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Presenilin mutants subvert chaperone function

Abstract

Mutant presenilin proteins, known to promote the development of Alzheimer’s disease through increased generation of Aβ42 peptides, appear to compound this insult by downregulating the signalling pathway that adjusts levels of molecular chaperones in the endoplasmic reticulum in response to stress.

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Figure 1: Generation of amyloid-β peptide (Aβ), the hallmark of Alzheimer’s disease.

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Gething, MJ. Presenilin mutants subvert chaperone function. Nat Cell Biol 2, E21–E23 (2000). https://doi.org/10.1038/35000090

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