A new study from the Jagust lab finds that excessive neural activity in brain networks could explain how the protein beta-amyloid drives accumulation of the protein tau, causing cognitive decline.
Medial temporal lobe (MTL) network excitation by the default mode network (DMN) during stimulus repetition
predicts the rate of subsequent tau deposition. Image courtesy of William Jagust.
In a study of human participants published in Neuron, Helen Wills Neuroscience Institute member William Jagust and collaborators reveal a mechanism that could explain the connection between two proteins and brain areas implicated in Alzheimer’s disease. The study, led by Jagust lab postdoctoral fellow Joseph Giorgio, showed that increased beta-amyloid protein causes increased excitability in the brain’s default mode network, which increases excitability in the medial temporal lobe of the brain, driving accumulation of the protein tau.
“As tau spreads, cognition declines. How these two proteins interact has been a major unanswered question in the field,” said Jagust.
Read the paper: Amyloid induced hyperexcitability in default mode network drives medial temporal hyperactivity and early tau accumulation (Neuron, December 13, 2023)