Anti-Amyloid Precursor Protein Antibody [bmAbetaN] (A269928)

Amyloid-ß (Aß) is the main constituent of amyloid deposits in Alzheimer's disease (AD). The neuropathology is associated with neuroinflammation. Here, we investigated effects of systemic lipopolysaccharide (LPS)-treatment on neuroinflammation and Aß deposition in AßPP-mice and double-transgenic mice with brain expression of AßPP and heparanase, an enzyme that degrades HS and generates an attenuated LPS-response. At 13 months of age, the mice received a single intraperitoneal injection of 50 µg LPS or vehicle, and were sacrificed 1.5 months thereafter. Aß in the brain was analyzed histologically and biochemically after sequential detergent extraction. Neuroinflammation was assessed by CD45 immunostaining and mesoscale cytokine/chemokine ELISA. In single-transgenic mice, LPS-treatment reduced total Aß deposition and increased Tween-soluble Aß. This was associated with a reduced CXCL1, IL-1ß, TNF-a-level and microgliosis, which correlated with amyloid deposition and total Aß. In contrast, LPS did not change Aß accumulation or inflammation marker in the double-transgenic mice. Our findings suggest that a single pro-inflammatory LPS-stimulus, if given sufficient time to act, triggers Aß-clearance in AßPP-transgenic mouse brain. The effects depend on HS and heparanase.