By Novartis Foundation
With the ever-increasing upward push in lifestyles expectancy, there's an pressing have to increase our figuring out of the connection among growing old and the pathogenesis of age-related ailments that allows you to determine better technique of prevention, amelioration and administration of such ailments. furthermore, there's a have to decrease the social and monetary impression of the getting older inhabitants. Age-related morbidity and mortality vary dramatically between contributors; this e-book focusses on person transformations in susceptibility to age-related problems.
It comprises contributions from top 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 approach and in bone, muscle and cardiovascular tissue. For all people with an curiosity within the biology of ageing, this can be obligatory reading.Content:
Read or Download Ageing Vulnerability: Causes and Interventions: Novartis Foundation Symposium 235 PDF
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Extra resources for Ageing Vulnerability: Causes and Interventions: Novartis Foundation Symposium 235
However, this does not mean that these metals are unavailable for reaction. Physiological events can result in marked £uctuation of metal levels in the local microenvironment. For example, the concentration of Zn (II) released into the synaptic cleft during neurotransmission reaches &300 mM (Cuajungco & Lees 1997) and Cu (II) rises to &15 mM (Hartter & Barnea 1988). Local microenvironment conditions can also favour release of bound metals. This e¡ect is observed under conditions of tissue acidosis, such as that seen during disease- PROTEIN OXIDATION IN AGEING 29 induced energy compromise or local in£ammation, where low pH fosters the liberation of protein-bound metals (Halliwell et al 1985, 1984, Gutteridge 1987).
It is possible that an abnormal elevation of tissue copper could contribute to both cataractogenesis and AD, since the eye is in the same anatomical compartment as the brain. An important implication of this hypothesis is that targeted chelation of redox-active metal ions or displacement with non-redox-active metals such as zinc may have therapeutic potential in preventing or treating these disorders. We are currently at work on developing such agents that may penetrate into susceptible tissue compartments and thus interfere with progression of pathogenic metalloprotein redox reactions.
Familial AD-linked mutations of amyloid precursor protein (APP), presenilin 1 (PS1) and PS2, increase both cerebral Ab burden and pathogenic Ab1^42 peptide production, underscoring the role that Ab metabolism plays in AD pathogenesis (reviewed in Atwood et al 1999). Furthermore, the deposition of Ab in the neocortex of transgenic mice overexpressing human Ab peptides is accompanied by many of the neuropathological features of AD, including intraneuronal tau abnormalities and neuronal loss, as well as signs of oxidative damage similar to those seen in ADa¡ected brain (Calhoun et al 1998).