CORDIS Project
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This research explores the role of Tau protein phosphorylation in dementia, particularly its connection to sleep and synaptic plasticity. It aims to uncover how sleep-induced changes in Tau may influence cognitive functions and offer new treatment avenues.
Dysfunction of protein Tau is the main cause of dementia.
Dementia associates with synaptic failure and sleep disturbances, but their connection remains elusive.
In dementia, Tau becomes hyperphosphorylated (p-Tau) causing synaptic loss.
Temperature fluctuations also associate with Tau phosphorylation, for example in hibernating animals.
Intriguingly, my work demonstrates that brain temperature decreases during sleep, and further evidence suggests there are Tau-sites phosphorylated during sleep.…
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