Evidence that the Amyloid beta Precursor Protein-intracellular domain lowers the stress threshold of neurons and has a 'regulated' transcriptional role
2008

Amyloid beta Precursor Protein's Role in Neuron Stress Response

publication Evidence: moderate

Author Information

Author(s): Giliberto Luca, Zhou Dawang, Weldon Richard, Tamagno Elena, De Luca Pasquale, Tabaton Massimo, D'Adamio Luciano

Primary Institution: Albert Einstein College of Medicine

Hypothesis

Does the APP intracellular domain lower the stress threshold of neurons and influence gene transcription?

Conclusion

The APP intracellular domain may increase neuronal sensitivity to toxic stimuli without affecting the expression of certain target genes.

Supporting Evidence

  • AID does not regulate the basal expression of APP, NEP, KAI1, and p53 in the adult mouse brain.
  • Transgenic mice expressing AID showed increased sensitivity to toxic stimuli.
  • LDH release indicated higher cell damage in AID positive neurons under stress.

Takeaway

This study found that a part of a protein related to Alzheimer's disease makes brain cells more sensitive to damage, but it doesn't change how certain genes work.

Methodology

Transgenic mice expressing the APP intracellular domain were analyzed for gene expression and susceptibility to stress.

Limitations

The study did not identify specific AID target genes and results may vary under different conditions.

Statistical Information

P-Value

0.001

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1750-1326-3-12

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