In a study published in Science Advances, Luca Ferrari, a postdoctoral researcher in the Martens group, compared how monomeric and pathological Tau proteins are targeted by this surveillance machinery. The team found that while Tau monomers are degraded normally, Tau fibrils, a hallmark of Alzheimer’s Disease, evade clearance by preventing the binding of a crucial mediator, TAX1BP1, which helps to recruit the autophagy machinery.
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