Research suggests that Alzheimer's disease (AD), a chronic neurodegenerative disease characterized by cognitive function impairment (Canas et al., 2009) is caused by soluble oligomeric Amyloid-beta (Abeta) proteins that disrupt synaptic mechanisms (Selkoe et al., 2004). Increased Abeta levels lead to a decrease in brain derived neurotrophic factor (BDNF), an agonist of the p75NTR receptor, an autophagy mediator (Florez et al., 2004). Evidence suggests that cross-talk occurs between the A2A adenosine receptor and the p75NTR receptor (Canas et al., 2009); however, the effect of this cross-talk on the regulation of autophagy in neuronal cells has not been elucidated. Using PC12 pheochromocytoma cells as a model neuronal cell line, analysis of the expression of autophagy markers after exposure to BDNF and CGS21680 (an A2A receptor agonist) in the presence of Abeta will provide insight into the effect of the interaction between these two receptors on the regulation of autophagy in neuronal cells.

Investigation of the roles of p75<sup>NTR</sup> and A<sub>2A</sub> receptors on the regulation of amyloid-beta-induced autophagy in PC12 pheochromocytoma cells

243rd National Meeting (2012)

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Investigation of the roles of p75NTR and A2A receptors on the regulation of amyloid-beta-induced autophagy in PC12 pheochromocytoma cells

Investigation of the roles of p75^NTR and A_2A receptors on the regulation of amyloid-beta-induced autophagy in PC12 pheochromocytoma cells