Skip to main content
Figure 7 | Molecular Neurodegeneration

Figure 7

From: Systemic treatment with liver X receptor agonists raises apolipoprotein E, cholesterol, and amyloid-β peptides in the cerebral spinal fluid of rats

Figure 7

Proposed mechanism by which LXR agonists improve apoE-mediated Aβ clearance from the brain. Based on the differential ability of the apoE isoforms to associate with lipids, Aβ, and LDLR, the model predicts that the "protective" apoE2, which has poor binding to LDLR and therefore increased association with lipids and ability to bind Aβ, favors elimination of amyloid to the CSF reducing amyloid deposition within the brain parenchyma (A). In contrast, apoE4, which has decreased association with lipids and reduced Aβ binding capacity when compared to apoE3 and apoE2, can lead to impaired Aβ clearance, increased Aβ oligomerization and deposition into amyloid plaques (B). By raising the levels and the lipidation of apoE and potentially decreasing apoE receptors within the brain, LXR agonists favor the transport of apoE and amyloid to the CSF with subsequent decrease in brain amyloid burden, similar to the "apoE2 effect" (C).

Back to article page