Enhancement of beta-amyloid peptide A beta(1-40)-mediated neurotoxicity by glutamine synthetase.

@article{MYu1995EnhancementOB,
  title={Enhancement of beta-amyloid peptide A beta(1-40)-mediated neurotoxicity by glutamine synthetase.},
  author={Aksenov MYu and Marina V. Aksenova and Meera E Harris and Kenneth Hensley and David Butterfield and John M. Carney},
  journal={Journal of neurochemistry},
  year={1995},
  volume={65 4},
  pages={1899-902}
}
The beta-amyloid peptide (A beta), a main constituent in both senile and diffuse plaques in Alzheimer's disease brains, was previously shown to be neurotoxic and to be able to interact with several macromolecular components of brain tissue. Previous investigations carried out in our laboratory demonstrated free radical species formation in aqueous solutions of A beta(1-40) and its C-end fragment, A beta(25-35). Toxic forms of A beta rapidly inactivate the oxidation-sensitive cytosolic enzyme… CONTINUE READING

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