A closer look at the launch symposium:
SESSION 1- RNA Binding Proteins & RNAs in Neurodegeneration
Mutations in RNA binding proteins (RBPs) as well as their aggregation are a common feature of neurodegeneration. Talks covered several aspects of RNA metabolism in neurodegeneration including a newly identified RBP involved in Amyotrophic Lateral Sclerosis, the consequences of disease causing mutations on the molecular and organism level, and how RNA could be used to prevent the aggregation of mutated RBPs.
SESSION 2- Glia in Neurodegeneration
Microglia are emerging as key players in neurodegenerative diseases such as Alzheimer’s disease. Thus far, microglia have rather been known as modulator of neurodegeneration with functions limited to neuroinflammation and release of neurotoxic molecules. However, several recent studies have demonstrated a direct role of microglia in “neuro”degeneration by promoting phagocytosis of neuronal, in particular, synaptic structures. Speakers shared advances in the field.
SESSION 3- Post-translational modifications in neurodegeneration
Post-translational modifications are a subtle and cunning way to modify protein function. Their relevance in neurodegenerative diseases is becoming increasingly obvious. This session discussed examples of post-translational modifications in Alzheimer and diabetes. We got to see how post-translational modifications can be studied experimentally.
SESSION 4- Advanced Imaging in Neurodegeneration
Advanced imaging in neurodegeneration: This session showcased the strength of the KCL dementia research community in advanced imaging technologies, showing how they can reveal mechanistic insight from single molecules to in vivo models and patient tissue.
SESSION 5- Synapse and Disease
Alzheimer’s disease (AD) is the leading cause of dementia. The pathophysiology of AD involves the weakening of synaptic connections and ultimately their elimination, which is thought to correlate with disease progression and severity. This session discussed how synapse loss in disease is underpinned by the aberrant activation of synapse weakening signalling cascades.
See more photos in our event album.