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PMID- 28103595
STAT- Publisher
DA  - 20170119
LR  - 20170119
IS  - 1660-2862 (Electronic)
IS  - 1660-2854 (Linking)
VI  - 17
IP  - 2-3
DP  - 2017 Jan 20
TI  - Identification of Small Peptides in Human Cerebrospinal Fluid upon Amyloid-beta
PG  - 103-109
LID - 10.1159/000453358 [doi]
AB  - BACKGROUND: Amyloid-beta (Abeta) degradation in brains of Alzheimer disease
      patients is a crucial focus for the clarification of disease pathogenesis.
      Nevertheless, the mechanisms underlying Abeta degradation in the human brain
      remain unclear. OBJECTIVE: This study aimed to quantify the levels of small
      C-terminal Abeta fragments generated upon Abeta degradation in human
      cerebrospinal fluid (CSF). METHODS: A fraction containing small peptides was
      isolated and purified from human CSF by high-pressure liquid chromatography.
      Degradation products of Abeta C termini were identified and measured by liquid
      chromatography-tandem mass spectrometry. The C-terminal fragments of Abeta in the
      conditioned medium of cultured cells transfected with the Swedish variant of
      betaAPP (sw betaAPP) were analyzed. These fragments in brains of PS1 I213T
      knock-in transgenic mice, overexpressing sw betaAPP, were also analyzed. RESULTS:
      The peptide fragments GGVV and GVV, produced by the cleavage of Abeta40, were
      identified in human CSF as well as in the brains of the transgenic mice and in
      the conditioned medium of the cultured cells. Relative to Abeta40 levels, GGVV
      and GVV levels were 7.6 +/- 0.81 and 1.5 +/- 0.18%, respectively, in human CSF.
      Levels of the GGVV fragment did not increase by the introduction of genes
      encoding neprilysin and insulin-degrading enzyme to the cultured cells.
      CONCLUSION: Our results indicate that a substantial amount of Abeta40 in human
      brains is degraded via a neprilysin- or insulin-degrading enzyme-independent
CI  - (c) 2017 S. Karger AG, Basel.
FAU - Mizuta, Naoki
AU  - Mizuta N
AD  - Psychiatry, Department of Integrated Medicine, Division of Internal Medicine,
      Osaka University Graduate School of Medicine, Osaka, Japan.
FAU - Yanagida, Kanta
AU  - Yanagida K
FAU - Kodama, Takashi
AU  - Kodama T
FAU - Tomonaga, Takeshi
AU  - Tomonaga T
FAU - Takami, Mako
AU  - Takami M
FAU - Oyama, Hiroshi
AU  - Oyama H
FAU - Kudo, Takashi
AU  - Kudo T
FAU - Ikeda, Manabu
AU  - Ikeda M
FAU - Takeda, Masatoshi
AU  - Takeda M
FAU - Tagami, Shinji
AU  - Tagami S
FAU - Okochi, Masayasu
AU  - Okochi M
LA  - eng
PT  - Journal Article
DEP - 20170120
PL  - Switzerland
TA  - Neurodegener Dis
JT  - Neuro-degenerative diseases
JID - 101189034
EDAT- 2017/01/20 06:00
MHDA- 2017/01/20 06:00
CRDT- 2017/01/20 06:00
PHST- 2016/04/04 [received]
PHST- 2016/11/10 [accepted]
AID - 000453358 [pii]
AID - 10.1159/000453358 [doi]
PST - aheadofprint
SO  - Neurodegener Dis. 2017 Jan 20;17(2-3):103-109. doi: 10.1159/000453358.

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