The following grants were approved prior to July 2016
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.
Tau imaging and cognition in Parkinson’s disease
Using new technology to determine how the accumulation of a protein in the brains of Parkinson’s disease patients affects cognitive decline
Most people with Parkinson’s develop cognitive problems and, in many cases, dementia. Suitable objective tools that measure the underlying brain changes that underpin this cognitive decline need to be identified. These tools are important for both trials of new preventative treatments and for use in the clinic. This study will measure accumulation in the brain of an abnormal protein, tau, which is associated with the development of Parkinson’s dementia. Professor Anderson’s study will involve the use of tau PET scans in 70 people with Parkinson’s disease with varying cognitive problems including dementia to show how tau accumulation in the brain reflects degree of cognitive decline. Positron emission tomography scanning is a diagnostic tool that uses a tracer to illuminate specific proteins or cancer cells.
Ms Kao will undertake her Neurological Foundation Philip Wrightson Postdoctoral Fellowship at the Royal Holloway, University of London in the United Kingdom. Ms Kao will be supervised by Professor George Dickson, who holds a Chair in Molecular Cell Biology and has spent most of his career studying neuromuscular disease and muscle cell biology. Following the completion of her fellowship Ms Kao aims to return to New Zealand and become a principal investigator of her own research group.
An investigation into the role of Rpl3l and regulation of ribosome biogenesis in the pathogenesis of Duchenne muscular dystrophy: implications for novel therapeutic strategies
Investigating the role of a protein called Rpl3l in the muscular changes of a Muscular Dystrophy model: a new treatment target may be identified
Duchenne muscular dystrophy (DMD) is the most common fatal genetic disorder in childhood. It is caused by mutations in a gene called DMD that result in the absence of an important structural protein in muscle, called dystrophin. Absence of dystrophin results in progressive muscle weakness caused by pathological changes at the molecular level that are as yet poorly understood. A recent study revealed a protein called ‘Rpl3l’ may play a role in the pathological changes associated with DMD. Ms Kao’s fellowship aims to elucidate the role of Rpl3l in DMD and speculates that it could be targeted as a treatment for this devastating disease.
Sex-dimorphic brain development and disease: the role a non-coding RNA encoded within the Anti-Müllerian hormone locus
Shedding light on the nature of neurodevelopmental disorders depending upon the sex of the child
Susceptibility to many common neurological and psychiatric conditions differs and shows a dramatic sex basis – whether the person is male or female. Formation of the human brain during foetal development follows a slightly different path depending upon the sex of the child. These differences arise even before sex-hormones are produced. By determining how male and female sex impacts on the developing brain we hope to shed light on the nature of how sex differences to neurodevelopmental disorders arise.