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. 2018 Sep 11;12:307. doi: 10.3389/fncel.2018.00307

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Copyright © 2018 Canet, Dias, Gabelle, Simonin, Gosselet, Marchi, Makinson, Tuaillon, Van de Perre, Givalois and Salinas.

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) and the copyright owner(s) 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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Proposed mechanisms by which glucocorticoids and their receptors modulate/potentiate the development of HAND and potentially AD. The dysregulation of the HPA axis is observed both in HIV patients and rodent models. GC overexposure, in combination with viral proteins or not, is able to induce the increase of Aβ production, Tau phosphorylation, excitotoxicity, oxidative stress, neuroinflammation and apoptosis. It should be also mentioned that Aβ itself can trigger Tau phosphorylation, excitotoxicity, oxidative stress, neuroinflammation and cell death. All these processes lead to neurodegeneration and synaptic deficits and potentially responsible for cognitive decline observed in HAND patients, all of which could progressively favor to the development of AD.