The DOI matches its Crossref record; 103 of the 103 references it cites were found in a registry or an index.
Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
Abstract
Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.
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In the citing paper
“Evidence also suggests that not only does Aβ increase cellular RS but that these RS may in turn increase production of Aβ in a destructive autocatalytic cycle (Misonou et al., 2000; Tamagno et al., 2002, 2005; Lin and Beal, 2006; Quiroz-Baez et al., 2009).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Lin and Beal, 2006
In the citing paper
“Aβ appears to enhance production of cellular RS, and these RS in turn may to contribute to Aβ toxicity.”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Lin and Beal, 2006
In the citing paper
“On the basis of evidence from post-mortem brain tissues from AD patients as well as different AD mouse models, damaged mitochondria and increased oxidative stress are common features of AD (Lin and Beal, 2006; Mattson et al., 2008).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Lin and Beal, 2006
In the citing paper
“Due to the content of multiple electron carriers and an extensive antioxidant defence, they represent a key centre for ROS/antioxidant balance regulation [56].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [56]
In the citing paper
“and the AD brain displays insulin resistance and impaired mitochondrial function (45,46)”
From Altered mitochondrial function in insulin-deficient and insulin-resistant states (2018) · cites this paper as [46]
In the citing paper
“a range of distinct aetologies, which manifest as a variety of different syndromes or diseases, converge at some point on an autocatalytic series of reactions, involving imperfectly liganded iron, in the production of the very damaging hydroxyl radical, that by causing the destruction of appropriate cellular structures and proteins liberates further ‘free’ iron and other reactive oxygen species,”
In the citing paper
“Aging-associated expression changes in genes associated with mitochondrial function, protein metabolism, and immune response have been identified in several tissues (173) and are consistent with some proposed mechanisms for late-onset neurodegenerative diseases (98, 113, 124, 166).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [98]
In the citing paper
“Mitochondrial dysfunction and oxidative stress, including mitochondrial DNA damage, have been implicated in all three diseases—AD, PD, and AMD (12, 17, 98, 165).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [98]
In the citing paper
“Numerous studies have demonstrated a central role of mitochondria and energy homeostasis in the pathogenesis of aging-associated neurodegenerative diseases (98, 157, 166).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [98]
In the citing paper
“Much evidence suggests a role for mitochondrial dysfunction in the pathophysiology of PD, a common age-associated neurodegenerative disease characterized by progressive degeneration of the nigrostriatal dopamine (DA) pathway and presence of the intraneuronal protein inclusions (Lewy bodies)1-3.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [2]
In the citing paper
“Several different pathogenic mechanisms have been identified in the CNS and peripheral tissues during the disease course in ALS, but mitochondrial and bioenergetic defects are implicated widely in ALS pathogenesis2.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [2]
In the citing paper
“These studies provide compelling evidence for a role of PGC-1α in the pathogenesis of neurodegenerative diseases, and thus it is a promising therapeutic target for neurodegenerative disorders2, 72.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [2]
In the citing paper
“Second, high cellular ROS levels are associated with cancer, diabetes, inflammatory diseases, ischemia-related diseases, and neurodegeneration, and are thus commonly thought to contribute to human pathologies and aging 80–83.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [81]
Citations
Cites
Danial, N. N., & Korsmeyer, S. J. (2004) · Cell · doi:10.1016/s0092-8674(04)00046-7 · Cited by 4,651
Chronic systemic pesticide exposure reproduces features of Parkinson's disease
Betarbet, R. S., Sherer, T., MacKenzie, G. M., Garcia‐Osuna, M., Panov, A. V., & Greenamyre, J. T. (2000) · Nature Neuroscience · doi:10.1038/81834 · Cited by 3,770
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
Wallace, D. C. (2005) · Annual Review of Genetics · doi:10.1146/annurev.genet.39.110304.095751 · Cited by 3,185
Mutations in the DJ-1 Gene Associated with Autosomal Recessive Early-Onset Parkinsonism
Bonifati, V., Rizzu, P., van Baren, M. J., Schaap, O., Breedveld, G. J., Krieger, E., Dekker, M. C. J., Squitieri, F., Ibáñez, P., Joosse, M., et al. (2003) · Science · doi:10.1126/science.1077209 · Cited by 2,854
Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
Chipuk, J. E., Kuwana, T., Bouchier-Hayes, L., Droin, N. M., Newmeyer, D. D., Schuler, M., & Green, D. R. (2004) · Science · doi:10.1126/science.1092734 · Cited by 2,108
Oxidative Damage Is the Earliest Event in Alzheimer Disease
Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., et al. (2001) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/60.8.759 · Cited by 1,885
Gene regulation and DNA damage in the ageing human brain
Lu, T., Pan, Y., Kao, S.-Y., Li, C., Kohane, I., Chan, J., & Yankner, B. A. (2004) · Nature · doi:10.1038/nature02661 · Cited by 1,874
MITOCHONDRIAL COMPLEX I DEFICIENCY IN PARKINSON'S DISEASE
Schapira, A. H. V., Cooper, J. A. D., Dexter, D. T., Jenner, P. G., Clark, J. B., & MARSDEN, C. D. (1989) · The Lancet · doi:10.1016/s0140-6736(89)92366-0 · Cited by 1,757
Extension of murine life span by overexpression of catalase targeted to mitochondria
Schriner, S. E., Linford, N. J., Martin, G. M., Treuting, P., Ogburn, C. E., Emond, M., Coskun, P. E., Ladiges, W., Wolf, N., Van Remmen, H., et al. (2005) · Science · doi:10.1126/science.1106653 · Cited by 1,724
Bender, A., Krishnan, K. J., Morris, C. M., Taylor, G. A., Reeve, A. K., Perry, R. H., Jaros, E., Hersheson, J. S., Betts, J., Klopstock, T., et al. (2006) · Nature Genetics · doi:10.1038/ng1769 · Cited by 1,570
Mitochondrial metabolism of reactive oxygen species
Andreyev, A. Y., Kushnareva, Y. E., & Starkov, A. A. (2005) · Biochemistry (Moscow) · doi:10.1007/s10541-005-0102-7 · Cited by 1,336
ABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer's Disease
Lustbader, J. W., Cirilli, M., Lin, C., Xu, H. W., Takuma, K., Wang, N., Caspersen, C., Chen, X., Pollak, S., Chaney, M., et al. (2004) · Science · doi:10.1126/science.1091230 · Cited by 1,303
PUMA Induces the Rapid Apoptosis of Colorectal Cancer Cells
Yu, J., Zhang, L., Hwang, P. M., Kinzler, K. W., & Vogelstein, B. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00213-1 · Cited by 1,289
Parkinson's disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity
West, A. B., Moore, D. J., Biskup, S., Bugayenko, A., Smith, W. W., Ross, C. A., Dawson, V. L., & Dawson, T. M. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0507360102 · Cited by 1,228
Defects in Adaptive Energy Metabolism with CNS-Linked Hyperactivity in PGC-1α Null Mice
Lin, J., Wu, P.-H., Tarr, P. T., Lindenberg, K. S., St-Pierre, J., Zhang, C.-Y., Mootha, V. K., Jäger, S., Vianna, C. R., Reznick, R. M., et al. (2004) · Cell · doi:10.1016/j.cell.2004.09.013 · Cited by 1,162
Canet-Aviles, R., Wilson, M. A., Miller, D. W., Ahmad, R., McLendon, C., Bandyopadhyay, S., Baptista, M. J., Ringe, D., Petsko, G. A., & Cookson, M. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0402959101 · Cited by 1,115
Manczak, M., Anekonda, T. S., Henson, E., Park, B. S., Quinn, J., & Reddy, P. H. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl066 · Cited by 1,104
Mechanism of Toxicity in Rotenone Models of Parkinson's Disease
Sherer, T., Betarbet, R. S., Testa, C. M., Seo, B. B., Richardson, J. R., Kim, J. H., Miller, G. W., Yagi, T., Matsuno‐Yagi, A., & Greenamyre, J. T. (2003) · Journal of Neuroscience · doi:10.1523/jneurosci.23-34-10756.2003 · Cited by 1,102
Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines
Panov, A. V., Gutekunst, C.-A., Leavitt, B. R., Hayden, M. R., Burke, J. R., Strittmatter, W. J., & Greenamyre, J. T. (2002) · Nature Neuroscience · doi:10.1038/nn884 · Cited by 1,030
Mitochondrial Dysfunction and Oxidative Damage in parkin-deficient Mice
Palacino, J. J., Sagi, D., Goldberg, M. S., Krauss, S., Motz, C., Wacker, M., Klose, J., & Shen, J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m401135200 · Cited by 995
Kraytsberg, Y., Kudryavtseva, E., McKee, A. C., Geula, C., Kowall, N. W., & Khrapko, K. (2006) · Nature Genetics · doi:10.1038/ng1778 · Cited by 896
Mitochondrial DNA deletions in human brain: regional variability and increase with advanced age
Corral-Debrinski, M., Horton, T., Lott, M. T., Shoffner, J. M., Flint Beal, M., & Wallace, D. C. (1992) · Nature Genetics · doi:10.1038/ng1292-324 · Cited by 890
Yang, Y., Gehrke, S., Imai, Y., Huang, Z., Ouyang, Y., Wang, J.-W., Yang, L., Beal, M. F., Vogel, H., & Lu, B. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0602493103 · Cited by 798
Self-citationPraticò, D., Uryu, K., Leight, S., Trojanoswki, J. Q., & Lee, V. M.-Y. (2001) · The Journal of Neuroscience · doi:10.1523/jneurosci.21-12-04183.2001 · Cited by 777
S -Nitrosylation of Parkin Regulates Ubiquitination and Compromises Parkin's Protective Function
Chung, K. K. K., Thomas, B., Li, X., Pletniková, O., Troncoso, J. C., Marsh, L., Dawson, V. L., & Dawson, T. M. (2004) · Science · doi:10.1126/science.1093891 · Cited by 772
Mitochondrial defect in Huntington's disease caudate nucleus
Gu, M., Gash, M. T., Mann, V. M., Javoy‐Agid, F., Cooper, J. M., & Schapira, A. H. V. (1996) · Annals of Neurology · doi:10.1002/ana.410390317 · Cited by 758
Kong, J., & Xu, Z. (1998) · Journal of Neuroscience · doi:10.1523/jneurosci.18-09-03241.1998 · Cited by 723
Kim, R. H., Smith, P. D., Aleyasin, H., Hayley, S. P., Mount, M. P., Pownall, S., Wakeham, A. C., You-Ten, A. J., Kalia, S. K., Horne, P., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0501282102 · Cited by 711
Martin, L. J., Pan, Y., Price, A. C., Sterling, W., Copeland, N. G., Jenkins, N. A., Price, D. L., & Lee, M. K. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.4308-05.2006 · Cited by 684
Mattiazzi, M., D’Aurelio, M., Gajewski, C. D., Martushova, K., Kiaei, M., Beal, M. F., & Manfredi, G. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m203065200 · Cited by 639
Self-citationCytochrome oxidase deficiency in Alzheimer’s disease
Parker, W. D., Filley, C. M., & Parks, J. K. (1990) · Neurology · doi:10.1212/wnl.40.8.1302 · Cited by 598
Anandatheerthavarada, H. K., Biswas, G., Robin, M.-A., & Avadhani, N. G. (2003) · The Journal of Cell Biology · doi:10.1083/jcb.200207030 · Cited by 571
Loss of function mutations in the gene encoding Omi/HtrA2 in Parkinson's disease
Strauss, K. M., Martins, L. M., Plun‐Favreau, H., Marx, F. P., Kautzmann, S., Berg, D., Gasser, T., Wszolek, Z., Müller, T. H., Bornemann, A., et al. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi215 · Cited by 569
Coskun, P. E., Beal, M. F., & Wallace, D. C. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0403649101 · Cited by 556
Self-citationLuoma, P., Melberg, A., Rinne, J. O., Kaukonen, J. A., Nupponen, N. N., Chalmers, R. M., Oldfors, A., Rautakorpi, I., Peltonen, L., Majamaa, K., et al. (2004) · The Lancet · doi:10.1016/s0140-6736(04)16983-3 · Cited by 548
DJ-1, a novel regulator of the tumor suppressor PTEN
Kim, R. H., Peters, M., Jang, Y., Shi, W., Pintilie, M., Fletcher, G. C., DeLuca, C., Silvester, J., Zhou, L., Snow, B. E., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.02.010 · Cited by 547
Transcriptional abnormalities in Huntington disease
Sugars, K. L., & Rubinsztein, D. C. (2003) · Trends in Genetics · doi:10.1016/s0168-9525(03)00074-x · Cited by 535
Fornai, F., Schlüter, O. M., Lenzi, P., Gesi, M., Ruffoli, R., Ferrucci, M., Lazzeri, G., Busceti, C. L., Pontarelli, F., Battaglia, G., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0409713102 · Cited by 526
Toxicity of Familial ALS-Linked SOD1 Mutants from Selective Recruitment to Spinal Mitochondria
Liu, J., Lillo, C., Jonsson, P. A., Velde, C. V., Ward, C. M., Miller, T. M., Subramaniam, J. R., Rothstein, J. D., Marklund, S. L., Andersen, P. M., et al. (2004) · Neuron · doi:10.1016/j.neuron.2004.06.016 · Cited by 525
Choo, Y. S. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddh162 · Cited by 515
Pasinelli, P., Belford, M. E., Lennon, N. J., Bacskai, B. J., Hyman, B. T., Trotti, D., & Brown, R. H. (2004) · Neuron · doi:10.1016/j.neuron.2004.06.021 · Cited by 506
p53 Mediates Cellular Dysfunction and Behavioral Abnormalities in Huntington’s Disease
Bae, B.-I., Xu, H., Igarashi, S., Fujimuro, M., Agrawal, N., Taya, Y., Hayward, S. D., Moran, T. H., Montell, C., Ross, C. A., et al. (2005) · Neuron · doi:10.1016/j.neuron.2005.06.005 · Cited by 495
The prolyl isomerase Pin1 regulates amyloid precursor protein processing and amyloid-β production
Pastorino, L., Sun, A., Lu, P.-J., Zhou, X. Z., Balastik, M., Finn, G., Wulf, G., Lim, J., Li, S.-H., Li, X., et al. (2006) · Nature · doi:10.1038/nature04543 · Cited by 487
β‐Amyloid inhibits integrated mitochondrial respiration and key enzyme activities
Casley, C. S., Canevari, L., Land, J. M., Clark, J. B., & Sharpe, M. A. (2001) · Journal of Neurochemistry · doi:10.1046/j.0022-3042.2001.00681.x · Cited by 485
Brouillet, E., Hantraye, P., Ferrante, R. J., Dolan, R., Leroy‐Willig, A., Kowall, N. W., & Beal, M. F. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.15.7105 · Cited by 485
Self-citationJenkins, B. G., Koroshetz, W. J., Beal, M. F., & Rosen, B. R. (1993) · Neurology · doi:10.1212/wnl.43.12.2689 · Cited by 479
Self-citationHigh-quality life extension by the enzyme peptide methionine sulfoxide reductase
Ruan, H., Tang, X. D., Chen, M.-L., Joiner, M.-L. A., Sun, G., Brot, N., Weissbach, H., Heinemann, S. H., Iverson, L., Wu, C., et al. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.032671199 · Cited by 454
Mitochondrial import and enzymatic activity of PINK1 mutants associated to recessive parkinsonism
Silvestri, L., Caputo, V., Bellacchio, E., Atorino, L., Dallapiccola, B., Valente, E. M., & Casari, G. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi377 · Cited by 449
Pesah, Y., Pham, T., Burgess, H., Middlebrooks, B. W., Verstreken, P., Zhou, Y., Harding, M. J., Bellen, H. J., & Mardon, G. (2004) · Development · doi:10.1242/dev.01095 · Cited by 448
Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration
Liou, Y., Sun, A., Ryo, A., Zhou, X. Z., Yu, Z.-X., Huang, H.-K., Uchida, T., Bronson, R. T., Bing, G., Li, X., et al. (2003) · Nature · doi:10.1038/nature01832 · Cited by 432
Gibson, G. E., Sheu, K. ‐. R., Blass, J. P., Baker, A., Carlson, K., Harding, B. N., & Perrino, P. (1988) · Archives of Neurology · doi:10.1001/archneur.1988.00520320022009 · Cited by 425
Whitworth, A. J., Theodore, D. A., Greene, J. C., Beneš, H., Wes, P. D., & Pallanck, L. J. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0501078102 · Cited by 421
Parkin prevents mitochondrial swelling and cytochrome c release in mitochondria-dependent cell death
Darios, F. D. (2003) · Human Molecular Genetics · doi:10.1093/hmg/ddg044 · Cited by 407
Martins, L. M., Morrison, A., Klupsch, K., Fedele, V., Moisoi, N., Teismann, P., Abuin, A., Grau, E., Geppert, M., Livi, G. P., et al. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.22.9848-9862.2004 · Cited by 395
Busciglio, J., Pelsman, A., Wong, C., Pigino, G., Yuan, M., Mori, H., & Yankner, B. A. (2002) · Neuron · doi:10.1016/s0896-6273(02)00604-9 · Cited by 387
Sun, J., Folk, D. G., Bradley, T. J., & Tower, J. (2002) · Genetics · doi:10.1093/genetics/161.2.661 · Cited by 381
High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer's disease brain
Lin, M. T. (2002) · Human Molecular Genetics · doi:10.1093/hmg/11.2.133 · Cited by 366
Self-citationYang, Y., Gehrke, S., Haque, M. E., Imai, Y., Kosek, J. C., Yang, L., Beal, M. F., Nishimura, I., Wakamatsu, K., Ito, S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0504610102 · Cited by 338
Self-citationReddy, P. H., McWeeney, S. K., Park, B. S., Mańczak, M., Gutala, R. V., Partovi, D., Jung, Y., Yau, V., Searles, R. P., Mori, M., et al. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddh140 · Cited by 332
Petit-Paitel, A., Kawarai, T., Paitel, E., Sanjo, N., Maj, M. C., Scheid, M. P., Chen, F., Gu, Y., Hasegawa, H., Salehi‐Rad, S., et al. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m505143200 · Cited by 331
Copper-Dependent Inhibition of Human Cytochrome c Oxidase by a Dimeric Conformer of Amyloid-β1-42
Crouch, P. J., Blake, R., Duce, J. A., Ciccotosto, G. D., Li, Q.-X., Barnham, K. J., Curtain, C. C., Cherny, R. A., Cappai, R., Dyrks, T., et al. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.4276-04.2005 · Cited by 327
Tamagno, E., Parola, M., Bardini, P., Piccini, A., Borghi, R., Guglielmotto, M., Santoro, G., Davit, A., Danni, O., Smith, M. A., et al. (2005) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02895.x · Cited by 324
Song, D. D., Shults, C. W., Sisk, A., Rockenstein, E. M., & Masliah, E. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00342-x · Cited by 301
Higgins, C. M. J., Jung, C., & Xu, Z. (2003) · BMC Neuroscience · doi:10.1186/1471-2202-4-16 · Cited by 288
Jaarsma, D., Rognoni, F., van Duijn, W., Verspaget, H. W., Haasdijk, E. D., & Holstege, J. C. (2001) · Acta Neuropathologica · doi:10.1007/s004010100399 · Cited by 281
Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice
Li, F., Calingasan, N. Y., Yu, F., Mauck, W. M., Toidze, M., Almeida, C. G., Takahashi, R. H., Carlson, G. A., Beal, M. F., Lin, M. T. S., et al. (2004) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2004.02455.x · Cited by 277
Self-citationCybrids in Alzheimer's disease: a cellular model of the disease?
Swerdlow, R. H., Parks, J. K., Cassarino, D. S., Maguire, D. J., Maguire, R. S., Bennett, J. P., Davis, R. E., & Parker, W. D. (1997) · Neurology · doi:10.1212/wnl.49.4.918 · Cited by 272
Parkin enhances mitochondrial biogenesis in proliferating cells
Kuroda, Y., Mitsui, T., Kunishige, M., Shono, M., Akaike, M., Azuma, H., & Matsumoto, T. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl006 · Cited by 268
Damiano, M. G., Starkov, A. A., Petri, S., Kipiani, K., Kiaei, M., Mattiazzi, M., Beal, M. F., & Manfredi, G. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03619.x · Cited by 267
Self-citationCybrids in Alzheimer's disease: A cellular model of the disease?
Swerdlow, R. H., & Parker, D. W. (1998) · Neurology · doi:10.1212/wnl.51.1.326-a · Cited by 260
Milakovic, T., & Johnson, G. V. W. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m504749200 · Cited by 259
Vijayvergiya, C., Beal, M. F., Buck, J., & Manfredi, G. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.4385-04.2005 · Cited by 257
Self-citationNicastrin, Presenilin, APH-1, and PEN-2 Form Active γ-Secretase Complexes in Mitochondria
Hansson, C. A., Frykman, S., Farmery, M. R., Tjernberg, L. O., Nilsberth, C., Pursglove, S. E., Ito, A., Winblad, B., Cowburn, R. F., Thyberg, J., et al. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m404500200 · Cited by 256
Rukhsana Sultana, A., Debra Boyd-kimball, A., Poon, H. F., Cai, J., Pierce, W. M. J., Klein, J. B., Markesbery, W. R., Zhou, X. Z., Lu, K. P., & Butterfield, D. A. (2005) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2005.05.005 · Cited by 255
Velliquette, R. A., O'Connor, T., & Vassar, R. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.2350-05.2005 · Cited by 254
Benchoua, A., Trioulier, Y., Zala, D., Gaillard, M., Lefort, N., Dufour, N., Saudou, F., Elalouf, J., Hirsch, É. C., Hantraye, P., et al. (2006) · Molecular Biology of the Cell · doi:10.1091/mbc.e05-07-0607 · Cited by 248
Association of DJ-1 and parkin mediated by pathogenic DJ-1 mutations and oxidative stress
Moore, D. J., Zhang, L., Troncoso, J. C., Lee, M. K., Hattori, N., Mizuno, Y., Dawson, T. M., & Dawson, V. L. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddi007 · Cited by 248
Amyotrophic lateral sclerosis: A proposed mechanism
Okado‐Matsumoto, A., & Fridovich, I. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.132260399 · Cited by 247
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Tang, B., Xiong, H., Sun, P., Zhang, Y., Wang, D., Hu, Z., Zhu, Z.-H., Ma, H., Pan, Q., Xia, J., et al. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl104 · Cited by 218
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Brouillet, M. (1995) · Medical Entomology and Zoology · Cited by 190
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Metadata
- Authors
- Lin, M. T., & Beal, M. F.
- Affiliations
- Cornell University (US)
- Corresponding author
- Beal, M. Flint
- ORCID
- Beal, M. Flint
- Venue
- Nature
- Published
- 2006-10
- Volume
- 443
- Issue
- 7113
- Pages
- 787-795
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2152165298
- Cited by
- 6,455
- References
- 103
- Citations by year
- 2026: 266 · 2025: 386 · 2024: 393 · 2023: 362 · 2022: 408 · 2021: 454 · 2020: 412 · 2019: 366 · 2018: 450 · 2017: 373 · 2016: 356 · 2015: 326 · 2014: 290 · 2013: 296 · 2012: 293
- FWCI
- 13.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- American Federation for Aging Research
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, oxidative stress, neurodegenerative diseases, aging, mitochondrial DNA mutations, cell death, energy metabolism, free radicals, pathogenesis, mitochondrial-targeted therapy
- MeSH terms
- Aging, Animals, Humans, Mitochondria, Apoptosis, Oxidative Stress, Neurodegenerative Diseases
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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