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Perspectives of drug-based neuroprotection targeting mitochondria.
Rev Neurol (Paris). 2014 May; 170(5):390-400.RN

Abstract

Mitochondrial dysfunction has been reported in most neurodegenerative diseases. These anomalies include bioenergetic defect, respiratory chain-induced oxidative stress, defects of mitochondrial dynamics, increase sensitivity to apoptosis, and accumulation of damaged mitochondria with instable mitochondrial DNA. Significant progress has been made in our understanding of the pathophysiology of inherited mitochondrial disorders but most have no effective therapies. The development of new metabolic treatments will be useful not only for rare mitochondrial disorders but also for the wide spectrum of common age-related neurodegenerative diseases shown to be associated with mitochondrial dysfunction. A better understanding of the mitochondrial regulating pathways raised several promising perspectives of neuroprotection. This review focuses on the pharmacological approaches to modulate mitochondrial biogenesis, the removal of damaged mitochondria through mitophagy, scavenging free radicals and also dietary measures such as ketogenic diet.

Authors+Show Affiliations

UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France.UMR CNRS6214, Inserm1083 and department of biochemistry and genetics, CHU d'Angers, 4, rue Larrey, 49933 Angers, France. Electronic address: pareynier@chu-angers.fr.

Pub Type(s)

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

Language

eng

PubMed ID

24792485

Citation

Procaccio, V, et al. "Perspectives of Drug-based Neuroprotection Targeting Mitochondria." Revue Neurologique, vol. 170, no. 5, 2014, pp. 390-400.
Procaccio V, Bris C, Chao de la Barca JM, et al. Perspectives of drug-based neuroprotection targeting mitochondria. Rev Neurol (Paris). 2014;170(5):390-400.
Procaccio, V., Bris, C., Chao de la Barca, J. M., Oca, F., Chevrollier, A., Amati-Bonneau, P., Bonneau, D., & Reynier, P. (2014). Perspectives of drug-based neuroprotection targeting mitochondria. Revue Neurologique, 170(5), 390-400. https://doi.org/10.1016/j.neurol.2014.03.005
Procaccio V, et al. Perspectives of Drug-based Neuroprotection Targeting Mitochondria. Rev Neurol (Paris). 2014;170(5):390-400. PubMed PMID: 24792485.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Perspectives of drug-based neuroprotection targeting mitochondria. AU - Procaccio,V, AU - Bris,C, AU - Chao de la Barca,J M, AU - Oca,F, AU - Chevrollier,A, AU - Amati-Bonneau,P, AU - Bonneau,D, AU - Reynier,P, Y1 - 2014/05/01/ PY - 2014/01/27/received PY - 2014/03/25/accepted PY - 2014/5/6/entrez PY - 2014/5/6/pubmed PY - 2015/1/13/medline KW - 5-aminoimidazole-4-carboxamide ribonucleoside KW - AD KW - AICAR KW - ALS KW - AMP KW - ATP KW - Acide N-methyl-D-aspartic KW - Adenosine monophosphate KW - Adenosine triphosphate KW - Alzheimer's disease KW - Amyotrophic lateral sclerosis KW - CCCP KW - CNS KW - Carbonylcyanide m-chlorophenylhydrazone KW - Central nervous system KW - CoQ KW - Coenzyme Q KW - Cyclic AMP KW - ERR KW - ETC KW - Electron transport chain KW - Estrogen-related receptors KW - FAD/FADH KW - Flavin adenine nucleotide KW - GDAP1 KW - Ganglioside-induced differentiation-associated protein 1 KW - HD KW - Huntington disease KW - KTP KW - Kinetin triphosphate KW - LHON KW - Leber hereditary optic neuropathy KW - MAPK KW - MELAS KW - MERRF KW - MFN1/MFN2 KW - Maladies mitochondriales KW - Maladies neurodégénératives KW - Mammalian target of rapamycin KW - Manganese superoxide dismutase KW - Mitochondria KW - Mitochondrial diseases KW - Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes KW - Mitochondrial genome or DNA KW - Mitochondrial permeability transition pore KW - Mitochondrial transcription factor A KW - Mitochondrie KW - Mitofusin KW - Mitogen-activated protein kinases KW - MnSOD KW - Myoclonic epilepsy and ragged red fibers KW - NAD/NADH KW - NARP KW - NMDA KW - NOS KW - NRF1/NRF2 KW - Neurodegenerative disorders KW - Neurogenic muscle weakness, ataxia, and retinitis pigmentosa KW - Neuroprotection pharmacologique KW - Nicotinamide adenine dinucleotide KW - Nitric oxide synthase KW - Nuclear genome or DNA KW - Nuclear respiratory factors KW - OPA1 KW - OXPHOS KW - Optic atrophy 1 KW - Oxidative phosphorylation KW - PARL KW - PD KW - PGC-1-α KW - PGC1-related coactivator KW - PINK1 KW - PKA KW - PPAR KW - PPAR gamma coactivator 1-alpha KW - PRC KW - PTEN-induced putative kinase1 KW - Parkinson's disease KW - Peroxisome proliferators-activated receptors KW - Pharmacological neuroprotection KW - Presenilins-associated rhomboid-like protein KW - Protein kinase A KW - RC KW - ROS KW - RXR KW - Reactive oxygen species KW - Respiratory chain KW - Retinoid X receptors KW - SIRT KW - Sirtuins KW - TFAM KW - TFB2/TFB2 KW - Transcription factors B1 and B2 KW - cAMP KW - mTOR KW - mtDNA KW - mtPTP KW - nDNA SP - 390 EP - 400 JF - Revue neurologique JO - Rev Neurol (Paris) VL - 170 IS - 5 N2 - Mitochondrial dysfunction has been reported in most neurodegenerative diseases. These anomalies include bioenergetic defect, respiratory chain-induced oxidative stress, defects of mitochondrial dynamics, increase sensitivity to apoptosis, and accumulation of damaged mitochondria with instable mitochondrial DNA. Significant progress has been made in our understanding of the pathophysiology of inherited mitochondrial disorders but most have no effective therapies. The development of new metabolic treatments will be useful not only for rare mitochondrial disorders but also for the wide spectrum of common age-related neurodegenerative diseases shown to be associated with mitochondrial dysfunction. A better understanding of the mitochondrial regulating pathways raised several promising perspectives of neuroprotection. This review focuses on the pharmacological approaches to modulate mitochondrial biogenesis, the removal of damaged mitochondria through mitophagy, scavenging free radicals and also dietary measures such as ketogenic diet. SN - 0035-3787 UR - https://www.unboundmedicine.com/medline/citation/24792485/Perspectives_of_drug_based_neuroprotection_targeting_mitochondria_ DB - PRIME DP - Unbound Medicine ER -