Mitochondria in aging and Alzheimer's disease

Rejuvenation Research

Volumn 10, Issue 3, 2007, Pages 349-357

  Crouch, P J ^a,c   Cimdins, K ^a,b   Duce, J A ^c   Bush, A I ^c,d   Trounce, Ian A ^a,b  

^a UNIVERSITY OF MELBOURNE   (Australia)

^b ST VINCENT S HOSPITAL   (Australia)

^c FLOREY INSTITUTE OF NEUROSCIENCE AND MENTAL HEALTH   (Australia)

^d MASSACHUSETTS GENERAL HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; AMYLOID BETA PROTEIN; AMYLOID PRECURSOR PROTEIN; CARBONYL CYANIDE CHLOROPHENYLHYDRAZONE; CYTOCHROME C; GAMMA SECRETASE; HYDROGEN PEROXIDE; HYDROXYL RADICAL; MITOCHONDRIAL DNA; MITOGEN ACTIVATED PROTEIN KINASE; PROTON TRANSPORTING ADENOSINE TRIPHOSPHATE SYNTHASE; REACTIVE OXYGEN METABOLITE;

AGED; AGING; ALZHEIMER DISEASE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; BRAIN MITOCHONDRION; CONFERENCE PAPER; DEGENERATIVE DISEASE; ENZYME PHOSPHORYLATION; ENZYME RELEASE; GENOME; HISTOPATHOLOGY; HUMAN; HUMAN CELL; MOUSE; NERVE CELL CULTURE; NEUROLOGIC DISEASE; NEUROTOXICITY; NONHUMAN; OXIDATION REDUCTION REACTION; OXIDATIVE PHOSPHORYLATION; OXIDATIVE STRESS; PRIORITY JOURNAL; SENILE PLAQUE; SIGNAL TRANSDUCTION; SOMATIC MUTATION; TRANSGENIC MOUSE;

AGED; AGING; ALZHEIMER DISEASE; AMYLOID; ANIMALS; DNA, MITOCHONDRIAL; HUMANS; LONGEVITY; MITOCHONDRIA; MODELS, BIOLOGICAL; NEURONS; OXIDATIVE STRESS;

EID: 34548486918     PISSN: 15491684     EISSN: None     Source Type: Journal    
DOI: 10.1089/rej.2007.0592     Document Type: Conference Paper

References (69)

1. Boveris A, Chance B. The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen. Biochem J 1973;134:707-716.
2. Shulman RG, Rothman DL, Behar KL, Hyder F. Energetic basis of brain activity: implications for neuroimaging. Trends Neurosci 2004;27:489-495.
3. Cooper AJL. Glutathione in the brain: disorders of glutathione metabolism. In: Rosenberg RN, Prusiner SB, DiMauro S, et al. (eds.): The Molecular and Genetic Basis of Neurological Disease. Boston: Butterworth-Heinemann, 1997, pp. 1195-1230.
4. Clarke DD, Sokoloff L. Circulation and energy metabolism of the brain. In: Sigel GJ, Agranoff BW, Albers RW, et al., (eds.): Basic Neurochemistry: Molecular, Cellular and Medical Aspects. Philadelphia: Lippincott-Raven, 1999, pp. 637-669.
5. Wallace DC. Mitochondrial diseases in man and mouse. Science 1999;283:1482-1488.
6. Loeb LA, Wallace DC, Martin GM. The mitochondrial theory of aging and its relationship to reactive oxygen species damage and somatic mtDNA mutations. Proc Natl Acad Sci USA 2005;102:18769-18770.
7. Trifunovic A, Wredenberg A, Falkenberg M, Spelbrink JN, Rovio AT, Bruder CE, Bohlooly YM, Gidlof S, Oldfors A, Wibom R, Tornell J, Jacobs HT, Larsson NG. Premature ageing in mice expressing defective mitochondrial DNA polymerase. Nature 2004;429:417-423.
8. Kujoth GC, Hiona A, Pugh TD, Someya S, Panzer K, Wohlgemuth SE, Hofer T, Seo AY, Sullivan R, Jobling WA, Morrow JD, Van Remmen H, Sedivy JM, Yamasoba T, Tanokura M, Weindruch R, Leeuwenburgh C, Prolla TA. Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging. Science 2005;309:481-484.
9. Trifunovic A, Hansson A, Wredenberg A, Rovio AT, Dufour E, Khvorostov I, Spelbrink JN, Wibom R, Jacobs HT, Larsson NG. Somatic mtDNA mutations cause aging phenotypes without affecting reactive oxygen species production. Proc Natl Acad Sci USA 2005;102:17993-17998.
10. Schriner SE, Linford NJ, Martin GM, Treuting P, Ogburn CE, Emond M, Coskun PE, Ladiges W, Wolf N, Van Remmen H, Wallace DC, Rabinovitch PS. Extension of murine life span by overexpression of catalase targeted to mitochondria. Science 2005;308:1909-1911.
11. Vermulst M, Bielas JH, Kujoth GC, Ladiges WC, Rabinovitch PS, Prolla TA, Loeb LA. Mitochondrial point mutations do not limit the natural lifespan of mice. Nat Genet 2007; 39:540-543.
12. Bender A, Krishnan KJ, Morris CM, Taylor GA, Reeve AK, Perry RH, Jaros E, Hersheson JS, Betts J, Klopstock T, Taylor RW, Turnbull DM. High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease. Nat Genet 2006;38:515-517.
13. Cantuti-Castelvetri I, Lin MT, Zheng K, Keller-McGandy CE, Betensky RA, Johns DR, Beal MF, Standaert DG, Simon DK. Somatic mitochondrial DNA mutations in single neurons and glia. Neurobiol Aging 2005;26:1343-1355.
14. Kraytsberg Y, Kudryavtseva E, McKee AC, Geula C, Kowall NW, Khrapko K. Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons. Nat Genet 2006;38:518-520.
15. Lin MT, Simon DK, Ahn CH, Kim LM, Beal MF. High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer's disease brain. Hum Mol Genet 2002;11:133-145.
16. Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci USA 1985;82:4245-4249.
17. Selkoe DJ, Abraham CR, Podlisny MB, Duffy LK. Isolation of low-molecular-weight proteins from amyloid plaque fibers in Alzheimer's disease. J Neurochem 1986;46:1820-1834.
18. Hardy JA, Higgins GA. Alzheimer's disease: The amyloid cascade hypothesis. Science 1992;256:184-185.
19. Hartley DM, Walsh DM, Ye CP, Diehl T, Vasquez S, Vassilev PM, Teplow DB, Selkoe DJ. Protofibrillar intermediates of amyloid β-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons. J Neurosci 1999;19:8876-8884.
20. Lambert MP, Barlow AK, Chromy BA, Edwards C, Freed R, Liosatos M, Morgan TE, Rozovsky I, Trommer B, Viola KL, Wals P, Zhang C, Finch CE, Krafft GA, Klein WL. Diffusible, nonfibrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 1998;95:6448-6453.
21. Lambert MP, Viola KL, Chromy BA, Chang L, Morgan TE, Yu J, Venton DL, Krafft GA, Finch CE, Klein WL. Vaccination with soluble Aβ oligomers generates toxicity-neutralizing antibodies. J Neurochem 2001;79:595-605.
22. Walsh DM, Hartley DM, Kusumoto Y, Fezoui Y, Condron MM, Lomakin A, Benedek GB, Selkoe DJ, Teplow DB. Amyloid β-protein fibrillogenesis. Structure and biological activity of protofibrillar intermediates. J Biol Chem 1999;274:25945-25952.
23. Walsh DM, Klyubin I, Fadeeva JV, Cullen WK, Anwyl R, Wolfe MS, Rowan MJ, Selkoe DJ. Naturally secreted oligomers of amyloidβ protein potently inhibit hippocampal long-term potentiation in vivo. Nature 2002;416:535-539.
24. Mattson MP, Carney JW, Butterfield DA. A tombstone in Alzheimer's? Nature 1995;373:481.
25. Curtain CC, Ali F, Volitakis I, Cherny RA, Norton RS, Beyreuther K, Barrow CJ, Masters CL, Bush AI, Barnham KJ. Alzheimer's disease amyloid-β binds copper and zinc to generate an allosterically ordered membrane-penetrating structure containing superoxide dismutase-like subunits. J Biol Chem 2001;276:20466-20473.
26. Ciccotosto GD, Tew D, Curtain CC, Smith D, Carrington D, Masters CL, Bush AI, Cherny RA, Cappai R, Barnham KJ. Enhanced toxicity and cellular binding of a modified amyloid β peptide with a methionine to valine substitution. J Biol Chem 2004;279:42528-42534.
27. Klyubin I, Walsh DM, Lemere CA, Cullen WK, Shankar GM, Betts V, Spooner ET, Jiang L, Anwyl R, Selkoe DJ, Rowan MJ. Amyloid β protein immunotherapy neutralizes Aβ oligomers that disrupt synaptic plasticity in vivo. Nat Med 2005;11:556-561.
28. 1-42. J Neurosci 2005;25:672-679.
29. Yan SD, Shi Y, Zhu A, Fu J, Zhu H, Zhu Y, Gibson L, Stern E, Collison K, Al-Mohanna F, Ogawa S, Roher A, Clarke S, Stern D. Role of ERAB/L-3- hydroxyacylcoenzyme A dehydrogenase type II activity in Aβ-induced cytotoxicity. J Biol Chem 1999;274:2145-2156.
30. Martins RN, Harper CG, Stokes GB, Masters CL. Increased cerebral glucose-6-phosphate dehydrogenase activity in Alzheimer's disease may reflect oxidative stress. J Neurochem 1986;46:1042-1045.
31. Butterfield DA, Drake J, Pocernich C, Castegna A. Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptide. Trends Mol Med 2001;7:548-554.
32. Li F, Calingasan NY, Yu F, Mauck WM, Toidze M, Almeida CG, Takahashi RH, Carlson GA, Flint Beal M, Lin MT, Gouras GK. Increased plaque burden in brains of APP mutant MnSOD heterozygous knock-out mice. J Neurochem 2004;89:1308-1312.
33. Gabuzda D, Busciglio J, Chen LB, Matsudaira P, Yankner BA. Inhibition of energy metabolism alters the processing of amyloid precursor protein and induces a potentially amyloidogenic derivative. J Biol Chem 1994;269:13623-13628.
34. Busciglio J, Pelsman A, Wong C, Pigino G, Yuan M, Mori H, Yankner BA. Altered metabolism of the amyloid β precursor protein is associated with mitochondrial dysfunction in Down's syndrome. Neuron 2002;33:677-688.
35. Velliquette RA, O'Connor T, Vassar R. Energy inhibition elevates β-secretase levels and activity and is potentially amyloidogenic in APP transgenic mice: possible early events in Alzheimer's disease pathogenesis. J Neurosci 2005;25:10874-10883.
36. 2-induced apoptosis in human neuronal cells. Biochem Biophys Res Commun 1997;235:845-848.
37. Tamagno E, Bardini P, Obbili A, Vitali A, Borghi R, Zaccheo D, Pronzato MA, Danni O, Smith MA, Perry G, Tabaton M. Oxidative stress increases expression and activity of BACE in NT2 neurons. Neurobiol Dis 2002;10:279-288.
38. Coma M, Guix FX, Ill-Raga G, Uribesalgo I, Alameda F, Valverde MA, Munoz FJ. Oxidative stress triggers the amyloidogenic pathway in human vascular smooth muscle cells. Neurobiol Aging (in press).
39. Muresan Z, Muresan V. c-Jun NH2-terminal kinase-interacting protein-3 facilitates phosphorylation and controls localization of amyloid-β precursor protein. J Neurosci 2005;25:3741-3751.
40. McDonald DR, Bamberger ME, Combs CK, Landreth GE. β-Amyloid fibrils activate parallel mitogen-activated protein kinase pathways in microglia and THP1 monocytes. J Neurosci 1998;18:4451-4460.
41. Nunomura A, Perry G, Aliev G, Hirai K, Takeda A, Balraj EK, Jones PK, Ghanbari H, Wataya T, Shimohama S, Chiba S, Atwood CS, Petersen RB, Smith MA. Oxidative damage is the earliest event in Alzheimer disease. J Neuropathol Exp Neurol 2001;60:759-767.
42. Castellani RJ, Lee H, Perry G, Smith MA. Antioxidant protection and neurodegenerative disease: the role of amyloid-β and tau. Am J Alzheimer Dis Dement 2006;21:126-130.
43. Reddy PH. Amyloid precursor protein-mediated free radicals and oxidative damage: implications for the development and progression of Alzheimer's disease. J Neurochem 2006;96:1-13.
44. Cottrell DA, Blakely EL, Johnson MA, Ince PG, Turnbull DM. Mitochondrial enzyme-deficient hippocampal neurons and choroidal cells in AD. Neurology 2001;57:260-264.
45. Duara R, Grady C, Haxby J, Sundaram M, Cutler NR, Heston L, Moore A, Schlageter N, Larson S, Rapoport SI. Positron emission tomography in Alzheimer's disease. Neurology 1986;36:879-887.
46. Hirai K, Aliev G, Nunomura A, Fujioka H, Russell RL, Atwood CS, Johnson AB, Kress Y, Vinters HV, Tabaton M, Shimohama S, Cash AD, Siedlak SL, Harris PL, Jones PK, Petersen RB, Perry G, Smith MA. Mitochondrial abnormalities in Alzheimer's disease. J Neurosci 2001;21:3017-3023.
47. Coskun PE, Beal MF, Wallace DC. Alzheimer's brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication. Proc Natl Acad Sci USA 2004;101:10726-10731.
48. Wang J, Xiong S, Xie C, Markesbery WR, Lovell MA. Increased oxidative damage in nuclear and mitochondrial DNA in Alzheimer's disease. J Neurochem 2005;93:953-962.
49. Casley CS, Canevari L, Land JM, Clark JB, Sharpe MA. β-Amyloid inhibits integrated mitochondrial respiration and key enzyme activities. J Neurochem 2002;80:91-100.
50. Crouch PJ, Barnham KJ, Duce JA, Blake RE, Masters CL, Trounce IA. Copper-dependent inhibition of cytochrome c oxidase by Aβ(1-42) requires reduced methionine at residue 35 of the Aβ peptide. J Neurochem 2006;99:226-236.
51. Canevari L, Clark JB, Bates TE. β-Amyloid fragment 25-35 selectively decreases complex IV activity in isolated mitochondria. FEBS Lett 1999;457:131-134.
52. Parks JK, Smith TS, Trimmer PA, Bennett JPJ, Parker WDJ. Neurotoxic Aβ peptides increase oxidative stress in vivo through NMDA-receptor and nitric-oxide-synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro. J Neurochem 2001;76:1050-1056.
53. Cardoso SM, Santos S, Swerdlow RH, Oliveira CR. Functional mitochondria are required for amyloid β-mediated neurotoxicity. FASEB J 2001;15:1439-1441.
54. Cardoso SM, Swerdlow RH, Oliveira CR. Induction of cytochrome c-mediated apoptosis by amyloid β 25-35 requires functional mitochondria. Brain Res 2002;931:117-125.
55. Clementi ME, Marini S, Coletta M, Orsini F, Giardina B, Misiti F. Abeta(31-35) and Aβ(25-35) fragments of amyloid β-protein induce cellular death through apoptotic signals: Role of the redox state of methionine-35. FEBS Lett 2005;579:2913-2918.
56. Keil U, Bonert A, Marques CA, Scherping I, Weyermann J, Strosznajder JB, Muller-Spahn F, Haass C, Czech C, Pradier L, Muller WE, Eckert A. Amyloid-β induced changes in nitric oxide production and mitochondrial activity lead to apoptosis. J Biol Chem 2004;279:50310-50320.
57. Kim HS, Lee JH, Lee JP, Kim EM, Chang KA, Park CH, Jeong SJ, Wittendorp MC, Seo JH, Choi SH, Suh HY. Amyloid β peptide induces cytochrome c release from isolated mitochondria. Mol Neurosci 2002;13:1989-1993.
58. Misiti F, Martorana GE, Nocca G, Di Stasio E, Giardina B, Clementi ME. Methionine 35 oxidation reduces toxic and pro-apoptotic effects of the amyloid β-protein fragment (31-35) on isolated brain mitochondria. Neuroscience 2004;126:297-303.
59. Moreira PI, Santos MS, Moreno A, Rego AC, Oliveira C. Effect of amyloid β-peptide on permeability transition pore: a comparative study. J Neurosci Res 2002;69:257-267.
60. Mungarro-Menchaca X, Ferrera P, Moran J, Arias C. β-Amyloid peptide induces ultrastructural changes in synaptosomes and potentiates mitochondrial dysfunction in the presence of ryanodine. J Neurosci Res 2002;68:89-96.
61. Aleardi AM, Benard G, Augereau O, Malgat M, Talbot JC, Mazat JP, Letellier T, Dachary-Prigent J, Solaini GC, Rossignol R. Gradual alteration of mitochondrial structure and function by β-amyloids: importance of membrane viscosity changes, energy deprivation, reactive oxygen species production, and cytochrome c release. J Bioenerg Biomembr 2005;37:207-225.
62. Takuma K, Yao J, Huang J, Xu H, Chen X, Luddy J, Trillat AC, Stern DM, Arancio O, Yan SS. ABAD enhances Aβ-induced cell stress via mitochondrial dysfunction. FASEB J 2005;19:597-598.
63. Yan SD, Fu D, Soto C, Chen X, Zhu H, Al-Mohanna F, Collison K, Zhu A, Stern E, Saido T, Tohyama M, Ogawa S, Roher A, Stern D. An intracellular protein that binds amyloid-β peptide and mediates neurotoxicity in Alzheimer's disease. Nature 1997;389:689-695.
64. Furuta S, Kobayashi A, Miyazawa S, Hashimoto T. Cloning and expression of cDNA for a newly identified isozyme of bovine liver 3-hydroxyacyl-CoA dehydrogenase and its import into mitochondria. Biochim Biophys Acta 1997;1350:317-324.
65. Anandatheerthavarada HK, Biswas G, Robin M-A, Avadhani NG. Mitochondrial targeting and a novel transmembrane arrest of Alzheimer's amyloid precursor protein impairs mitochondrial function in neuronal cells. J Cell Biol 2003;161:41-54.
66. Hansson CA, Frykman S, Farmery MR, Tjernberg LO, Nilsberth C, Pursglove SE, Ito A, Winblad B, Cowburn RF, Thyberg J, Ankarcrona M. Nicastrin, presenilin, APH-1 and PEN-2 form active γ-secretase complexes in mitochondria. J Biol Chem 2004;279:51654-51660.
67. Lustbader JW, Cirilli M, Lin C, Xu HW, Takuma K, Wang N, Caspersen C, Chen X, Pollak S, Chaney M, Trinchese F, Liu S, Gunn-Moore F, Lue LF, Walker DG, Kuppusamy P, Zewier ZL, Arancio O, Stern D, Yan SS, Wu H. ABAD directly links Aβ to mitochondrial toxicity in Alzheimer's disease. Science 2004;304:448-452.
68. Caspersen C, Wang N, Yao J, Sosunov A, Chen X, Lustbader JW, Xu HW, Stern D, McKhann G, Yan SD. Mitochondrial Aβ: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease. FASEB J 2005;19:2040-2041.
69. Manczak M, Anekonda TS, Henson E, Park BS, Quinn J, Reddy PH. Mitochondria are a direct site of Aβ accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. Hum Mol Genet 2006;15:1437-1449.