By Novartis Foundation
With the ever-increasing upward thrust in existence expectancy, there's an pressing have to enhance our realizing of the connection among getting older and the pathogenesis of age-related illnesses so one can determine more suitable technique of prevention, amelioration and administration of such illnesses. furthermore, there's a have to decrease the social and monetary impression of the growing old inhabitants. Age-related morbidity and mortality vary dramatically between contributors; this booklet focusses on person alterations 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 procedures 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 getting older, this can be obligatory reading.Content:
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Extra resources for Ageing Vulnerability: Causes and Interventions: Novartis Foundation Symposium 235
The proteins comprising these deposits rapidly aggregate and frequently result in direct cytotoxicity. Recent evidence suggests that these abnormal protein deposits may directly involve trace quantities of redox-active metals such as copper, iron and manganese (Bush 2000). A large and growing literature now supports the notion that aberrant metal-catalysed protein redox reactions ö those involving local reactions of redox-active metals, oxygen and proteins (Stadtman & Oliver 1991, Stadtman 1993) ö may be a common denominator in the underlying alterations in protein secondary structure which result in protein deposition and accumulation in these diseases.
He showed that with Ab up to 40 residues long, the toxicity occurred when the concentration rose above 1 mM. What people forgot was that he also showed that there was a signi¢cant trophic activity of Ab1À40 in the nanomolar concentration range. Ab’s original activity in its physiologically plausible concentration is trophic. We have reproduced that result and we also ¢nd that Ab1À42 in the same system has greater trophic activity, but you have to keep the concentration low. In the case of Ab1À42, it has to be kept below 1 nM, because when it rises above 10 nM it begins to become toxic.
This was very e¡ective, giving the rats a 10 day increase in life span and improved motor function. But the most important thing was that this proves the principle that the oral supplement can be transduced to bene¢t the GSH system of the brain. We are next testing this out with Alzheimer’s disease mice, because we have also found out that there is a 30% decrease in the levels of plasma cysteine in individuals with Alzheimer’s disease. Andersen: In terms of the improved motor function, did you look speci¢cally for changes in nigrostriatal pathology?
Ageing Vulnerability: Causes and Interventions: Novartis Foundation Symposium 235 by Novartis Foundation