Syntaxin 5 Overexpression and <i>β</i>-Amyloid 1–42 Accumulation in Endoplasmic Reticulum of Hippocampal Cells in Rat Brain Induced by Ozone Exposure

<div>Schematic representation of the suggested mechanisms related with <i>β</i>A42 accumulation in ER. (a) Normal metabolism of mitochondria and ER under no oxidant stress conditions. Normal processing of <i>β</i>A42. (b) Metabolism alterations under oxidant stress conditions. (1) O<sub>3</sub> induces an oxidative stress state causing PS1 and Syx5 overexpression. (1b) ROS induces by itself the overcleavage of APP by PS1 and PS2. (2) PS1 and Syx5 accumulate in mitochondria, MAM, and ER. (3) <i>β</i>A42 accumulation in mitochondria, MAM, and ER. (4) Transport of PS1, Syx5, and <i>β</i>A42 through MAM. (5) Syx5 excess in ER. (6) Interaction Syx5/PS1 blocks the PS1 normal efflux. (7) PS1 accumulation. (8) PS1 transport to <i>γ</i>-secretase complex. (9) Accumulation of <i>β</i>A42 in ER. (10) ER dysfunction.</div>

BioMed Research International

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Figure 4: Syntaxin 5 Overexpression and <i>β</i>-Amyloid 1–42 Accumulation in Endoplasmic Reticulum of Hippocampal Cells in Rat Brain Induced by Ozone Exposure 

Figure 4 | Syntaxin 5 Overexpression and β-Amyloid 1–42 Accumulation in Endoplasmic Reticulum of Hippocampal Cells in Rat Brain Induced by Ozone Exposure 