Showing papers on "Aging brain published in 1977"
TL;DR: Findings show that specific alterations occur in the activities of several mitochondrial enzymes in aging brain, including 3-hydroxybutyrate dehydrogenase, acetoacetyl CoA thiolase, and NAD-isocitrate dehydrogen enzyme.
Abstract: The effects of aging on the oxidation of labeled glucose and 3-hydroxybutyrate and on several mitochondrial enzymes in rat brain were investigated. The oxidation of labeled glucose and labeled 3-hydroxybutyrate was diminished by about 40 and 35%, respectively, in cerebral cortex slices from 2-year-old rats compared to those from 3-mo-old animals. A significant reduction in the activities of 3-hydroxybutyrate dehydrogenase, 3-oxo acid CoA transferase, acetoacetyl CoA thiolase, and NAD-isocitrate dehydrogenase was observed in brains of 1- and 2-year-old rats compared to 3-mo-old animals. However, aging had no effect on the activities of citrate synthase and pyruvate carboxylase. These findings show that specific alterations occur in the activities of several mitochondrial enzymes in aging brain.
83 citations
01 Jan 1977
TL;DR: There is evidence that the rate of aging may be mediated by the brain, especially by the hypothalamus and the closely linked pituitary and peripheral endocrine system, which in turn cause the development of age-related pathology.
Abstract: Aging may be considered a progressive deterioration of an organism after maturation that leads to physiological decline, increasing incidence of pathological lesions, and death. The rate of aging and duration of life appear to result from an interaction between the genetic program in the cell and influences from the external environment. While the causes of aging are unknown, there is evidence that the rate of aging may be mediated by the brain, especially by the hypothalamus and the closely linked pituitary and peripheral endocrine system (Everitt, 1976). Disproportionate changes in this system may result in “disregulation” of the organism (Frolkis, 1976), or an elevation of hypothalamic threshold to feed back control (Dilman, 1971), which in turn cause the development of age-related pathology.
1 citations