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Article

FAD mutants unable to increase neurotoxic Abeta 42 suggest that mutation effects on neurodegeneration may be independent of effects on Abeta.

Journal of neurochemistry - 1 May 2007

Shioi Junichi, Georgakopoulos Anastasios, Mehta Pankaj, Kouchi Zen, Litterst Claudia M, Baki Lia, Robakis Nikolaos K

Abstract excerpt

Strong support for a primary causative role of the Abeta peptides in the development of Alzheimer's disease (AD) neurodegeneration derives from reports that presenilin familial AD (FAD) mutants alter amyloid precursor protein processing, thus increasing production of neurotoxic Abeta 1-42 (Abeta 42). This effect of FAD mutants is also reflected in an increased ratio of peptides Abeta 42 over Abeta 1-40 (Abeta...

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Identifiers

PMID: 17254019
DOI: 10.1111/j.1471-4159.2006.04391.x

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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FAD mutants unable to increase neurotoxic Abeta 42 suggest that mutation effects on neurodegeneration may be independent of effects on Abeta.PMID 17254019Read ↗

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