Abeta exacerbates the neuronal dysfunction caused by human tau expression in a Drosophila model of Alzheimer's disease.

@article{Folwell2010AbetaET,
  title={Abeta exacerbates the neuronal dysfunction caused by human tau expression in a Drosophila model of Alzheimer's disease.},
  author={James Folwell and Catherine M. Cowan and Kiren K. Ubhi and Hassan Shiabh and Tracey A. Newman and David Shepherd and Amritpal Mudher},
  journal={Experimental neurology},
  year={2010},
  volume={223 2},
  pages={401-9}
}
Alzheimer's disease (AD) is characterised by neurofibrillary tangles composed of hyper-phosphorylated tau, and neuritic plaques composed of misfolded amyloid peptide (Abeta(42)). It is generally believed that the hyper-phosphorylated tau and oligomeric Abeta(42) are responsible for the neuronal dysfunction and cognitive impairments that underlie the early stages of AD, but the mechanism by which they interact in the pathogenic process is not clear. Mounting evidence suggests that Abeta(42… CONTINUE READING
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