Challenging but essential targets for genuine anti-ageing drugs

被引:11
作者
de Grey, ADNJ [1 ]
机构
[1] Univ Cambridge, Dept Genet, Cambridge CB2 3EH, England
关键词
ageing; anti-ageing drugs; atherosclerosis; cell senescence; cell therapy; gene therapy; glycation; mitochondria; mutations;
D O I
10.1517/14728222.7.1.1
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Contrary to what one might conclude from the popular press, anti-ageing drugs do not yet exist, in the sense in which the term 'drug' is normally used. Since a drug is assumed to be effective against its target human pathology and since the vast majority of deaths in the developed world are from ageing-related causes, it is inappropriate to describe something as an anti-ageing drug unless one has good reason to believe that it will appreciably, extend the life expectancy of those in the developed world who receive it. A drug that rejuvenates aspects of the aged body but does not increase life expectancy is an antifrailty drug, not an anti-ageing one. This distinction is critical for decision makers in the drug discovery sphere because, while the market for antifrailty drugs (even unproven ones) is large, that for genuine anti-ageing drugs - which, as the author explains, are now foreseeable - will certainly be far larger. in this article, the author surveys the main aspects of age-related degeneration that are believed to be essential targets for genuine anti-ageing drugs - that is, without whose amelioration human life expectancy probably cannot be greatly increased - and some promising strategies for the design of such drugs.
引用
收藏
页码:1 / 5
页数:5
相关论文
共 34 条
[1]   The neuropathogenic contributions of lysosomal dysfunction [J].
Bahr, BA ;
Bendiske, J .
JOURNAL OF NEUROCHEMISTRY, 2002, 83 (03) :481-489
[2]   Role of oxidative stress in diabetic complications - A new perspective on an old paradigm [J].
Baynes, JW ;
Thorpe, SR .
DIABETES, 1999, 48 (01) :1-9
[3]   The mitochondrial-lysosomal axis theory of aging - Accumulation of damaged mitochondria as a result of imperfect autophagocytosis [J].
Brunk, UT ;
Terman, A .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (08) :1996-2002
[4]  
De Grey A.D.N.J., 1998, EUR RESPIR J, V1, P53, DOI [10.1089/rej.1.1998.1.53, DOI 10.1089/REJ.1.1998.1.53]
[5]   Mitochondrial gene therapy: an arena for the biomedical use of inteins [J].
de Grey, ADNJ .
TRENDS IN BIOTECHNOLOGY, 2000, 18 (09) :394-399
[6]   The reductive hotspot hypothesis of mammalian aging - Membrane metabolism magnifies mutant mitochondrial mischief [J].
de Grey, ADNJ .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (08) :2003-2009
[7]   Bioremediation meets biomedicine: therapeutic translation of microbial catabolism to the lysosome [J].
de Grey, ADNJ .
TRENDS IN BIOTECHNOLOGY, 2002, 20 (11) :452-455
[8]   Time to talk SENS: Critiquing the immutability of human aging [J].
De Grey, ADNJ ;
Ames, CN ;
Andersen, JK ;
Bartke, A ;
Campisi, J ;
Heward, CB ;
McCarter, RJM ;
Stock, G .
INCREASING HEALTHY LIFE SPAN: CONVENTIONAL MEASURES AND SLOWING THE INNATE AGING PROCESS, 2002, 959 :452-462
[9]   Is human aging still mysterious enough to be left only to scientists? [J].
de Grey, ADNJ ;
Baynes, JW ;
Berd, D ;
Heward, CB ;
Pawelec, G ;
Stock, G .
BIOESSAYS, 2002, 24 (07) :667-676
[10]  
DEGREY ADN, 2000, J AM AGING ASSOC, V23, P170