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. 2021 Nov 24;13:705594. doi: 10.3389/fnagi.2021.705594

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Copyright © 2021 Zhan, Hakoupian, Jin and Sharp.

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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Colocalization of LPS with dMBP, LPS LAL assay, and Western blot analysis of dMBP in the PVWM of AD and control brains. (A) LPS (A1) and dMBP (A2) in control PVWM were colocalized (A3). (B) LPS (B1) and dMBP (B2) in AD PVWM were colocalized (B3). (C) The LAL assay for LPS of PVWM showed significantly greater LPS activity in AD (77.3 ± 3.1 EU/g, n = 12) compared to controls (65 ± 2.1 EU/g, n = 10, p = 0.0022). (D) The dMBP band intensity in PVWM was greater in AD (4.8 ± 0.8, n = 13) compared to controls (1 ± 0.3, n = 5, p = 0.007). (E) Western blots of PVWM for dMBP and β-actin for 5 controls (C1-C5) and 13 AD samples (AD1-AD13). β-actin was used as a loading control. Note: LAL, Limulus Amoebocyte Lysate assay for LPS; dMBP, degraded myelin basic protein; LPS, lipopolysaccharide; AD, Alzheimer's disease; Bar = 50 μm.