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. 2014 May 1;7:36. doi: 10.3389/fnmol.2014.00036

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Copyright © 2014 Giese.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Models of p25 dysregulation in Alzheimer’s disease. (A) The first model implicating p25 in AD is shown. This model proposes that p25 expression is increased in AD. This increased expression is caused by amyloid oligomers that increase calcium signaling enhancing cleavage of p35 into p25. Increased p25 expression leads to an overactivation and mislocalization of Cdk5, which results in tau hyperphosphorylation, which is a prerequisite for neurofibrillary tangle formation and neurodegeneration. (B) Revised model of p25 dysregulation in AD. This model proposes that p25 expression is not increased but reduced in AD. This decreased expression is caused by amyloid oligomers that decrease NMDA receptor-dependent calcium signaling at the synapse (due to internalization and desensitization of NMDA receptors) impairing cleavage of p35 into p25. Decreased p25 expression reduces synthesis of particular synaptic proteins, which affects synaptogenesis, late LTP and memory formation.