Cited by 49

The DOI matches its Crossref record.

Attenuation of the Neurotoxic Effect of Aβ Amyloid Peptide by Apolipoprotein E

Whitson, J.S., Mims, M.P., Strittmatter, W.J., Yamaki, T., Morrisett, J.D., Appel, S.H.·1994·Biochemical and Biophysical Research Communications

Abstract

Alzheimer's disease patients have increased frequency of apolipoprotein E allele c4, suggesting apoE4 is a risk factor determining disease. ApoE binds A beta amyloid peptide with great avidity in vitro and in the neuritic plaque. Potentially, binding of A beta to apolipoprotein E could increase A beta neurotoxicity. However, in hippocampal cultures, 0.1 microM apolipoprotein E eliminated the neurotoxicity of 10 microM A beta. Neuronal rescue was dose-dependent and occurred even after 48 hours exposure to A beta, but was overwhelmed by excess A beta. Thus, interaction between these proteins does not directly increase A beta neurotoxicity, and the role of ApoE in Alzheimer's disease remains to be elucidated.

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Crossref · 10.1006/bbrc.1994.1209

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  • The addition of exogenous apoE protects against Aβ-induced toxicity in neuronal cell cultures and against Aβ-induced activation of astrocyte cultures.

    “The addition of exogenous apoE protects against A␤-induced toxicity in neuronal cell cultures, as well as A␤-induced activation of astrocyte cultures (24,25,38,52,53).”

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Authors
Whitson, J. S., Mims, M. P., Strittmatter, W. J., Yamaki, T., Morrisett, J. D., & Appel, S. H.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
1994-02
Volume
199
Issue
1
Pages
163-170
ISSN
0006-291X
Cited by
49
References
0
Language
en

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