Bibliographic Details
| Title: |
Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line. |
| Authors: |
Yuki Yasutaka1 yasutaka@fukuoka-u.ac.jp, Takuya Watanabe2 twatanabe@fukuoka-u.ac.jp, Akio Nakashima1 anakashima@fukuoka-u.ac.jp, Junichi Matsumoto1 jmatsumoto@fukuoka-u.ac.jp, Koujiro Futagami1 futagami@fukuoka-u.ac.jp, Atsushi Yamauchi2 atyama@fukuoka-u.ac.jp, Yasufumi Kataoka2 ykataoka@fukuoka-u.ac.jp |
| Source: |
FEBS Letters. Jan2015, p263-268. 6p. |
| Subjects: |
Tumor necrosis factors, Amyloid beta-protein, Prions, Blood-brain barrier, Endothelial cells, Alzheimer's disease |
| Abstract: |
Disruption of beta-amyloid (Aß) transport across the blood-brain barrier is thought to cause Aß accumulation in the brain, thus leading to the development of Alzheimer's disease (AD). As AD patients show increased serum tumor necrosis factor-a (TNFa) levels, we examined the effect of TNFa on the function and expression of Aß transport-related proteins including cellular prion protein (PrPC) in the mouse brain microvascular endothelial cell line MBEC4. TNFa decreased PrPC levels and intracellular radiolabeled Aß. Similarly, anti-prion protein antibody also decreased radiolabeled Aß. These results suggest that TNFa lowers PrPC levels, which in turn, reduces Aß in the brain endothelium. [ABSTRACT FROM AUTHOR] |
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| Database: |
Engineering Source |
