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By Novartis Foundation

With the ever-increasing upward thrust in lifestyles expectancy, there's an pressing have to enhance our knowing of the connection among aging and the pathogenesis of age-related ailments in an effort to determine more advantageous technique of prevention, amelioration and administration of such illnesses. additionally, there's a have to decrease the social and monetary impression of the ageing inhabitants. Age-related morbidity and mortality vary dramatically between contributors; this ebook focusses on person variations in susceptibility to age-related issues.

It comprises contributions from best specialists within the box on subject matters such as:
age-related pathology within the mind, age-related strategies in stem cells, and age-related results at the immune process and in bone, muscle and cardiovascular tissue. For all people with an curiosity within the biology of growing older, this can be obligatory reading.Content:

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Proc Natl Acad Sci USA 89:10449^10453 Huang X, Atwood CS, Moir RD et al 1997 Zinc-induced Alzheimer’s Ab1-40 aggregation is mediated by conformational factors. J Biol Chem 272:26464^26470 Huang X, Cuajungco MP, Atwood CS et al 1999a Cu (II) potentiation of Alzheimer Ab neurotoxicity. Correlation with cell-free hydrogen peroxide production and metal reduction. J Biol Chem 274:37111^37116 PROTEIN OXIDATION IN AGEING 37 Huang X, Atwood CS, Hartshorn MA et al 1999b The Ab peptide of Alzheimer’s disease directly produces hydrogen peroxide through metal ion reduction.

Thus, understanding the metalloprotein biochemistry of the local microenvironment in which these proteins are converted into toxic pro-oxidants is critical for unravelling the mechanisms which underlie these diseases. A common misunderstanding that arises when metals are implicated in disease processes is the notion that only high-level exposure to free metals such as Cu, Fe, Zn and Mn are toxic. This is an important misconception to clarify. In terms of total tissue concentrations, most tissues including the brain contain a plenitude of these trace metal ions.

Kirkwood: Early on you referred to the co-localization of the zinc, copper and iron in the plaques. Aluminium is another mechanism also found in the plaques. What do you think is the background metal that leads to these concentrations of metal ions within the plaques? Bush: Once the plaque begins to form I think it becomes a kind of protein ‘£ypaper’ for metal ions. The concentration of aluminium in biological bu¡ers is very low, in the region of 1 nM. The fact that it is enriched in the plaque could be because there are non-speci¢c metal ion binding sites that start developing on the oxidised version of the amyloid.

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