Topic
Aging brain
About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.
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TL;DR: The presence of RACK1 immunoreactivity in human brain frontal cortex for the first time is reported and a decrease in Rack1 content in cytosol and membrane extracts in AD is demonstrated when compared with non-AD controls, indicating that a decreases in an anchoring protein for PKC is an additional determinant of this deficit.
82 citations
TL;DR: Estrogen-containing hormone therapy should not be initiated after age 65 to prevent dementia or remediate cognitive aging, and further research is needed to understand short-term and long-term cognitive effects of estrogen exposures closer to the age of menopause.
82 citations
TL;DR: An enhanced endogenous expression of Hb in aging brain cells is revealed, probably serving as a compensatory mechanism against hypoxia, and Aβ binds to Hb and other hemoproteins via the iron-containing heme moiety, thereby reducing Hb/heme/iron-induced cytotoxicity.
Abstract: Accumulation of amyloid-β (Aβ) peptides in the brain is one of the central pathogenic events in Alzheimer's disease (AD). However, why and how Aβ aggregates within the brain of AD patients remains elusive. Previously, we demonstrated hemoglobin (Hb) binds to Aβ and co-localizes with the plaque and vascular amyloid deposits in post-mortem AD brains. In this study, we further characterize the interactions between Hb and Aβ in vitro and in vivo and report the following observations: 1) the binding of Hb to Aβ required iron-containing heme; 2) other heme-containing proteins, such as myoglobin and cytochrome C, also bound to Aβ; 3) hemin-induced cytotoxicity was reduced in neuroblastoma cells by low levels of Aβ; 4) Hb was detected in neurons and glial cells of post-mortem AD brains and was up-regulated in aging and APP/PS1 transgenic mice; 5) microinjection of human Hb into the dorsal hippocampi of the APP/PS1 transgenic mice induced the formation of an envelope-like structure composed of Aβ surrounding the Hb droplets. Our results reveal an enhanced endogenous expression of Hb in aging brain cells, probably serving as a compensatory mechanism against hypoxia. In addition, Aβ binds to Hb and other hemoproteins via the iron-containing heme moiety, thereby reducing Hb/heme/iron-induced cytotoxicity. As some of the brain Hb could be derived from the peripheral circulation due to a compromised blood-brain barrier frequently observed in aged and AD brains, our work also suggests the genesis of some plaques may be a consequence of sustained amyloid accretion at sites of vascular injury.
82 citations
TL;DR: The hippocampus, an area with abundant glucocorticoid receptors, continues to be the focus of research on effects of glucocORTicoids on the aging brain, and new ways in which glucOCorticoids may contribute to brain aging are discussed, including decreased responses to glucoc Corticoids possibly as a result of decreased glucoc Torticoids receptors and also altered regulation of neuronal turnover in the dentate gyrus.
81 citations
TL;DR: In this article, the potential role of age-related metabolic disturbances serving as an important basis for deleterious perturbations in the aging brain was discussed, which not only have important implications for understanding the basis of brain aging, but also may be important to the development of therapeutic interventions which promote successful brain aging.
Abstract: Deleterious neurochemical, structural, and behavioral alterations are a seemingly unavoidable aspect of brain aging. However, the basis for these alterations, as well as the basis for the tremendous variability in regards to the degree to which these aspects are altered in aging individuals, remains to be elucidated. An increasing number of individuals regularly consume a diet high in fat, with high-fat diet consumption known to be sufficient to promote metabolic dysfunction, although the links between high-fat diet consumption and aging are only now beginning to be elucidated. In this review we discuss the potential role for age-related metabolic disturbances serving as an important basis for deleterious perturbations in the aging brain. These data not only have important implications for understanding the basis of brain aging, but also may be important to the development of therapeutic interventions which promote successful brain aging.
81 citations