title: Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line.
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.
authors.affiliation: Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: yasutaka@fukuoka-u.ac.jp.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Yasutaka
authors.affiliation: Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: twatanabe@fukuoka-u.ac.jp.
authors.forename: Takuya
authors.initials: T
authors.lastname: Watanabe
authors.affiliation: Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: anakashima@fukuoka-u.ac.jp.
authors.forename: Akio
authors.initials: A
authors.lastname: Nakashima
authors.affiliation: Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: jmatsumoto@fukuoka-u.ac.jp.
authors.forename: Junichi
authors.initials: J
authors.lastname: Matsumoto
authors.affiliation: Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: futagami@fukuoka-u.ac.jp.
authors.forename: Koujiro
authors.initials: K
authors.lastname: Futagami
authors.affiliation: Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: atyama@fukuoka-u.ac.jp.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Yamauchi
authors.affiliation: Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. Electronic address: ykataoka@fukuoka-u.ac.jp.
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Kataoka
mesh_terms: D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002460:Cell Line; D051379:Mice; D011328:Prions / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D011328:Prions; D014409:Tumor Necrosis Factor-alpha
keywords: Alzheimer’s disease; Beta-amyloid; Brain endothelial cell; Prion protein; Tumor necrosis factor-α