Spike bursts increase amyloid-β 40/42 ratio by inducing a presenilin-1 conformational change

Relative amounts of amyloid-β peptides of different length are altered in the brains of Alzheimer's disease patients. Here the authors show that neuronal patterns differentially regulate the production of amyloid-β isoforms by modifying the molecular conformation of presenilin-1, the catalytic subunit of γ-secretase that cleaves amyloid precursor protein to release amyloid-β.