Difference between revisions of "Eckert 2012 Mol Neurobiol"
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{{Publication | {{Publication | ||
|title=Eckert GP, Renner K, Eckert SH, Eckmann J, Hagl S, Abdel-Kader RM, Kurz C, Leuner K, Muller WE (2012) Mitochondrial dysfunction - a pharmacological target in Alzheimer's disease. Mol Neurobiol 46: 136- | |title=Eckert GP, Renner K, Eckert SH, Eckmann J, Hagl S, Abdel-Kader RM, Kurz C, Leuner K, Muller WE (2012) Mitochondrial dysfunction - a pharmacological target in Alzheimer's disease. Mol Neurobiol 46:136-50. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/22552779 PMID: 22552779] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/22552779 PMID: 22552779] | ||
|authors=Eckert GP, Renner K, Eckert SH, Eckmann J, Hagl S, Abdel-Kader RM, Kurz C, Leuner K, Muller WE | |authors=Eckert GP, Renner K, Eckert SH, Eckmann J, Hagl S, Abdel-Kader RM, Kurz C, Leuner K, Muller WE | ||
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|abstract=Increasing evidences suggest that mitochondrial dysfunction plays an important role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD). Alterations of mitochondrial efficiency and function are mainly related to alterations in mitochondrial content, amount of respiratory enzymes, or changes in enzyme activities leading to oxidative stress, mitochondrial permeability transition pore opening, and enhanced apoptosis. More recently, structural changes of the network are related to bioenergetic function, and its consequences are a matter of intensive research. Several mitochondria-targeting compounds with potential efficacy in AD including dimebon, methylene blue, piracetam, simvastatin, Ginkgo biloba, curcumin, and omega-3 polyunsaturated fatty acids have been identified. The majority of preclinical data indicate beneficial effects, whereas most controlled clinical trials did not meet the expectations. Since mitochondrial dysfunction represents an early event in disease progression, one reason for the disappointing clinical results could be that pharmacological interventions might came too late. Thus, more studies are needed that focus on therapeutic strategies starting before severe disease progress. | |abstract=Increasing evidences suggest that mitochondrial dysfunction plays an important role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD). Alterations of mitochondrial efficiency and function are mainly related to alterations in mitochondrial content, amount of respiratory enzymes, or changes in enzyme activities leading to oxidative stress, mitochondrial permeability transition pore opening, and enhanced apoptosis. More recently, structural changes of the network are related to bioenergetic function, and its consequences are a matter of intensive research. Several mitochondria-targeting compounds with potential efficacy in AD including dimebon, methylene blue, piracetam, simvastatin, Ginkgo biloba, curcumin, and omega-3 polyunsaturated fatty acids have been identified. The majority of preclinical data indicate beneficial effects, whereas most controlled clinical trials did not meet the expectations. Since mitochondrial dysfunction represents an early event in disease progression, one reason for the disappointing clinical results could be that pharmacological interventions might came too late. Thus, more studies are needed that focus on therapeutic strategies starting before severe disease progress. | ||
|keywords=Alzheimer's disease, Dimebon, Methylene blue, Piracetam, Simvastatin, Ginkgo biloba, Curcumin, Omega-3 polyunsaturated fatty acids | |keywords=Alzheimer's disease, Dimebon, Methylene blue, Piracetam, Simvastatin, Ginkgo biloba, Curcumin, Omega-3 polyunsaturated fatty acids | ||
|mipnetlab=DE Frankfurt Mueller WE | |mipnetlab=DE Frankfurt Mueller WE, DE Frankfurt Eckert GP, DE Giessen Eckert GP, DE Regensburg Renner-Sattler K | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|injuries=Mitochondrial | |area=Patients, Pharmacology;toxicology | ||
|injuries=Mitochondrial disease | |||
|organism=Human | |organism=Human | ||
|preparations=Intact organism | |||
|additional=Curcumin, | |||
}} | }} | ||
Latest revision as of 07:53, 21 February 2020
| Eckert GP, Renner K, Eckert SH, Eckmann J, Hagl S, Abdel-Kader RM, Kurz C, Leuner K, Muller WE (2012) Mitochondrial dysfunction - a pharmacological target in Alzheimer's disease. Mol Neurobiol 46:136-50. |
Eckert GP, Renner K, Eckert SH, Eckmann J, Hagl S, Abdel-Kader RM, Kurz C, Leuner K, Muller WE (2012) Mol Neurobiol
Abstract: Increasing evidences suggest that mitochondrial dysfunction plays an important role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD). Alterations of mitochondrial efficiency and function are mainly related to alterations in mitochondrial content, amount of respiratory enzymes, or changes in enzyme activities leading to oxidative stress, mitochondrial permeability transition pore opening, and enhanced apoptosis. More recently, structural changes of the network are related to bioenergetic function, and its consequences are a matter of intensive research. Several mitochondria-targeting compounds with potential efficacy in AD including dimebon, methylene blue, piracetam, simvastatin, Ginkgo biloba, curcumin, and omega-3 polyunsaturated fatty acids have been identified. The majority of preclinical data indicate beneficial effects, whereas most controlled clinical trials did not meet the expectations. Since mitochondrial dysfunction represents an early event in disease progression, one reason for the disappointing clinical results could be that pharmacological interventions might came too late. Thus, more studies are needed that focus on therapeutic strategies starting before severe disease progress. • Keywords: Alzheimer's disease, Dimebon, Methylene blue, Piracetam, Simvastatin, Ginkgo biloba, Curcumin, Omega-3 polyunsaturated fatty acids
• O2k-Network Lab: DE Frankfurt Mueller WE, DE Frankfurt Eckert GP, DE Giessen Eckert GP, DE Regensburg Renner-Sattler K
Labels: MiParea: Patients, Pharmacology;toxicology
Stress:Mitochondrial disease Organism: Human
Preparation: Intact organism
Curcumin
