Familial Alzheimer mutations stabilize synaptotoxic g-secretase-substrate complexes
Devkota et al. find that mutations that cause hereditary Alzheimer’s disease, located in the substrate and protease that produce amyloid b-peptides, result in reduced proteolytic function and stabilized enzyme-substrate complexes. These stalled complexes trigger synaptic loss in C. elegans that is independent of amyloid b-peptide production.Read more