Adenosine A2A receptor blockade prevents synaptotoxicity and memory dysfunction caused by beta-amyloid peptides via p38 mitogen-activated protein kinase pathway.

@article{Canas2009AdenosineAR,
  title={Adenosine A2A receptor blockade prevents synaptotoxicity and memory dysfunction caused by beta-amyloid peptides via p38 mitogen-activated protein kinase pathway.},
  author={Paula M Canas and Lisiane de Oliveira Porci{\'u}ncula and Geanne Matos de Andrade Cunha and Carla Sofia Gomes da Silva and Nuno J Machado and Jorge Oliveira and Catarina Resende de Oliveira and Rodrigo A Cunha},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2009},
  volume={29 47},
  pages={14741-51}
}
Alzheimer's disease (AD) is characterized by memory impairment, neurochemically by accumulation of beta-amyloid peptide (namely Abeta(1-42)) and morphologically by an initial loss of nerve terminals. Caffeine consumption prevents memory dysfunction in different models, which is mimicked by antagonists of adenosine A(2A) receptors (A(2A)Rs), which are located in synapses. Thus, we now tested whether A(2A)R blockade prevents the early Abeta(1-42)-induced synaptotoxicity and memory dysfunction and… CONTINUE READING

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