Amyloid β protein 42(43) in cerebrospinal fluid of patients with Alzheimer's disease

Akira Tamaoka, Naoya Sawamura, Tetsuo Fukushima, Shin'ichi Shoji, Etsuro Matsubara, Mikio Shoji, Shunsaku Hirai, Yoshiko Furiya, Riuko Endoh, Hiroshi Mori

研究成果: Article査読

117 被引用数 (Scopus)

抄録

To investigate the pathomechanism of amyloid β protein (Aβ) deposition in brains with Alzheimer's disease (AD), cerebrospinal fluid (CSF) levels of Aβ species (CSF-Aβ) with different carboxy termini, i.e. AβX-40 and AβX-42(43) as well as Aβ1-40 and Aβ1-42(43), were measured in patients with AD and age-matched controls without dementia (CTR) using sandwich enzyme-linked immunosorbent assays (ELISAs). The present study revealed that both CSF-AβX-42(43) and Aβ1-42(43) levels were significantly lower in the AD patients (P<0.005) than in the CTR group, whereas neither CSF-AβX-40 nor CSF-Aβ1-40 levels showed any differences between the two groups. In addition, although there was no difference between the ratios of AβX-40 to Aβ1-40 in the AD and CTR groups, the ratios of AβX-42(43)to Aβ1-42(43) were increased in the AD group compared with those in the CTR group (P<0.05). Therefore, it can be assumed that the ratios of amino terminal truncations and/or modifications of CSF-Aβ42(43) with carboxy termini ending at residue 42(43) were more increased in the AD group than in the CTR group. Increased adsorption of Aβ42(43) to Aβ deposition in AD brains, decreased secretion of Aβ42(43) to CSF and/or increased clearance of Aβ42(43) from CSF might explain the diminished levels of Aβ42(43) in the CSF of AD patients. In addition, CSF-Aβ42(43) could reflect increased amino terminal truncations and/or modifications of Aβ42(43) in AD brains.

本文言語English
ページ(範囲)41-45
ページ数5
ジャーナルJournal of the Neurological Sciences
148
1
DOI
出版ステータスPublished - 1997 5 1
外部発表はい

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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