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. 2019 Jun 18;11:1759091419855541. doi: 10.1177/1759091419855541

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© The Author(s) 2019

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Changes in glutamatergic synapse component expression and signaling with AD progression. (a) Preclinical AD upregulation of several neuronal components contributing to hyperactivation and building the foundation for excitotoxicity. (b) Clinical AD is characterized by hypoactivation of the glutamatergic system, possibly a consequence of the earlier preclinical stage. This results in cognitive deficits due to signal-to-noise ratio imbalance.

AD = Alzheimer’s disease; α7nAChR = alpha-7 nicotinic acetylcholine receptor; Aβ_o = amyloid beta oligomer; VGluT1 = vesicular glutamate transporter 1; AMPAR = α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; E-NMDAR = extrasynaptic N-methyl-D-aspartic acid receptor; mGluR = metabotropic glutamate receptor; S-NMDAR = synaptic N-methyl-D-aspartic acid receptor; EAAT = excitatory amino acid transporter.