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Considerable evidence, particularly from genetics, points to the aggregation-prone amyloid β-peptide as a pathogenic entity in Alzheimer's disease. Hence, the proteases that produce this peptide from its precursor protein have been prime targets for the development of potential therapeutics. One of these proteases, γ-secretase, has been a particular focus. Many inhibitors and modulators of this membrane-embedded protease complex have been identified, with some brought into late-stage clinical trials, where they have spectacularly failed. The reasons for these failures will be discussed, along with recent findings on the mechanism of γ-secretase and of Alzheimer-causing mutations that may suggest new strategies for targeting this enzyme.

Unlocking Truths of γ-Secretase In Alzheimer'S Disease: What Is the Translational Potential?