Many researchers now believe that misfolded proteins spread from cell to cell across the brain, corrupting normal proteins as they go, yet exactly how this propagation would happen remains unclear. At the Society for Neuroscience annual meeting scientists identified specific mechanisms that may be involved in the spread of pathological proteins in Parkinson’s and Alzheimer’s diseases. They argued that astrocytes transmit α-synuclein aggregates by cell-to-cell contact; for tau, they argued that its trans-synaptic spread depends on the secretory vesicles known as exosomes. In addition, researchers debuted a new method for following tau aggregates over time in living mouse brain.
“Up until a few years ago, we did not understand how Parkinson’s disease progresses at the molecular level,” noted Alice Chen-Plotkin of the University of Pennsylvania. “Now, we may be starting to discover how the disease worsens, which could give insights into ways to slow it down or stop it,” she wrote to Alzforum.
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