Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment

CNS Neuroscience and Therapeutics - Tập 23 Số 1 - Trang 5-22 - 2017
Mojtaba Golpich1, Elham Amini1, Zahurin Mohamed2, Azman Ali Raymond1, Norlinah Mohamed Ibrahim1, Abolhassan Ahmadiani3
1Department of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Cheras, Kuala Lumpur, Malaysia
2Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
3Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Tóm tắt

Summary

Neurodegenerative diseases are a heterogeneous group of disorders that are incurable and characterized by the progressive degeneration of the function and structure of the central nervous system (CNS) for reasons that are not yet understood. Neurodegeneration is the umbrella term for the progressive death of nerve cells and loss of brain tissue. Because of their high energy requirements, neurons are especially vulnerable to injury and death from dysfunctional mitochondria. Widespread damage to mitochondria causes cells to die because they can no longer produce enough energy. Several lines of pathological and physiological evidence reveal that impaired mitochondrial function and dynamics play crucial roles in aging and pathogenesis of neurodegenerative diseases. As mitochondria are the major intracellular organelles that regulate both cell survival and death, they are highly considered as a potential target for pharmacological‐based therapies. The purpose of this review was to present the current status of our knowledge and understanding of the involvement of mitochondrial dysfunction in pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) and the importance of mitochondrial biogenesis as a potential novel therapeutic target for their treatment. Likewise, we highlight a concise overview of the key roles of mitochondrial electron transport chain (ETC.) complexes as well as mitochondrial biogenesis regulators regarding those diseases.

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Tài liệu tham khảo

10.1007/s00415-011-6104-z

10.1016/j.tibs.2010.07.003

10.1038/nature05292

10.1016/j.phrs.2015.03.010

10.1074/jbc.M110.200311

10.1016/j.bbagen.2011.08.001

10.1016/j.freeradbiomed.2012.09.014

10.1371/journal.pone.0011468

10.1016/S1474-4422(10)70116-2

10.1016/j.freeradbiomed.2013.03.018

10.1073/pnas.0903563106

10.1002/mnfr.200700075

10.1016/j.tibs.2012.02.004

10.1016/j.cell.2008.06.016

10.1016/j.exger.2010.01.003

10.1016/j.bbadis.2011.04.006

10.1101/cshperspect.a011072

10.1186/1471-2202-15-9

10.2174/156720511795745401

10.1111/j.1471-4159.2011.07581.x

10.1093/brain/awp293

10.1016/j.bbadis.2011.10.016

10.1016/j.pneurobio.2011.06.003

10.1083/jcb.201007013

10.1038/nrm3013

10.1038/nrm3028

10.1371/journal.pone.0121328

10.1126/science.1201940

10.1093/hmg/ddg346

10.3389/fonc.2012.00182

10.2337/diabetes.51.10.2944

10.1016/j.cmet.2010.04.004

10.1073/pnas.0707060104

Hirschey M, 2011, SIRT3 regulates mitochondrial protein acetylation and intermediary metabolism. Cold Spring Harbor symposia on quantitative biology

10.1371/journal.pmed.0020233

10.1113/jphysiol.2007.135871

10.1074/jbc.M111.250092

10.1172/JCI46405

10.1056/NEJMra022567

10.1146/annurev.genet.39.110304.095751

10.1056/NEJMoa031314

10.1016/j.tibs.2011.01.004

10.1016/j.bbadis.2009.07.014

10.1007/s00702-011-0758-7

10.1016/j.freeradbiomed.2009.12.004

10.1007/s12035-010-8141-5

10.1016/j.neuroscience.2006.10.056

10.1186/1742-2094-9-184

10.1016/j.bbabio.2010.03.001

10.1111/j.1750-3639.2000.tb00278.x

10.1016/j.neurobiolaging.2011.04.011

10.1016/j.neurobiolaging.2007.12.005

10.1016/j.neurobiolaging.2012.12.005

10.1523/JNEUROSCI.3987-04.2004

10.1016/j.neuint.2009.11.011

10.1016/S0014-2999(02)01842-3

10.1186/1750-1326-8-6

10.3390/nu5020468

10.1074/jbc.M504749200

10.1093/hmg/ddi319

10.1093/hmg/ddq322

10.1016/j.cell.2006.09.015

10.1074/jbc.M700447200

10.1016/j.cmet.2012.03.019

10.1016/j.neurobiolaging.2013.03.024

10.1073/pnas.1014862107

10.1016/j.nbd.2012.08.015

10.1155/2008/418765

10.1016/j.ceca.2011.02.004

10.1093/hmg/ddp326

10.1093/hmg/ddm023

10.1186/1750-1326-6-53

10.1002/ana.20624

10.1016/j.expneurol.2013.12.017

10.1046/j.1471-4159.2003.01952.x

10.1093/brain/awf167

10.1136/jmg.2003.014316

10.1001/archgenpsychiatry.2010.22

10.1016/S0006-291X(02)03016-4

10.1074/jbc.M112.374629

10.1007/978-1-4614-3722-2_13

10.1016/j.bbabio.2013.01.004

10.1007/s00439-003-0946-0

10.1016/S0098-2997(02)00013-4

10.1128/MCB.01767-05

Li X, 2013, Mitochondrial disorders associated with mitochondrial respiratory chain complex V deficiency, Zhongguo Dang Dai Er Ke Za Zhi, 15, 596

10.1007/s10545-011-9382-9

10.1111/j.1471-4159.2011.07171.x

10.1007/s12035-014-8689-6

Rosenstock TR, 2012, Modified mitochondrial dynamics, turnover and function in neurodegeneration: A focus on Huntington's Disease, Cell Bioener Health Dis: New Perspectives in Mitochondrial Biology, 149

10.1016/j.neuroscience.2011.12.053

10.2174/1381612820666140305224906

10.1101/cshperspect.a015008

10.1152/physrev.00025.2007

10.1161/CIRCRESAHA.109.213645

10.1128/MCB.00585-06

10.1073/pnas.0606714103

10.1016/j.bbamcr.2010.09.019

10.1161/STROKEAHA.108.520114

10.1007/s12035-012-8259-8

10.1038/nature07813

10.1152/physrev.00011.2008

10.1046/j.1365-313X.2001.01167.x

10.1124/jpet.112.192138

10.1113/jphysiol.2006.109512

10.1152/ajpheart.00731.2011

10.1038/sj.onc.1207542

10.1016/j.tibs.2003.11.007

10.1074/jbc.M508805200

10.3389/fnagi.2013.00053

10.1038/cr.2013.70

10.1038/nature10815

10.1371/journal.pone.0011707

10.1073/pnas.0308686101

10.1210/er.2006-0037

10.1016/j.yjmcc.2008.03.021

10.1136/jmg.2004.026278

10.4161/cc.4.11.2121

10.1074/jbc.M707389200

10.2174/138161210793292519

10.1111/bph.12461

10.1111/j.1471-4159.2006.04018.x

10.1146/annurev.pharmtox.47.120505.105110

10.1016/j.mito.2007.02.007

Dumont M, 2011, Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease, J Alzheimers Dis, 27, 211, 10.3233/JAD-2011-110209

10.1016/j.bbadis.2013.09.007

10.1111/j.1471-4159.2009.06074.x

10.1016/j.freeradbiomed.2014.02.019

10.1152/ajprenal.00574.2014

10.1074/jbc.M609388200

Szeto HH, 2008, Cell‐permeable, mitochondrial‐targeted, peptide antioxidants, 535

10.3233/JAD-2010-100564

10.1089/ars.2009.2445

10.1002/mds.25835

10.1038/nature11060

10.1038/nature11729

10.1038/nature10821

10.3233/JAD-2010-100342

10.1111/j.1582-4934.2008.00390.x

10.1111/j.1471-4159.2009.05932.x

10.1016/j.bbadis.2013.08.013

10.1155/2014/175062

10.1016/j.ebiom.2015.03.009

10.1186/1750-1326-5-8

10.1111/j.1471-4159.2004.02884.x

10.1073/pnas.0709259105

Diana A, 2008, Mitochondria morphology and DNA content upon sublethal exposure to beta‐amyloid(1‐42) peptide, Coll Anthropol, 32, 51

10.1016/j.bbrc.2006.01.007

10.5772/59980

10.1016/j.brainres.2010.10.074

10.1093/hmg/ddg007

10.1016/j.neulet.2004.07.070

10.1111/j.1471-4159.2006.03931.x

Du L‐L, 2015, AMPK activation ameliorates Alzheimer's disease‐like pathology and spatial memory impairment in a streptozotocin‐induced Alzheimer's disease model in rats, J Alzheimers Dis, 43, 775

10.1038/sj.emboj.7601758

10.1007/s10038-008-0336-5

10.1016/j.nbd.2004.01.010

Korecka JA, 2013, Modeling early Parkinson's disease pathology with chronic low dose MPTP treatment, Restor Neurol Neurosci, 31, 155

10.1126/science.1098966

10.1007/s11064-011-0451-0

10.1016/j.nbd.2004.10.025

10.1523/JNEUROSCI.0499-12.2012

10.1016/j.neuint.2005.10.011

10.1523/JNEUROSCI.0984-06.2006

10.1016/j.tox.2012.12.011

10.1007/s00018-010-0435-2

10.1038/nrn1868

10.1523/JNEUROSCI.22-16-07006.2002

10.1002/jnr.10777

10.1016/j.expneurol.2012.06.032

10.3233/JPD-2012-11074

10.1016/j.neuron.2011.06.003

10.1038/cddis.2012.46

10.1126/scitranslmed.3001059

10.1093/hmg/ddq143

10.1093/hmg/ddq564

10.1093/hmg/ddl006

10.1007/s00401-011-0902-3

10.1038/emboj.2012.170

10.1111/jnc.12494

10.1371/journal.pbio.1000298

10.1083/jcb.201210111

10.1371/journal.pone.0004756

10.1016/j.freeradbiomed.2015.04.036

Lin T‐K, 2009, Mitochondrial dysfunction and biogenesis in the pathogenesis of Parkinson's disease, Chang Gung Med J, 32, 589

10.1016/j.neulet.2009.11.037

10.1089/hum.2009.023

10.1046/j.1471-4159.2002.00990.x

10.1038/ncpneuro0586

10.1016/j.expneurol.2012.02.017

10.1007/s12017-016-8398-6

10.1523/JNEUROSCI.3442-11.2012

10.1038/nature06022

10.1038/nature06975

10.1074/jbc.M804291200

10.1016/j.bbadis.2011.05.006

10.1093/hmg/ddq229

10.1093/hmg/ddp243

10.1093/hmg/ddn428

10.1016/j.cmet.2006.10.004

10.1016/j.nbd.2011.08.016

10.1016/j.brainresrev.2009.04.001

10.1111/j.1471-4159.2007.04996.x

10.1093/hmg/ddq306

10.1016/j.bbamcr.2008.06.004

10.1038/nrn2417

10.1016/j.freeradbiomed.2013.04.016

10.1093/hmg/ddr541

10.1126/scitranslmed.3003799

10.1210/jc.2007-1701

10.1111/j.1582-4934.2010.01223.x

10.1038/nm.2558

10.1046/j.1471-4159.2002.01112.x

10.1111/j.1365-2990.2011.01166.x

10.1096/fj.08-121046

10.1074/jbc.M112.366419

10.1371/journal.pone.0090449