By Novartis Foundation
With the ever-increasing upward thrust in existence expectancy, there's an pressing have to enhance our figuring out of the connection among growing older and the pathogenesis of age-related ailments with a purpose to determine more beneficial technique of prevention, amelioration and administration of such illnesses. additionally, there's a have to lessen the social and fiscal influence of the getting old inhabitants. Age-related morbidity and mortality vary dramatically between participants; this ebook focusses on person changes in susceptibility to age-related issues.
It comprises contributions from prime specialists within the box on issues such as:
age-related pathology within the mind, age-related techniques in stem cells, and age-related results at the immune method and in bone, muscle and cardiovascular tissue. For all people with an curiosity within the biology of getting older, this can be obligatory reading.Content:
Read or Download Ageing Vulnerability: Causes and Interventions: Novartis Foundation Symposium 235 PDF
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Additional resources for Ageing Vulnerability: Causes and Interventions: Novartis Foundation Symposium 235
J Biol Chem 27:12817^12826 PROTEIN OXIDATION IN AGEING 35 Atwood CS, Huang X, Moir RD, Tanzi RE, Bush AI 1999 Role of free radicals and metal ions in the pathogenesis of Alzheimer’s disease. Met Ions Biol Syst 36:309^364 Atwood CS, Huang X, Khatri A et al 2000a Copper catalyzed oxidation of Alzheimer Ab. Cell Mol Biol (Noisy-Le-Grand) 46:777^783 Atwood CS, Scarpa RC, Huang X et al 2000b Characterization of copper interactions with Alzheimer amyloid b peptides: identi¢cation of an attomolar-a⁄nity copper binding site on amyloid b1^42.
Isn’t there a problem with this, in that there is very little evidence for neuronal loss in that model, despite the large Ab depositions? Presumably there are some Ab dimers there, although I don’t know to what extent this has been measured. Bush: There is a small amount of neuronal toxicity, but your point is well taken. It is an inadequate model, but it is the only one available to academics like myself. Novartis has a fantastic mouse model for AD, but has not made it available. Martin: My understanding was that they might make it available with collaboration.
The human body has highly e⁄cient homeostatic mechanisms and bu¡er systems to prevent toxic decompartmentalization and pathological reactivity of metal ions. When these mechanisms and bu¡er systems fail, aberrant localized metalloprotein reactions may occur, even in the absence of globally elevated metal levels. We will examine two common chronic and progressive disorders of ageing, AD and age-related cataracts, to illustrate these considerations. Alzheimer’s disease AD is characterized by neuronal demise and cerebral oxidative stress in the setting of deposition of the Alzheimer’s disease Ab peptides within the neocortex.