scholarly journals Accumulation of Amyloid β-Protein in the Low-Density Membrane Domain Accurately Reflects the Extent of β-Amyloid Deposition in the Brain

2001 ◽  
Vol 158 (6) ◽  
pp. 2209-2218 ◽  
Author(s):  
Noriko Oshima ◽  
Maho Morishima-Kawashima ◽  
Haruyasu Yamaguchi ◽  
Masahiro Yoshimura ◽  
Shiro Sugihara ◽  
...  
2002 ◽  
Vol 71 (1) ◽  
pp. 313-322 ◽  
Author(s):  
Fumitaka Oyama ◽  
Naoya Sawamura ◽  
Kimio Kobayashi ◽  
Maho Morishima-Kawashima ◽  
Takashi Kuramochi ◽  
...  

2014 ◽  
Vol 92 (5) ◽  
pp. 351-355 ◽  
Author(s):  
Hironori Fujiwara ◽  
Junko Kimura ◽  
Masahiro Sakamoto ◽  
Akihito Yokosuka ◽  
Yoshihiro Mimaki ◽  
...  

Neprilysin (NEP) is one of the candidate amyloid β protein (Aβ) degrading enzymes affecting brain Aβ clearance. This enzyme declines in the brain with age, which leads to the increased Aβ deposition in Alzheimer’s disease (AD). Pharmacological activation of NEP during the aging process, therefore, represents a potential strategy to prevent the development of AD. To examine the influence of nobiletin on neprilysin activity, we measured cellular NEP activity in SK-N-SH cells. Moreover, NEP expression was examined by using reverse transcription – polymerase chain reaction and Western blotting. Measurement of cellular NEP activity showed that nobiletin stimulated this in a dose- and time-dependent manner in SK-N-SH cells. Moreover, nobiletin increased the expression of NEP mRNA, and then the levels of NEP protein, also in a dose- and time-dependent manner. Our findings showed that nobiletin promoted NEP gene and protein expression, resulting in enhancement of cellular NEP activity in SK-N-SH cells. This compound could be a novel Aβ-degrading compound for use in the development of disease-modifying drugs to prevent and (or) cure AD.


2003 ◽  
Vol 278 (27) ◽  
pp. 24294-24301 ◽  
Author(s):  
Toru Sato ◽  
Naoshi Dohmae ◽  
Yue Qi ◽  
Nobuto Kakuda ◽  
Hiroaki Misonou ◽  
...  

2006 ◽  
Vol 101 (4) ◽  
pp. 949-958 ◽  
Author(s):  
Maho Morishima‐Kawashima ◽  
Xianlin Han ◽  
Yu Tanimura ◽  
Hiroki Hamanaka ◽  
Mariko Kobayashi ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yu Fujita ◽  
Kuniyuki Kano ◽  
Shigenobu Kishino ◽  
Toshihiro Nagao ◽  
Xuefeng Shen ◽  
...  

AbstractConjugated linoleic acid (CLA) is an isomer of linoleic acid (LA). The predominant dietary CLA is cis-9, trans-11-CLA (c-9, t-11-CLA), which constitutes up to ~ 90% of total CLA and is thought to be responsible for the positive health benefits associated with CLA. However, the effects of c-9, t-11-CLA on Alzheimer’s disease (AD) remain to be elucidated. In this study, we investigated the effect of dietary intake of c-9, t-11-CLA on the pathogenesis of an AD mouse model. We found that c-9, t-11-CLA diet-fed AD model mice significantly exhibited (1) a decrease in amyloid-β protein (Aβ) levels in the hippocampus, (2) an increase in the number of microglia, and (3) an increase in the number of astrocytes expressing the anti-inflammatory cytokines, interleukin-10 and 19 (IL-10, IL-19), with no change in the total number of astrocytes. In addition, liquid chromatography–tandem mass spectrometry (LC–MS/MS) and gas chromatographic analysis revealed that the levels of lysophosphatidylcholine (LPC) containing c-9, t-11-CLA (CLA-LPC) and free c-9, t-11-CLA were significantly increased in the brain of c-9, t-11-CLA diet-fed mice. Thus, dietary c-9, t-11-CLA entered the brain and appeared to exhibit beneficial effects on AD, including a decrease in Aβ levels and suppression of inflammation.


2017 ◽  
Vol 18 (10) ◽  
pp. 2154 ◽  
Author(s):  
Werner Müller ◽  
Shunfeng Wang ◽  
Maximilian Ackermann ◽  
Meik Neufurth ◽  
Renate Steffen ◽  
...  

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