognitive decline, a precursor to dementia is also a symptom that can accompany ageing. Fortunately, neuroscience research into the brain’s ability to change (plasticity) may hold the key to early detection of sensory and cognitive decline. A greater understanding of brain plasticity in the elderly is also key to developing methods to enhance recovery and compensatory processes; we know that the brain becomes less plastic as we age.
This research aims to develop a simple objective measurement of plasticity in sensory brain regions, which could be used to identify early signs of cognitive decline. We will also examine the effects of multisensory processing on enhancing plasticity and perception in the elderly. We will be using electroencephalography (EEG), a non-invasive neuroimaging technique, to examine brain responses to sensory stimuli before and after the induction of plasticity with uni- and multisensory stimuli.
Renita Martis – The University of Auckland
The role of the cystine/glutamate antiporter in the eye: a target for delaying age related eye diseases?
Age-related eye disease such as cataract, glaucoma and age-related macular degeneration are responsible for more than 70% of blindness in New Zealanders over the age of 50 years and are associated with increased levels of oxidative stress. The tissues of the eye are constantly exposed to high levels of oxidative stress due to ultraviolet radiation from sunlight and are therefore particularly susceptible to oxidative damage.
The use of antioxidants to reduce oxidative stress has been promoted as therapies to prevent age related eye diseases however; studies have shown inconsistent results due to a lack of understanding on the molecular pathways involved in minimising oxidative stress in the tissues of the eye.
To date, no one has examined the roles of cystine/glutamate antiporter (CGAP) in the eye and hence for my PhD project I will investigate the roles of CGAP in the eye and determine whether it represents a pathway that could be targeted to minimise oxidative stress. Collectively, I believe that the findings from my PhD project will lead to new strategies for enhancing antioxidant levels and restoring redox balance in the eye thus delaying the onset of age related eye diseases for which currently no preventative treatments exist.
Kay Shannon - Auckland University of Technology.
The transition of Whare Aroha Care residents to a new dementia-friendly village.
Rotorua Continuing Care Trust operate an aged residential care facility, Whare Aroha Care, providing rest home, private hospital and secure dementia care. The trust is building a village, primarily but not exclusively for people with dementia. Based on the Hogeweyk model, people will live in domestic scale environments with like-minded others. The village will be the first based on the Hogeweyk model completed outside The Netherlands, with the setting adapted to New Zealand lifestyles.
The aim of the research is to explain the resettlement of Whare Aroha Care residents into the village and the effects of the resettlement on the lives of the residents. The study will utilise a critical realist methodology and a single case study research design. Study participants will be facility management, staff, residents and family members as well as other key informants from organisations such as the Ministry of Health. Study data will be collected using interviews, focused observation and key relevant documents. There are two thesis questions for the study:
There are two thesis questions for the study:
- Why and how has the decision for Whare Aroha Care to transition to a new facility been made and implemented, and:
- How has the transition affected the way residents live their lives?
Cobus Kilian - AUT University
Purposes, Principles and Profit – An investigation into the organisational legitimacy of residential aged care providers
This research focuses on the perception(s) of strategic decision-makers in social purpose businesses about how legitimacy is created and maintained in their businesses. It is specifically looking at community-based residential aged-care providers in the Waikato region.
It is focusing on three specific aspects of legitimacy. Firstly, the factors the strategic decision-makers identify as influencing their legitimacy; secondly, the sources that makes assessments of these organisations’ legitimacy and thirdly, motivations behind these legitimacy actions (for instance, moral or pragmatic reasons). Organisational legitimacy relates to the extent the organisation being assessed reflects the values or norms of the community it is a part of. Simply put, if an aged care facility is providing its services in a way that aligns with the values and norms held by that community, then the organisation is likely to be seen by community as legitimate, and will have a mandate to operate
Once completed, this study will be an original contribution to management research in the aged care sector. The study will provide clarity to community-based residential aged care providers, researchers and policy-makers on how the legitimacy of these organisations is constructed. I will highlight systemic factors that detract from improving the quality of life of frail elderly New Zealanders, and suggest improvements to aged care that enhances the dignity and quality of care of the frail elderly.
Navneet Lal - University of Otago
Myofibre death in Elderly Mouse Skeletal Muscle
Our ability to move and to maintain our physical independence rests heavily upon the health and integrity of our skeletal muscles. As we age, we lose muscle mass and strength, and become frail. This constellation of symptoms has been termed Sarcopenia. The details of how this phenomenon occurs at the cellular level is presently unclear, and investigation of the biological mechanisms that drive age-related losses in muscle mass is difficult due to the complexity of skeletal muscle tissue.
Currently, it is understood that losses in muscle mass correlate with declining strength and mobility. Furthermore, losses in muscle mass also appear to occur in conjunction with decreases in the number (cell death) and size (atrophy) of muscle cells (muscle fibres). Muscle fibre atrophy is thought to result partly from disuse due to denervation (motor nerve contact is lost). However, the processes driving muscle fibre death are unclear.
Although loss of whole muscle fibres with age is accepted, we have been the only group to describe elderly muscle fibres with microscopic features consistent with dying cells. In order to develop strategies to attenuate or even reverse sarcopenia, we require a comprehensive understanding of muscle fibre death: what triggers it; by what mechanism is it enacted; how long does it take; what are the functional consequences?
During the course of my PhD, I will attempt to further our understanding of muscle fibre death by carefully examining dying muscle fibres in elderly mouse and human muscle tissues. My study will involve detailing microscopic morphological, sub-cellular and biochemical features that differentiate dying muscle fibres from young healthy muscle fibres. I will attempt to reconcile these findings with the functional impact they have on whole muscles by examining their performance characteristics. Finally, I will attempt to recreate these features within young healthy muscles in order to validate my findings and to nominate potential pharmacological targets for future therapeutic intervention.
Jessica Young - University of Otago
Pathways to end of life care
Assisted dying is highly topical, of national interest, and globally significant; it presents challenging moral, philosophical, legal and practical considerations. Debate about assisted dying takes place in a context of ageing populations, unparalleled advances in medical technology, fears of dying badly, consumer driven pressure for more choice in end-of-life care, and changing ideas about choice, human rights, autonomy, suffering and compassion. Presently, New Zealand is considering legalising assisted dying for those who meet specific criteria. It is in light of the New Zealand End of Life Choice Bill, which may be chosen from the ballot at any time, that further research is needed, particularly about how it may effect older people with terminal illness. A recent NZ study found 82% of the public support legalising assisted dying.
However, the voice of individuals for whom assisted dying might be an immediate choice, were there to be a law change, is absent from the NZ discourse. My PhD research will focus on assisted dying and end-of-life decision-making by people with terminal illness and the members of their care networks (comprising significant individuals and multidisciplinary health professionals). While assisted dying is a highly complex and sensitive subject, in order to prepare for an ageing future, it is important to gain insight into the issue of assisted dying as New Zealanders are living longer and the public shows strong support for assisted dying.
Ashley Gillon - University of Otago
Nucleocytoplasmic transport defects as drivers for neurogeneration in elderly neurons.
Sarcopenia is the age related loss of skeletal muscle, and is a condition that will at some stage affect everyone. The resultant muscular weakness is associated with increased falls and decreasing independence within the aged community. The death of the nerve cells (motoneurons) that activate muscle fibres is now thought to be a major cause of muscle weakness in old age, but we do not know why these old motoneurons die. Nerve cell death is not unique to old age and recently many well described conditions that feature loss of neurons (motoneuron disease, Parkinson’s, Alzheimer’s and Fronto-temporal lobe dementia) have been associated with dysfunctional nucleocytoplasmic transport (movement of substances between the cell nucleus and surrounding cytoplasm).
Due to the shared pathophysiological manifestations between these conditions and sarcopenia (motoneuron death, muscle wasting and reduced strength), my PhD will investigate whether dysfunctional or altered nucleocytoplasmic transport is a feature of the ageing phenotype in mice and whether this in turn leads to motoneuron death and the muscular atrophy/weakness we associate with sarcopenia. In addition, one of the few documented therapeutic interventions for sarcopenia is exercise, so my research will also conduct an exercise program (mice on running wheels) to investigate whether exercise attenuates or reverses any effects of ageing on the nuclear transport system, with the overall goal of better understanding the physiological underpinnings of sarcopenia and opening up new avenues for development of therapeutic interventions for prolonging independence further into old age.
Tim van Ginkel – University of Canterbury
Cellular Coupling in the Neurovascular System
This project is being undertaken within the University of Canterbury’s Brains Trust Research Group. This group investigates mathematical and numerical models of blood flow in the brain. They use super computers to virtually model slices of brain tissue. Due to the close relationship between cerebral blood flow and brain health this will lead to a better understanding of the neurogenerative diseases that afflict the elderly such as Alzheimer’s disease, vascular dementia, hypertension and stroke. Improved understanding of these pathologies will aid in the development of new treatment options and coping strategies.
A model such as the one currently being developed is critical to allow researchers to carry out experiments on brain tissue without any risk of harming a human being. Treatments can be simulated and their effects observed both with and without the presence of pathological conditions. This will enable pharmacologists and chemical engineers to develop drugs that inhibit the effects of ageing related pathologies. There is also the potential for the development of better coping strategies for patients suffering from neurodegenerative diseases through changes in diet, exercise etc. as the effects of these on the brain can be simulated directly.
Most importantly as the complexity of the model being developed advances and it makes more accurate long term predictions it will provide increasingly helpful information to aid in every aspect of an ageing persons health. From studying factors such as dietary intake, sleep requirements and exercise we should be able to better look after the ageing brain.
Yanita McLeay - School of Sport & Exercise Science Massey University
The physiological effect of keratin protein supplementation in endurance athletes
Oxidative stress occurs when the body’s antioxidant system is unable to remove reactive oxygen species (ROS) at an appropriate rate. Elevated levels of ROS, and associated oxidative stress, is a primary cause of aging and age-related diseases including Alzheimer’s disease, age-related macular degeneration, muscle wasting, heart disease and cancer. It may therefore be suggested that increasing antioxidant status throughout life and in the aging population may help prevent these ROS associated diseases.
Keratins are animal-based proteins high in the sulphur amino acid cysteine; an important precursor for the intracellular antioxidants glutathione (GSH) and taurine. GSH is involved in both the breakdown and removal ROS and therefore plays a key role in the antioxidant status of the body. Taurine is a non-protein amino acid involved in many processes including antioxidant activity, lipid metabolism, mitochondrial protein synthesis and muscle function. Taurine levels in the retina have been shown to decrease with age and contribute to macular degeneration, and taurine replenishment is known to alleviate retinal oxidative stress in rats. Therefore, an elevation in GSH and taurine status may decrease oxidative stress, protect the body from associated oxidative damage and contribute to the prevention of age-related diseases.
The primary aim of this doctorate is to determine the effect of a novel proprietary keratin supplement antioxidant status; using casein-based protein as a control. This is being tested in male cyclists in a blinded, cross-over, and randomized study design protocol. Using exercise as a model for oxidative stress, both with and without keratin supplementation, blood and tissue antioxidant status, oxidative stress levels, body composition, and associated impact on physical work capacity are being tested prior to and following an acute and chronic intake of the each supplement. Preliminary results from this study suggest keratin may have a beneficial effect on body composition, specifically lean body mass. This may have significant implications for those experiencing age-related muscle atrophy and associated health issues. Further results from this study will have significant applications for enhancement of the health of the aging population and will contribute valuable information to the NZ health system for dealing with age-related diseases. Furthermore, this research will set the scene for future researchers to use these preliminary results in the design of projects focused on improving health in the aging population.
Alexia Mengelberg – Massey University
Effects of fish oil supplementation on cognitive performance in older adults with mild cognitive impairment
Nutritional research has shown that older adults are not eating enough fish and seafood to reach the recommended daily allowance of docosahexaenoic acid (DHA), and yet epidemiological research has shown positive associations between fish consumption and both higher scores on cognitive tests and a slower rate in cognitive decline. DHA is an omega-3, poly-unsaturated fatty acid found in high amounts in oily fish such as salmon, sardines and mackerel. DHA is commonly referred to as ‘essential fatty acid’ which reflects the fact that the human body cannot synthesise the precursors and therefore it must be consumed through food or taken as a supplement.
The extent to which environmental and genetic factors affect the progression from healthy age-related cognitive functioning to dementia remains unclear. Of particular interest is the APOE gene which is involved in the transport of fats and cholesterol within the brain. Research has shown that APOE4 allele carriers have an increased likelihood of developing Alzheimer’s disease and also of gaining a cognitive improvement from taking fish oil supplementation. This study aims to conduct a randomised, double-blind, placebo-controlled trial to investigate the effects of a high DHA fish oil supplement on cognitive performance in older adults with Mild Cognitive Impairment (MCI), as well as to investigate the modulating effect of the APOE4 allele on changes in cognitive performance.
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