In vivo effects of beta-amyloid implants in rodents: lack of potentiation of damage associated with transient global forebrain ischemia.

@article{Stephenson1992InVE,
  title={In vivo effects of beta-amyloid implants in rodents: lack of potentiation of damage associated with transient global forebrain ischemia.},
  author={Diane Stephenson and James A. Clemens},
  journal={Brain research},
  year={1992},
  volume={586 2},
  pages={235-46}
}
Recent studies have shown that the principal component of the senile plaque in Alzheimer's disease (AD), beta-amyloid protein (beta AP) can exert direct and indirect neurotoxicity in vitro. Because of the studies that demonstrated potentiation of excitatory amino acid toxicity by beta AP, we decided to test whether beta AP was able to potentiate damage in an in vivo model where excitotoxic damage is thought to be important. The present study evaluated the in vivo effects of beta AP implants in… CONTINUE READING

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Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
Recent studies have shown that the principal component of the senile plaque in Alzheimer 's disease ( AD ) , beta - amyloid protein ( beta AP ) can exert direct and indirect neurotoxicity in vitro .
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