By Caleb E. Finch (Auth.)
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Additional resources for The Biology of Human Longevity. Inflammation, Nutrition, and Aging in the Evolution of Life Spans
Combinations of risk indicators and disease load are also being intensively studied of the inflammatory marker, C-reactive protein (CRP). In the Women’s Health Study, future heart attacks occurred most frequently in those with both elevated CRP and LDL (Ridker, 2002). New models are needed to resolve the links between the diverse subtle subclinical aging changes that interact to cause circulatory failure on the background of declining organ reserves. It is shocking that 30% of diet-restricted old rats had no gross lesions at necropsy and cause of death was unknown (Shimokawa et al, 1993).
These metabolic level aging processes thus tend to accelerate the accumulation of oxidized damage. The effectiveness of diet restriction in slowing aging may be due in part to the accelerated protein turnover and decreased oxidative load (Chapter 3). The balance of reduction:oxidation (‘redox’) in glutathione and other key homeostatic regulators (Fig. 11) is shifted to a more oxidized state (GSSG and protein-SSG) in blood, liver, and other tissues (Lang et al, 1989; Lang et al, 1990; Rebrin et al, 2003; Rebrin and Sohal, 2004), and in whole aging flies (Rebrin et al, 2004).
These huge differences are unexplained. 8 White matter (myelinated pathway) aging. A. Microglial activation in cortico-striatal myelinated tracts of aging F344 rats. Note the increased immunostaining (dark area) in 24 m markers of microglial activation; MHC-2, antigen of activated macrophage/microglia; CR3, complement receptor. ) B. Myelin integrity declines with aging in the corpus callosum (subcortical white matter) of normal brain (o) after age 50, with greater deterioration in Alzheimer disease ( ).
The Biology of Human Longevity. Inflammation, Nutrition, and Aging in the Evolution of Life Spans by Caleb E. Finch (Auth.)