The following grants were approved prior to July 2016
Assessing RRMS patient sera for soluble blood brain barrier disrupting factors
Does a subset of multiple sclerosis patients have a dysfunction to the barrier protecting the brain?
Relapsing remitting multiple sclerosis (RRMS) is a chronic neurological condition where the immune system attacks structures in the brain. The disruption to the blood vessels in the brain in the regions where the lesions form is a key feature of multiple sclerosis pathology. Dr Graham’s research aims to investigate whether RRMS patients have soluble factors circulating in their blood that can directly cause disruption to the special vascular structure known as the blood brain barrier (BBB). The BBB protects the brain from foreign substances in the blood that may injure the brain. Identification of these factors will provide an understanding of mechanisms involved in blood brain barrier dysfunction and in the future lead to strategies that directly strengthen the compromised vessels.
Characterising the electroencephalogram profiles of Alzheimer’s disease mouse models
Studying brain activity recordings in a mouse model of Alzheimer’s disease to better understand the pathology of the disease
Alzheimer’s disease (AD) is a neurodegenerative disease that presents an immense burden for patients, caregivers and society, with the number of affected individuals rising steadily. Current mouse models used to study AD do not present the full range of pathology, perhaps contributing to the lack of a cure or efficient treatment. New research indicates that sleep patterns and electroencephalograms (EEG) of AD patients differ from the normal population and that these recordings help diagnose and predict patient outcomes. Dr Schweitzer will use a novel, wireless system to study EEG changes in a newly created mouse model. The results will provide a better understanding of the pathology in these mice, and will provide a baseline data for future tests of therapeutic approaches in both model systems.
Voluntary tremor suppression in Parkinson’s disease
Why can some Parkinson’s disease patients suppress involuntary tremors? Investigating this phenomenon for the first time
Tremor is the most well-known symptom of Parkinson’s disease but unfortunately is not very responsive to the standard pharmacological treatments. Dr Blakemore’s team has, however, encountered a number of patients who are able to temporarily suppress their tremor simply by effort of will. This ability does not appear to be uncommon and is surprising, especially as it has not yet been described in the literature. Dr Blakemore proposes to investigate this phenomenon systematically for the first time, adding functional brain imaging to a suite of movement and muscle measures to understand how people can suppress involuntary tremors.
Do basal ganglia inputs activate motor thalamus neurons?
Investigating the changes in a brain pathway in a model of Parkinson’s disease to improve our understanding of how the brain controls movement
In Parkinson’s disease (PD), loss of the brain chemical dopamine alters activity throughout movement control pathways. Dr Parr-Brownlie will investigate how one brain pathway, between two parts of the brain known as the basal ganglia and motor thalamus, usually works and if this is altered in PD. Using selective optogenetic stimulation, a cutting-edge technology, Dr Parr-Brownlie will investigate if this connection simultaneously releases two chemicals, thus is more complex than previously thought. Furthermore, this study will determine if this chemical release is altered in a model of PD. These data will improve our understanding of how the brain controls movement and the changes that occur in PD, thus highlighting new potential treatment sites.
Ms MacDonald will undertake her Neurological Foundation Philip Wrightson Postdoctoral Fellowship at the University of Birmingham, United Kingdom, and will be supervised by Dr Ned Jenkinson. Dr Jenkinson has spent his career investigating how the brain controls movement, and has extensive research experience in positions at Vanderbilt University in the United States and at the University of Oxford.
Following the completion of her fellowship Ms MacDonald plans to return to New Zealand and integrate the skills and knowledge gained overseas with her current experience, to advance her research career in clinical neuroscience.
Memory encoding and beta de-synchronisation in Parkinson’s disease
Does excessive brain activity contribute to memory deficits in Parkinson’s disease?
Although Parkinson’s disease (PD) is a movement disorder, there is increasing awareness of significant non-motor (non-movement) burdens experienced by patients. Excessively synchronised brain activity is linked to some motor symptoms of PD, however less is known about how this brain activity contributes to the non-motor symptoms. This project aims to shed new light on the relationship between hyper-synchronised brain activity and the memory deficits experienced in PD. Establishing that such a relationship exists will not only increase our understanding of the neurobiology underpinning PD symptoms, but will pave the way to addressing memory deficits by applying techniques shown to normalise brain activity.