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Disability and dementia define the devastating diseases Multiple Sclerosis (MS) and Alzheimer’s Disease (AD), but what drives the neuroinflammation and neurodegeneration? New research is focusing
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responses (Barrow et al., 2024). In this project drosophila will be used as model organism for investigating the functionality of p62/RNP interactions in models of neurodegeneration in vivo, including AD and
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, to generate a step-change in our understanding of neurodegeneration. The hypothesis underlying this work is that a significant lack of data and inaccuracies in our knowledge of the genomic structure and
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University. The project is focused on applying state-of-the-art tools and technologies to learn how inflammatory signals traverse the blood-brain-barrier and contribute to neurodegeneration in cerebrovascular
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neurodegeneration, but their physiological functions are often poorly understood. Defining these functions would increase our understanding of the behaviour and importance of PrLPs, and how and why they become
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neurodegeneration, emphasising the need to understand HIF's regulatory mechanisms. HIF is a heterodimeric transcription factor with oxygen-sensitive alpha subunits (HIF1-α and HIF-2α) and an oxygen-insensitive beta