The inflammatory response to amyloid-β in Alzheimer's disease
The comorbid nature of Alzheimer's disease (AD) and the difficulty of viewing neurobiological processes in action in real time are major obstacles for determining what changes in the AD brain actually cause the synaptic and neuronal damage that leads to behavioural symptoms. As such, there has been no success in developing drugs that can cure AD, or other common forms of dementia. The EU-funded AlzheimersInAction project proposes to develop an in-depth understanding of how the first known stage of AD, an overproduction of amyloid-β, causes downstream pathologies. Researchers will employ a multi-disciplinary approach that combines cell biology, molecular biology, time-lapse imaging, computational modelling, and electrophysiology techniques in the versatile Drosophila melanogaster genetic model.
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