Parkinson’s Disease & Movement Disorders

Led by Professor Kay Double, our laboratory-based research is focused on understanding how Parkinson’s disease damages brain cells and how we can intervene to halt this process. We are also working to develop better diagnostic tools and targeted treatment strategies for this debilitating disease.

We are currently focused on understanding neuronal vulnerability; that is, how and why Parkinson’s disease kills certain cells in the brain. This can help us to find better ways to make cells more resilient and develop new treatments that can protect brain cells. For example, we are investigating whether modifying metal levels in the brain, such as copper and iron, can slow the disease’s progress.

We are also investigating whether brain changes in Parkinson’s disease are similar to those in other brains disorders and what we might learn from these overlapping disease mechanisms.

Finally, our work aims to improve the methods used to diagnose Parkinson’s disease such that it may be identified early in the trajectory of the disease and with greater accuracy.

Our research is dedicated to improving the quality of life for people with Parkinson’s and, ultimately, to finding a cure for the disease.

Our clinical research, led by Professor Simon Lewis, focuses on targeting some specific symptoms of the disease, such as ‘freezing of gait’ and hallucinations. We work closely with people affected by Parkinson’s on a day-to-day basis. By working together, we aim to find ways to predict the disease and to stem its progression.

Through our Parkinson’s Disease Research Clinic we coordinate clinical research studies that investigate the symptoms of Parkinson’s disease.

Our research is part of the ForeFront Ageing and Neurodegeneration Program. We take a holistic approach, working closely with researchers who focus on brain conditions related to Parkinson’s disease. Together, we screen people who are considered to be ‘at risk’ of developing neurological disease and examine genetic risk factors to try to understand why some people develop Parkinson’s disease, others develop other neurodegenerative diseases such as frontotemporal dementia, while other ‘at risk’ patients never transition to disease at all.

We also collaborate with NeuroSleep, the Centre for Translational Sleep and Circadian Neurobiology, which seeks to better understand the relationship between sleep and a healthy brain. Collectively, we look at whether targeted sleep-wake interventions can influence the progression of neurodegenerative diseases and whether sleep-wake disturbances could be used as a predictor of disease in at-risk populations. 

Led by Professor Carolyn Sue, our genetic research aims to improve diagnostic methods and genetic testing for patients with Parkinson's disease and other inherited forms of movement disorders.

By identifying causative genes involved in these disorders, we are able to create patient-derived cell models with biologically relevant levels of abnormal proteins to further understand pathogenic mechanisms of disease. Our experiments have led to the discovery of novel disease pathways and new treatment approaches.

Iron accumulation is a cardinal feature of degenerating regions in the Parkinson’s disease brain. As a potent pro-oxidant, redox-active iron may be a key player in upstream mechanisms that precipitate cell death in this disorder. Although an elevation in brain iron levels is a normal feature of ageing, the increase is greater in Parkinson’s disease; on the other hand, the effects of the disease are most marked in the nigrostriatal dopaminergic system. In this Update, we explain that neurodegeneration in the affected regions may result from the potent redox couple formed by iron and dopamine itself, and discuss the clinical implications of this molecular trait in this dynamic and rapidly moving area of Parkinson’s disease research.

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Intracellular α-synuclein (α-syn)-rich protein aggregates called Lewy pathology (LP) and neuronal death are commonly found in the brains of patients with clinical Parkinson disease (cPD). It is widely believed that LP appears early in the disease and spreads in synaptically coupled brain networks, driving neuronal dysfunction and death. However, post-mortem analysis of human brains and connectome-mapping studies show that the pattern of LP in cPD is not consistent with this simple model, arguing that, if LP propagates in cPD, it must be gated by cell- or region-autonomous mechanisms. Moreover, the correlation between LP and neuronal death is weak. In this Review, we briefly discuss the evidence for and against the spreading LP model, as well as evidence that cell-autonomous factors govern both α-syn pathology and neuronal death.

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• Professor Simon Lewis
• Associate Professor Kay Double
• Professor Carolyn Sue
• Dr Jin-Sung Park
• Dr Kishore Kumar
• Dr Ryan Dacvis
• Dr Claire O’Callaghan
• Dr Brian Koentojoro
• Dr Ariandna Recasens
• Dr Guatam Wali
• Dr Katherine Phan