Tags

Type your tag names separated by a space and hit enter

Mitochondrial dysfunction, free radical generation and cellular stress response in neurodegenerative disorders.
Front Biosci. 2007 Jan 01; 12:1107-23.FB

Abstract

Protein conformational diseases, such as Alzheimer's, Parkinson's and Huntington's, affect a large portion of aging population. The pathogenic dysfunctional aggregation of proteins in non-native conformations is associated with metabolic derangements and excessive production of reactive oxygen species. Reduction of cellular expression and activity of antioxidant proteins result in increased oxidative stress. Free-radicals derived from mitochondrial dysfunction and from the cyclooxygenase enzyme activity play a role in oxidative damage of brain. Cyclooxygenase also mediates in neuro-inflammation by the production of pro-inflammatory prostaglandins which contribute to brain injury. The pathogenic role of cyclooxygenase has been demonstrated in Alzheimer and Parkinson diseases. The brain responses to detect and control diverse forms of stress are accomplished by a complex network of "longevity assurance processes" integrated to the expression of genes termed vitagenes. Heat shock proteins are a highly conserved system responsible for the preservation and repair of correct protein conformation. Heme oxygenase-1, a inducible and redox-regulated enzyme, is currently considered as having an important role in cellular antioxidant defense. A neuroprotective effect, due to its heme degrading activity, and tissue-specific pro-oxidant effects, due to its products CO and free iron, are under debate. There is a current interest in dietary compounds that can inhibit, retard or reverse the multi-stage pathophysiology of Alzheimer disease, with a chronic inflammatory response, brain injury and beta-amyloid associated pathology. Curcumin and ferulic acid, two powerful antioxidants, the first from the curry spice turmeric and the second a major constituent of fruit and vegetables, have emerged as strong inducers of the heat shock response. Food supplementation with curcumin and ferulic acid is considered a nutritional approach to reduce oxidative damage and amyloid pathology in Alzheimer disease.

Authors+Show Affiliations

Institute of Pharmacology, Catholic University School of Medicine, Rome, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

17127365

Citation

Mancuso, Cesare, et al. "Mitochondrial Dysfunction, Free Radical Generation and Cellular Stress Response in Neurodegenerative Disorders." Frontiers in Bioscience : a Journal and Virtual Library, vol. 12, 2007, pp. 1107-23.
Mancuso C, Scapagini G, Currò D, et al. Mitochondrial dysfunction, free radical generation and cellular stress response in neurodegenerative disorders. Front Biosci. 2007;12:1107-23.
Mancuso, C., Scapagini, G., Currò, D., Giuffrida Stella, A. M., De Marco, C., Butterfield, D. A., & Calabrese, V. (2007). Mitochondrial dysfunction, free radical generation and cellular stress response in neurodegenerative disorders. Frontiers in Bioscience : a Journal and Virtual Library, 12, 1107-23.
Mancuso C, et al. Mitochondrial Dysfunction, Free Radical Generation and Cellular Stress Response in Neurodegenerative Disorders. Front Biosci. 2007 Jan 1;12:1107-23. PubMed PMID: 17127365.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial dysfunction, free radical generation and cellular stress response in neurodegenerative disorders. AU - Mancuso,Cesare, AU - Scapagini,Giovanni, AU - Currò,Diego, AU - Giuffrida Stella,Anna Maria, AU - De Marco,Carlo, AU - Butterfield,D Allan, AU - Calabrese,Vittorio, Y1 - 2007/01/01/ PY - 2006/11/28/pubmed PY - 2007/8/24/medline PY - 2006/11/28/entrez SP - 1107 EP - 23 JF - Frontiers in bioscience : a journal and virtual library JO - Front. Biosci. VL - 12 N2 - Protein conformational diseases, such as Alzheimer's, Parkinson's and Huntington's, affect a large portion of aging population. The pathogenic dysfunctional aggregation of proteins in non-native conformations is associated with metabolic derangements and excessive production of reactive oxygen species. Reduction of cellular expression and activity of antioxidant proteins result in increased oxidative stress. Free-radicals derived from mitochondrial dysfunction and from the cyclooxygenase enzyme activity play a role in oxidative damage of brain. Cyclooxygenase also mediates in neuro-inflammation by the production of pro-inflammatory prostaglandins which contribute to brain injury. The pathogenic role of cyclooxygenase has been demonstrated in Alzheimer and Parkinson diseases. The brain responses to detect and control diverse forms of stress are accomplished by a complex network of "longevity assurance processes" integrated to the expression of genes termed vitagenes. Heat shock proteins are a highly conserved system responsible for the preservation and repair of correct protein conformation. Heme oxygenase-1, a inducible and redox-regulated enzyme, is currently considered as having an important role in cellular antioxidant defense. A neuroprotective effect, due to its heme degrading activity, and tissue-specific pro-oxidant effects, due to its products CO and free iron, are under debate. There is a current interest in dietary compounds that can inhibit, retard or reverse the multi-stage pathophysiology of Alzheimer disease, with a chronic inflammatory response, brain injury and beta-amyloid associated pathology. Curcumin and ferulic acid, two powerful antioxidants, the first from the curry spice turmeric and the second a major constituent of fruit and vegetables, have emerged as strong inducers of the heat shock response. Food supplementation with curcumin and ferulic acid is considered a nutritional approach to reduce oxidative damage and amyloid pathology in Alzheimer disease. SN - 1093-9946 UR - https://www.unboundmedicine.com/medline/citation/17127365/Mitochondrial_dysfunction_free_radical_generation_and_cellular_stress_response_in_neurodegenerative_disorders_ L2 - https://www.bioscience.org/2007/v12/af/2130/fulltext.htm DB - PRIME DP - Unbound Medicine ER -