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

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APOE in non-Alzheimer amyloidoses: transmissible spongiform encephalopathies.

BACKGROUND: The APOE genotype has been shown to influence the risk of developing sporadic and familial AD. This effect is isoform-dependent, the APOE epsilon4 allele increasing susceptibility and the APOE epsilon2 allele providing protection. Amyloid formation is an important part of the pathogenesis in AD as well as in spongiform encephalopathies; apoE deposition in amyloid plaques has been documented in both conditions. METHODS: We examined the frequency of the APOE alleles in patients with various forms of transmissible spongiform encephalopathies, or prion diseases, including sporadic and iatrogenic Creutzfeldt-Jakob disease; familial Creutzfeldt-Jakob disease associated with PRNP 178N/129V and 200K/129M point mutations and a 24-nucleotide repeat expansion; fatal familial insomnia caused by the 178N/129M mutation; Gerstmann-Sträussler-Scheinker disease associated with 102L/129M mutation; and kuru. RESULTS: None of the groups we studied had a significant excess of APOE epsilon4 allele when compared with appropriate controls. CONCLUSION: Our results do not support the contention that the APOE epsilon4 allele is a risk factor for developing Creutzfeldt-Jakob disease or related disorders.[1]

References

  1. APOE in non-Alzheimer amyloidoses: transmissible spongiform encephalopathies. Chapman, J., Cervenáková, L., Petersen, R.B., Lee, H.S., Estupinan, J., Richardson, S., Vnencak-Jones, C.L., Gajdusek, D.C., Korczyn, A.D., Brown, P., Goldfarb, L.G. Neurology (1998) [Pubmed]
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