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Headlines 11 commonest form of CMT. This information is important for designing rehabilitation programmes to reduce falls and prolong independence. Do neutrophil extracellular traps enhance inflammation around plaques in Alzheimer's disease? Dr Leon Smyth, University of Otago Christchurch $178,543 Cells called neutrophils get into the brain during Alzheimer’s disease, but what they do is unknown. We have seen remnants of neutrophils around plaques in the brains of people with Alzheimer’s disease, and we think these might be neutrophil extracellular traps (NETs). NETs are potent activators of the immune system and have proteins associated with them that can damage surrounding tissue. Dr Leon Smyth will investigate the effect of NETs on immune responses and cell death pathways in brain cells. They believe this will help uncover the connection between amyloid plaques and cellular dysfunction in Alzheimer’s disease. Advancing the therapeutic potential of sAPP α : an investigation of sAPP α -mediated glutamate receptor trafficking in rodent and human neurons Associate Professor Joanna Williams, University of Otago $223,385 Regulation of glutamate receptors is critical to memory formation and impaired in Alzheimer’s disease. Therapies that alter the course of Alzheimer’s disease are urgently needed and we have shown that “sAPP α ” enhances synthesis of glutamate receptors. Associate Professor Joanna Williams will investigate this subtype of glutamate receptor; those permeable to calcium and capable of fundamentally altering the connections between nerve cells. Crucially, they will study rodent neurons and human neurons donated by people with Alzheimer’s disease. These studies will deepen our understanding of how neurons communicate and provide a necessary next step in advancing sAPP α as a novel therapeutic agent. Small Project grants Understanding cognitive ageing and compensatory mechanisms: Neural correlates of better cognitive performance specific to older adults Dr Liana Machado, University of Otago $14,996 Proudly sponsored by the Withiel Fund Why do some older adults age more successfully than others in terms of their thinking abilities? Recent research suggests that during cognitive engagement older adults recruit additional brain areas, not used in young adults, that can help support better cognitive functioning. The purpose of this project is to better understand compensatory brain mechanisms used by older adults to cope with cognitive decline. The proposed research will investigate patterns of electrical brain activity alongside brain blood flow to help explain why some older adults age more successfully than others with regard to maintaining cognitive abilities and identify a therapeutic target. Identifying the relationship between cognition and swallowing in Parkinson's disease Dr Sarah Perry, University of Otago Christchurch $14,696 Parkinson’s disease (PD) is a common neurodegenerative disease. Cognitive decline and disordered swallowing contribute to the leading causes of death in PD. Although evidence suggests that cognition may influence swallowing, examination of the effects of cognitive decline on swallowing has not been undertaken. One of the goals of this study is to describe cognitive predictors of swallowing dysfunction in people with PD. Dr Sarah Perry will achieve this by analysing cognitive data and comparing this to swallowing test results. In the long-term, this should mean improved patient outcomes through earlier identification of high-risk patients and timely referral for swallowing rehabilitation. Cell type-specific TDP-43 nuclear clearing and aggregation in the Motor Neuron Disease brain Dr Molly Swanson, University of Auckland $15,000 Proudly sponsored by the Withiel Fund Motor Neuron Disease (MND) is a paralysing neurodegenerative disease caused by the death of neurons controlling movement. Clumping of a critical protein called TDP-43 occurs in motor neurons and other brain cells in 97% of MND cases. TDP-43 ordinarily resides in the nucleus, but is either clumped in the cytoplasm, absent from the nucleus, or both, in MND. Dr Molly Swanson will determine whether it is the clumping of TDP-43 or its ‘clearing’ from the nucleus that causes its dysfunction in MND, both in neurons and other brain cells. This research will reveal how TDP-43 dysfunction should be therapeutically targeted in MND.