2015 Scholars

Posted by on 2 March 2015

The cornerstone funding from the Selwyn Foundation plus additional grants from Family Trusts have enabled us to extend our grants to researchers in 2015. Specifically this has meant one extra Scholar for the Universities of Auckland and Massey plus for the first time a grant to a University of Canterbury Scholar.

Phillip Aitken - Department of Pharmacology & Toxicology University of Otago

Examining the vestibular modulation of hippocampal spatial memory

The vestibular system, located in the inner ear, is the group of sensory organs which detect linear and rotational acceleration. Vestibular dysfunction affects 35% of adults aged 40 years and older, with an increased incidence in patients suffering from neurodegenerative disease. The vestibular system is also implicated in higher cognitive function. Spatial memory, learning, exploration and object recognition have all been shown to be impaired following damage to the peripheral vestibular system. It is hypothesized that the cognitive dysfunction is due to the loss of sensory input into the hippocampus. Vestibular lesions disrupt several hippocampal processes involved in learning and memory such as place cell firing, theta rhythm and hippocampal field potentials. Vestibular lesions also produce atrophy of the hippocampus in humans, this atrophy is thought to increase the progression of neurodegenerative diseases which also atrophy the hippocampus. Conversely, activation of the vestibular system produces increased hippocampal activity. Currently our understanding of how hippocampal function may be influenced by vestibular information is poor.

One of the brain areas that may play an important role in mediating vestibular-hippocampal interaction is the pedunculopontine tegmental nucleus (PPT), an acetylcholine-containing nucleus located in the brainstem. By examining the electrophysiological and neurochemical effect of vestibular modulation and PPT inactivation in the hippocampus this project will attempt to determine the mechanism by which the vestibular system produces changes in spatial learning and memory. This could lead to therapeutic interventions for patients suffering from vestibular damage or even neurodegenerative diseases, in which the PPT or hippocampus are specifically damaged, such as Parkinson’s and Alzheimer’s diseases.

Alexia Mengelberg - School of Psychology Massey University

Investigating the effects of fish oil supplementation on cognitive performance in older adults with mild cognitive impairment

Nutritional research has shown that most elderly people are not eating enough fish and seafood to reach the recommended 100 mg per day of docosahexaenoic acid (DHA), and at the same time epidemiological research has shown positive associations between fish consumption and both higher scores on cognitive tests and a slower rate in cognitive decline. DHA and eicosapentaenoic acid (EPA) are omega-3, poly-unsaturated fatty acids (n-3 PUFAs) found in oily fish such as salmon, sardines and eel. These fatty acids are commonly referred to as ‘essential fatty acids’ which reflects the fact that the human body cannot synthesise the precursors and therefore they must be consumed through the diet. As well as being important for reducing inflammation and blood-clotting, DHA in particular is crucial for the integrity of neuronal cell membranes, for neuronal cell signalling, as well as providing a protective mechanism against neuro-toxicity. There has been an increase in the use of n-3 PUFA supplementation for the treatment of cognitive and behavioural conditions; however it is still unclear for which particular conditions and at what stages of those conditions it is most efficacious.

The extent to which genetic and environmental factors affect the progression from healthy age-related cognitive functioning to dementia, remains unclear. This research study proposes to conduct a randomized, double-blind, placebo-controlled intervention trial to investigate the effects of a high dose DHA supplement on cognitive performance in older adults with Mild Cognitive Impairment (MCI). Older adults with MCI have a selective memory impairment but with no sign of dementia and a preserved ability to carry out everyday activities. MCI is considered the earliest detectible stage of dementia and consequently this study hopes to contribute to our understanding of the effects of DHA supplementation on memory as well as the potential for using DHA as a preventative treatment for dementia. As more and more older adults use nutritional supplements as an alternative to or in addition to pharmaceutical treatments, it becomes increasingly important that we have the most up-to-date information especially about the risks and benefits of taking these supplements.

Yanita McLeay -School of Sport & Exercise Science Massey University

The antioxidant effect of a novel high cysteine protein supplement in healthy individuals

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 will be tested using exercise as a model for oxidative stress, both with and without keratin supplementation. Blood and tissue antioxidant status, oxidative stress levels and associated impact on physical work capacity will be tested. The 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. 

Rebecca Hickmott - Department of Management University of Canterbury

Responding to the Needs of Vulnerable People during a Disaster

An earthquake measuring 7.1 hit the Canterbury region on September 4, 2010. Some Aged and Residential Care (ARC) facilities sustained significant damage and the Canterbury District Health Board (CDHB), which funds nearly all health and disability services, set up a an interagency emergency response team to address the needs of vulnerable people with significant health and disability needs who were unable to access support through the usual channels or whose needs were much greater than can be provided for through other support/help agencies. This team was called the Vulnerable Peoples Team (VPT)

On February 2011 the region was again hit by a devastatingly shallow earthquake near the centre of Christchurch with hundreds injured, loss of life and severe damage to infrastructure. Many ARC facilities were badly damaged and several destroyed. Over 600 ARC beds were lost and 500 elderly and disabled people were displaced. The emergency response for vulnerable people was established again but on a much larger scale. The VPT coordinated the care needs, and for some elderly and disabled persons, evacuation and relocation either within Christchurch or to other locations. The response included representatives from a range of different agencies (e.g., Civil Defence, Ministry of Social Development, Police, and the Military), which had to collaborate in order to meet the needs of the vulnerable people.

This study focuses on the nature of the communication at the inter-agency interfaces responding to vulnerable people. It proposes to collect narratives from those interacting with operational members of the VPT as they sought to locate and secure the safety of people of concern. This interpretive study uses a critical incident method to capture participant’s perspectives and determines what constitutes best practice (and less than ideal practice) in a multi-agency emergency response team from their point of view. The narratives collected will be analysed to uncover accounts of communication events that stabilised (and destabilised) the interagency interfaces. These critical incidents will then be subjected to in-depth analysis in order to develop a framework for interagency communication best practice when responding to vulnerable people. This framework will then be presented to respondents and they will be provided with an anonymous forum (an online feedback process) that will allow them to assess how well the model accommodates their experiences and provide any other information that they may have felt unable to provide in the interview process.

The overarching question for this study is:
What can we learn about stabilising inter-agency interfaces from the communication that occurred between the agencies responding to the vulnerable people during the Christchurch earthquakes?

It is hoped that the findings will add to our understanding of the complexities of inter-agency response coordination, the challenges of inter-agency integration of crisis communication and suggest ways to enhance the quality of response delivery to vulnerable communities in times of disaster. The key goal will be to develop a framework for interagency communication best practice. The knowledge gained will assist in creating frameworks for managing the communication at such interfaces in future emergencies where vulnerable communities are involved.

Aleea Devitt - School of Psychology University of Auckland 

Age-Related Neural Correlates of Autobiographical Memory Conjunction Errors

Memory is a constructive process, whereby the individual details comprising a memory are stored in different locations across the brain, and these must be relocated and reintegrated to form a coherent memory at retrieval. This constructive process can leave us vulnerable to memory distortions, such as memory conjunction errors. A conjunction error occurs when details from one memory are incorrectly incorporated into another.

It is well known that as we grow older our memory tends to fade. However, what is less well known is that as we age we become more susceptible to making memory errors. My previous research has demonstrated that conjunction errors can occur within autobiographical memory (memory for personally experienced life events). In a more recent study, I have found that older adults are more likely to make conjunction errors than younger adults, especially if the erroneous combination of details feels plausible and familiar.

Despite the importance of autobiographical memory in particular for self-identity, independent living and social interaction, there is a lack of research exploring the influence of age on memory distortions in this domain. My current research uses functional magnetic resonance imaging (fMRI) to better understand the neural correlates of accuracy and errors in autobiographical memory, and how these may be affected by ageing. Age-related reductions in memory accuracy for laboratory stimuli (such as words) can be attributable to neural declines in the medial temporal and frontal lobes; brain regions that play vital roles in reactivating memories, and monitoring these memories for errors. We wish to explore whether these age effects hold true for more complex types of memory such as autobiographical memory.

Jane (Xi Hua) Wu - University of Auckland

Gene expression profiling in the human subthalamic nucleus in Parkinson’s disease

Parkinson’s disease (PD) is a progressive, neurodegenerative disorder estimated to affect 1-2% in the population over the age of 65. It is one of the most common age-related neurodegenerative disorders in New Zealand. Over the past decade, deep brain stimulation therapy of the subthalamic nucleus has been successful in alleviating symptoms in advanced PD patients. However, the cellular mechanisms and neuro-scientific basis of the surgical procedure are not fully understood. The subthalamic nucleus is considered as the “power-house” of the motor circuitry, playing an extremely important role in PD progression. Abnormal neuronal signaling within this nucleus has been previously demonstrated in many animal models to be related to PD symptoms such as bradykinesia, rigidity and resting tremor. This study intends to define pathological changes within the subthalamic nucleus during PD in order to discover the molecular mechanisms which may play an important role in facilitating the benefits of deep brain stimulation therapy.

Early results using immunohistochemistry in the subthalamic nucleus in post-mortem human brain tissue show significant neurochemical changes at the cell receptor level. In particular, the current project using RNA-sequencing technologies intends to elucidate cellular pathways at the genetic level, which lead to the observed neurochemical changes. This discovery would contribute to a better understanding and improved application of deep brain stimulation and other therapies in the future treatment of Parkinson’s disease.

Helen Murray - Centre for Brain Research University of Auckland

Understanding the Role of PSA-NCAM in Age-Related Neurodegenerative Diseases

The research performed by our lab focuses on how the brain reacts to degenerative diseases by mounting a reparative response. One such response is to shift new brain cells into the damaged brain region. To migrate to their new position, new brain cells make a slippery molecule called polysialic acid-neural cell adhesion molecule (PSA-NCAM) which reduces the friction between the cell and its environment and enables efficient migration to the site of repair. Once in place, the cell must remove PSA-NCAM in order to form connections with neighbouring cells and integrate into its new environment.

This removal process has been poorly understood for many years, however recent work by our lab has demonstrated that cells will internalise PSA-NCAM when they receive specific cues from the extracellular matrix (the material surrounding cells in the brain). It was also discovered that this process is inhibited by insulin and insulin-like growth factor 1 (IGF-1), both of which are elevated in the brain in Alzheimer’s disease. An inability to remove PSA-NCAM from the cell surface could prevent neurons from maturing and forming the synaptic connections necessary for survival, resulting in cell death.

This research will investigate whether PSA-NCAM expression and distribution is altered in degenerated regions of the human Alzheimer’s disease brain as well as in other neurodegenerative diseases such as Parkinson’s disease and Huntington’s disease. To do this I will be developing an innovative new technique called fresh tissue microarray to improve the efficiency of studying a large number of brain regions across a large number of cases. This project will help us understand how the process of cell replacement is affected in neurodegenerative diseases and potentially provide new therapeutic targets for treatments to be developed.