Transmissible spongiform encephalopathies: a family of etiologically complex diseases - a review

被引：14

作者：

Bounias, M

Purdey, M

机构：

[1] Univ Avignon, F-807470 Le Lac Dissarles, France

[2] INRA, DSPE, Biomath & Toxicol Unit, F-807470 Le Lac Dissarles, France

[3] High Barn Farm, Taunton T4 3PX, Somerset, England

来源：

SCIENCE OF THE TOTAL ENVIRONMENT | 2002年 / 297卷 / 1-3期

关键词：

amyloid forms; cupric ion; oxidative shocks; prion structure/pathogenicity;

D O I：

10.1016/S0048-9697(02)00140-7

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

The upsurge of 'mad cow disease' with its human implications has raised the problem of the etiological mechanisms and the similarities or differences underlying the family of transmissible spongiform encephalopathies. Structural properties of prions are reviewed in connection with their natural distribution and functions, factors of transmissibility and mechanisms of pathogenicity. Polymorphism is examined in relation to disease phenotype variants. The role of oxidative factors is emphasized, while raising complexity about the role of copper ions. Further investigation directions are suggested. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

收藏

页码：1 / 19

页数：19

相关论文

共 155 条

[101] Pitfalls in prion research [J].

Peuschel, KE .

MEDICAL HYPOTHESES, 2000, 54 (05) :698-700

[102] Quantifying the dynamics of prion infection: a bifurcation analysis of Laurent's model [J].

Porcher, E ;

Gatto, M .

JOURNAL OF THEORETICAL BIOLOGY, 2000, 205 (02) :283-296

[103] NOVEL PROTEINACEOUS INFECTIOUS PARTICLES CAUSE SCRAPIE [J].

PRUSINER, SB .

SCIENCE, 1982, 216 (4542) :136-144

[104] Does an ultra violet photooxidation of the manganese-loaded/copper-depleted prion protein in the retina initiate the pathogenesis of TSE? [J].

Purdey, M .

MEDICAL HYPOTHESES, 2001, 57 (01) :29-45

[105] Ecosystems supporting clusters of sporadic TSEs demonstrate excesses of the radical-generating divalent cation manganese and deficiencies of antioxidant co factors Co, Se, Fe, Zn - Does a foreign cation substitution at prion protein's Cu domain initiate TSE? [J].

Purdey, M .

MEDICAL HYPOTHESES, 2000, 54 (02) :278-306

[106] High-dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein: the origins of new variant transmissible spongiform encephalopathies? [J].

Purdey, M .

MEDICAL HYPOTHESES, 1998, 50 (02) :91-111

[107] The UK epidemic of BSE: Slow virus or chronic pesticide-initiated modification of the prion protein? .1. Mechanisms for a chemically induced pathogenesis/transmissibility [J].

Purdey, M .

MEDICAL HYPOTHESES, 1996, 46 (05) :429-443

[108] Copper converts the cellular prion protein into a protease-resistant species that is distinct from scrapie isoform [J].

Quaglio, E ;

Chiesa, R ;

Harris, DA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (14) :11432-11438

[109] Evidence of a molecular barrier limiting susceptibility of humans, cattle and sheep to chronic wasting disease [J].

Raymond, GJ ;

Bossers, A ;

Raymond, LD ;

O'Rourke, KI ;

McHolland, LE ;

Bryant, PK ;

Miller, MW ;

Williams, ES ;

Smits, M ;

Caughey, B .

EMBO JOURNAL, 2000, 19 (17) :4425-4430

[110] Anthelmintic actions on homomer-forming nicotinic acetylcholine receptor subunits:: chicken α7 and ACR-16 from the nematode Caenorhabditis elegans [J].

Raymond, V ;

Mongan, NP ;

Sattelle, DB .

NEUROSCIENCE, 2000, 101 (03) :785-791

← 6 7 8 9 10 11 12 13 14 15 →