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. 2018 Feb 22;10:42. doi: 10.3389/fnagi.2018.00042

Figure 8.

Figure 8

Proposed model of how LPS, in combination with other factors, might produce amyloid plaques, myelin injury and Tau hyperphosphorylation. In addition, the model includes a possible mechanism by which autosomal dominant mutations in AβPP and Presenilin could damage myelin via Aβ actions on TLR4/CD14 receptors to increase cytokines.