510
Views
13
CrossRef citations to date
0
Altmetric
Editorial

Challenging but essential targets for genuine anti-ageing drugs

Pages 1-5 | Published online: 02 Mar 2005

Bibliography

  • DE GREY ADNJ, AMES BN, ANDERSEN JK et al: Time to talk SENS: critiquing the immutability of human aging. Annals NY Acad. Sci. (2002) 959:452–462.
  • DE GREY ADNJ, BAYNES JW, BERD D, HEWARD CB, PAWELEC G, STOCK G: Is human aging still mysterious enough to be left only to scientists? BioEssays (2002) 24(7):667–676.
  • DE GREY ADNJ: An engineer's approach to the development of real anti-aging medicine. Sci. SAGE-KE (2003) 2(1).
  • LANZA RP, CIBELLI JB, WEST MD: Human therapeutic cloning. Nat. Med. (1999) 5(9):975–977.
  • HORNER PJ, GAGE FH: Regeneration in the adult and aging brain. Arch. Neurol. (2002) 59(11):1717–1720.
  • WEISSMAN IL, ANDERSON DJ, GAGE F: Stem and progenitor cells: origins, phenotypes, lineage commitments, and transdifferentiations. Anna. Rev Cell. Dev. Biol. (2001) 17:387–403.
  • LUSIS AJ: Atherosclerosis. Nature (2000) 407(680 1):233–241.
  • BAHR BA, BENDISKE J: The neuropathogenic contributions of lysosomal dysfunction. Neurochem. (2002) 83(3):481–489.
  • FINNEMANN SC, LEUNG LW, RODRIGUEZ-BOULAN E: The lipofuscin component A2E selectively inhibits phagolysosomal degradation of photoreceptor phospholipid by the retinal pigment epithelium. Proc. Natl. Acad. Sci. USA (2002) 99(6):3842–3847.
  • BRUNK UT, TERMAN A: The mitochondrial-lysosomal axis theory of aging: accumulation of damaged mitochondria as a result of imperfect autophagocytosis. Eur. Biochem. (2002) 269(8):1996–2002.
  • SCHENK D: Amyloid-beta immunotherapy for Alzheimer's disease: the end of the beginning. Nat. Rev Neurosci a(2002) 3(10):824–828.
  • TERMAN A, WELANDER M: Centrophenoxine slows down, but does not reverse, lipofuscin accumulation in cultured cells. J. Anti-Aging Med. (1999) 2(3):265–273.
  • DE GREY ADNJ: Bioremediation meets biomedicine: therapeutic translation of microbial catabolism to the lysosome. Trends Biotechnol (2002) 20(11):452–455.
  • VACCARO DE: Symbiosis therapy: the potential of using human protozoa for molecular therapy. Ma Ther. (2000) 2(6):535–538.
  • BAYNES JW, THORPE SR: Role of oxidative stress in diabetic complications: a new perspective on an old paradigm. Diabetes (1999) 48(1):1–9.
  • VASAN S, ZHANG X, ZHANG X et al.: An agent cleaving glucose-derived protein crosslinks in vitro and in vivo. Nature (1996) 382(6588):275–278.
  • KASS DA, SHAPIRO EP, KAWAGUCHI M et al.: Improved arterial compliance by a novel advanced glycation end-product crosslink breaker. Circulation (2001) 104(13):1464–1470.
  • DE GREY ADNJ: A proposed refinement of the mitochondrial free radical theory of aging. BioEssays (1997) 19(2):161–166.
  • MULLER-HOCKER J, SEIBEL P, SCHNEIDERBANGER K, KADENBACH B: Different M situ hybridization patterns of mitochondrial DNA in cytochrome c oxidase-deficient extraocular muscle fibres in the elderly. Virchows Arch. A Pathol Anat. Histopathol (1993) 422(1):7–15.
  • PEREZ-CAMPO R, LOPEZ-TORRES M, CADENAS S, ROJAS C, BARJA G: The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach. J. Comp. Physiol M(1998) 168(3):149–158.
  • MCKENZIE D, BUA E, MCKIERNAN S, CAO Z, AIKEN JM: Mitochondrial DNA deletion mutations: a causal role in sarcopenia. Eur: Biochem. (2002) 269(8):2010–2015.
  • LEXELL J: Human aging, muscle mass, and fiber type composition. J. Gerontol A Biol. Sci. Med. Sci (1995) 50 (Spec. No.):11–16.
  • JONES DP, MODY VC, CARLSON JL, LYNN MJ, STERNBERG P: Redox analysis of human plasma allows separation of pro-oxidant events of aging from decline in antioxidant defenses. Free Radic. Biol. Med. (2002) 33(9):1290–1300.
  • DE GREY ADNJ: A mechanism proposed to explain the rise in oxidative stress during aging. I Anti-Aging Med. (1998) 1(1):53–66.
  • DE GREY ADNJ: The reductive hotspot hypothesis of mammalian aging: membrane metabolism magnifies mutant mitochondrial mischief. Eur: j Biochem. (2002) 269(8):2003–2009.
  • DE GREY ADNJ: Reversing age-related mitochondrial DNA decline: alternatives to mitochondrial gene therapy. I Am. Aging. Assoc. (2000) 23:170–171.
  • TAYLOR RW, WARDELL TM, LIGHTOWLERS RN, TURNBULL DM: Molecular basis for treatment of mitochondrial myopathies. Neurol. Sci. (2000) 21\(Suppl. 5):5909–5912.
  • SEIBEL P, TRAPPE J, VILLANI G, KLOPSTOCK T, PAPA S, REICHMANN H: Transfection of mitochondria: strategy towards a gene therapy of mitochondrial DNA diseases. Nucleic Acids Res. (1995) 23(1):10–17.
  • DE GREY ADNJ: Mitochondrial gene therapy: an arena for the biomedical use of inteins. Trends Biotechnol (2000) 18(9):394–399.
  • ZULLO SJ: Gene therapy of mitochondrial DNA mutations: a brief, biased history of allotopic expression in mammalian cells. Semin. Neurof (2001) 21(3):327–335.
  • MANFREDI G, FU J, OJAIMI J et al.: Rescue of a deficiency in ATP synthesis by transfer of MTATP6, a mitochondrial DNA-encoded gene, to the nucleus. Nat. Genet. (2002) 30(4):394–399.
  • GUY J, QI X, PALLOTTI F et al.: Rescue of a mitochondrial deficiency causing Leber Hereditary Optic Neuropathy. Ann. Neurol (2002) 52(5):534–542.
  • DIMRI GP, LEE X, BASILE G et al.: A biomarker that identifies senescent human cells in culture and in aging skin in vivo. Proc. Natl. Acad. Sci. USA (1995) 92(20):9363–9367.
  • KRTOLICA A, CAMPISI J: Cancer and aging: a model for the cancer promoting effects of the aging stroma. Int. J. Biochem. Cell. Biol. (2002) 34(11):1401–1414.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.