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Redox metals and neurodegenerative disease.
Curr Opin Chem Biol 1999; 3(2):220-5CO

Abstract

Multiple lines of evidence implicate redox-active transition metals as mediators of oxidative stress in neurodegenerative diseases. Among the recent research discoveries is the finding that transition metals bind to proteins associated with neurodegeneration, including the prion protein. Whereas binding in the latter case may serve an antioxidant function, adventitious binding of metals to other proteins appears to preserve their catalytic redox activity in a manner that disturbs free radical homeostasis. Alterations in the levels of copper- and iron-containing metalloenzymes, involved in processing partially reduced oxygen species, are also likely to contribute to altered redox balance in neurodegenerative diseases. Nonetheless, even in familial forms of amyotrophic lateral sclerosis linked to mutations in superoxide dismutase, it is unclear whether an altered enzyme activity or, indirectly, a disturbance in transition-metal homeostasis is involved in the disease pathogenesis.

Authors+Show Affiliations

Department of Chemistry, Case Western Reserve University, Cleveland, OH44106, USA. LMS3@PO.CWRU.EDUNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

10226049

Citation

Sayre, L M., et al. "Redox Metals and Neurodegenerative Disease." Current Opinion in Chemical Biology, vol. 3, no. 2, 1999, pp. 220-5.
Sayre LM, Perry G, Smith MA. Redox metals and neurodegenerative disease. Curr Opin Chem Biol. 1999;3(2):220-5.
Sayre, L. M., Perry, G., & Smith, M. A. (1999). Redox metals and neurodegenerative disease. Current Opinion in Chemical Biology, 3(2), pp. 220-5.
Sayre LM, Perry G, Smith MA. Redox Metals and Neurodegenerative Disease. Curr Opin Chem Biol. 1999;3(2):220-5. PubMed PMID: 10226049.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Redox metals and neurodegenerative disease. AU - Sayre,L M, AU - Perry,G, AU - Smith,M A, PY - 1999/5/5/pubmed PY - 1999/5/5/medline PY - 1999/5/5/entrez SP - 220 EP - 5 JF - Current opinion in chemical biology JO - Curr Opin Chem Biol VL - 3 IS - 2 N2 - Multiple lines of evidence implicate redox-active transition metals as mediators of oxidative stress in neurodegenerative diseases. Among the recent research discoveries is the finding that transition metals bind to proteins associated with neurodegeneration, including the prion protein. Whereas binding in the latter case may serve an antioxidant function, adventitious binding of metals to other proteins appears to preserve their catalytic redox activity in a manner that disturbs free radical homeostasis. Alterations in the levels of copper- and iron-containing metalloenzymes, involved in processing partially reduced oxygen species, are also likely to contribute to altered redox balance in neurodegenerative diseases. Nonetheless, even in familial forms of amyotrophic lateral sclerosis linked to mutations in superoxide dismutase, it is unclear whether an altered enzyme activity or, indirectly, a disturbance in transition-metal homeostasis is involved in the disease pathogenesis. SN - 1367-5931 UR - https://www.unboundmedicine.com/medline/citation/10226049/Redox_metals_and_neurodegenerative_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1367-5931(99)80035-0 DB - PRIME DP - Unbound Medicine ER -