Multi-elemental analysis of serum and amyloid fibrils in familial amyloid polyneuropathy patients

被引:12
|
作者
Susuki, Seiko [1 ]
Ando, Yukio [2 ]
Sato, Takashi [1 ]
Nishiyama, Masami [3 ]
Miyata, Masanori [1 ]
Suico, Mary Ann [1 ]
Shuto, Tsuyoshi [1 ]
Kai, Hirofumi [1 ]
机构
[1] Kumamoto Univ, Dept Mol Med, Grad Sch Pharmaceut Sci, Global COE Cell Fate Regulat Res & Educ Unit, Kumamoto 8620973, Japan
[2] Kumamoto Univ, Grad Sch Med Sci, Dept Diagnost Med, Kumamoto 8600811, Japan
[3] Kumamoto Univ, Inst Resource Dev & Anal, Div Instrumental Anal, Kumamoto 8620973, Japan
来源
关键词
ICP-MS; FAP; amyloid; metals; FAP patients; serum;
D O I
10.1080/13506120802006013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
There is accumulating evidence of the involvement of biological metal imbalance in the progression of amyloid diseases such as Alzheimer's, Parkinson's and prion diseases. However, the mineral status in patients affected with familial amyloidotic polyneuropathy (FAP) has not been investigated. It is the aim of this study to determine the metal concentrations in the serum and in the transthyretin (TTR) amyloid fibrils of FAP amyloidogenic TTR (ATTR) V30M patients. Multi-elemental analysis of 17 metals by high-resolution inductively coupled plasma mass spectrometry (ICP-MS) revealed a significant decrease of the metals Fe, Cu, Zn, Cs and Ba in the serum of FAP patients (mean age 38.5 +/- 8.3 years; duration of disease 4 +/- 2.6 years) in comparison with that of healthy individuals (mean age 36.2 +/- 9.2 years). On the other hand, these metals, except Cs, were found at high levels in the amyloid fibrils of FAP patients (mean age 55.8 +/- 9.2; duration of disease 6.5 +/- 1.3 years) compared with other metals. These findings firstly suggest that the mineral status could be a candidate factor, which participates in the wide spectrum of clinical pictures of FAP patients.
引用
收藏
页码:108 / 116
页数:9
相关论文
共 50 条
  • [1] Ultrastructure of amyloid fibrils in familial amyloid polyneuropathy
    Katsuragi, S
    Ikegami, K
    Nishiyama, K
    Ohsawa, K
    Yamashita, K
    Miyakawa, T
    Ando, Y
    BRAIN PATHOLOGY, 2000, 10 (04) : 549 - 549
  • [2] Evolution of amyloid fibrils in transthyretin familial amyloid polyneuropathy: An ultrastructural study
    Koike, Haruki
    Nishi, Ryoji
    Ikeda, Shohei
    Kawagashira, Yuichi
    Iijima, Masahiro
    Katsuno, Masahisa
    Sobue, Gen
    JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, 2018, 23 (04) : 321 - 321
  • [3] Serum transthyretin monomer in patients with familial amyloid polyneuropathy
    Sekijima, Y
    Tokuda, T
    Kametani, F
    Tanaka, K
    Maruyama, K
    Ikeda, S
    AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS, 2001, 8 (04): : 257 - 262
  • [4] PREALBUMIN VARIANTS IN THE AMYLOID FIBRILS OF SWEDISH FAMILIAL AMYLOIDOTIC POLYNEUROPATHY
    WESTERMARK, P
    SLETTEN, K
    OLOFSSON, BO
    CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1987, 69 (03): : 695 - 701
  • [5] Histopathological analysis of familial amyloid polyneuropathy
    Ehara, T
    9TH ASIAN PACIFIC CONGRESS OF NEPHROLOGY, 2003, : 79 - 81
  • [6] Ultrastructure of familial amyloid polyneuropathy amyloid fibrils: Examination with high-resolution electron microscopy
    Inoue, S
    Kuroiwa, M
    Saraiva, MJ
    Guimaraes, A
    Kisilevsky, R
    JOURNAL OF STRUCTURAL BIOLOGY, 1998, 124 (01) : 1 - 12
  • [7] FAMILIAL AMYLOID POLYNEUROPATHY
    REILLY, MM
    KING, RHM
    BRAIN PATHOLOGY, 1993, 3 (02) : 165 - 176
  • [8] Familial Amyloid Polyneuropathy
    Cakar, Arman
    Durmus-Tekce, Hacer
    Parman, Yesim
    NOROPSIKIYATRI ARSIVI-ARCHIVES OF NEUROPSYCHIATRY, 2019, 56 (02): : 150 - 156
  • [9] Familial amyloid polyneuropathy
    Plante-Bordeneuve, V.
    JOURNAL OF THE NEUROLOGICAL SCIENCES, 2019, 405
  • [10] Familial amyloid polyneuropathy
    Fernández, JAB
    MEDICINA CLINICA, 2004, 122 (05): : 197 - 197