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Updated: Apr 19, 2026

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
Published on: June 20, 2017
Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a
Yuki Yasutaka1, Takuya Watanabe2, Akio Nakashima1
1Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan.
Abstract:
Disruption of beta-amyloid (Aβ) transport across the blood-brain barrier is thought to cause Aβ accumulation in the brain, thus leading to the development of Alzheimer's disease (AD). As AD patients show increased serum tumor necrosis factor-α (TNFα) levels, we examined the effect of TNFα on the function and expression of Aβ transport-related proteins including cellular prion protein (PrP(C)) in the mouse brain microvascular endothelial cell line MBEC4. TNFα decreased PrP(C) levels and intracellular radiolabeled Aβ. Similarly, anti-prion protein antibody also decreased radiolabeled Aβ. These results suggest that TNFα lowers PrP(C) levels, which in turn, reduces Aβ in the brain endothelium.
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