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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Alzheimer's disease. Molecular consequences of presenilin-1 mutation.

Alzheimer's disease is characterized by accumulation in the brain of a family of insoluble amyloid peptides (Abeta peptides), which are produced as a result of the normal processing of beta-amyloid precursor protein (beta-APP). Russo et al. claim that a truncated Abeta peptide that lacks the first ten amino acids accumulates in the brains of patients carrying a mutant form of pre-senilin 1 (PS1), a protein that is involved in cleavage of beta-APP. However, we have found that this same species is also overrepresented in Alzheimer's patients with mutations in beta-APP itself. Our findings do not support the conclusion of Russo et al. that pathogenic PS1 mutations may control cleavage of beta-APP by beta-secretase.[1]

References

  1. Alzheimer's disease. Molecular consequences of presenilin-1 mutation. Gandy, S., Naslund, J., Nordstedt, C. Nature (2001) [Pubmed]
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