Aging brain

About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.

The Calcium Rationale in Aging and Alzheimer's Disease

Abstract: Calcium is required for the function of all cells in the body, including neurons. Considerable research has described the function of calcium in the regulation of numerous processes including neurotransmitter release, cytoarchitecture and growth, and activation of enzyme systems including kinases and phosphatases. Calcium is intimately involved in a variety of “plastic” changes in the brain. For example, during adaptive processes such as learning and development, changes in transmembrane calcium fluxes correlate with changes in neuronal excitability and structural connectivity. Calcium thus is likely to have key roles in the cellular processes underlying aging-related changes in the brain, including normal age-associated memory impairments as well as more severe dementias, including Alzheimer’s disease. The pivotal role of calcium in so many neuronal processes dictates the need for precise regulation of its intracellular levels. Any dysregulation, however subtle, could lead to dramatic changes in normal neuronal function. Recent studies from our laboratory and those of others have implicated altered calcium influx with agingrelated changes at both the behavioral and the neurophysiological levels. These findings led to and continue to support the calcium hypothesis’s* which posits that in the aging brain, transient or sustained increases in the average concentration of intracellular free calcium contribute to impaired function, eventually leading to cell death. The hypothesis suggests that the final common pathway that may contribute to cognitive deterioration of aging vertebrates, including persons with Alzheimer’s disease or other aging-related dementias, is increased free calcium within neurons. The functional impairment that characterizes a patient at a particular time in the aging-related disease process may be relieved by reducing excessive calcium influx. Additionally, because calcium dysregulation terminating in cell death is likely to be

Sex hormones, aging, and Alzheimer's disease.

Abstract: A promising strategy to delay and perhaps prevent Alzheimer's disease (AD) is to identify the age-related changes that put the brain at risk for the disease. A significant normal age change known to result in tissue-specific dysfunction is the depletion of sex hormones. In women, menopause results in a relatively rapid loss of estradiol and progesterone. In men, aging is associated with a comparatively gradual yet significant decrease in testosterone. We review a broad literature that indicates age-related losses of estrogens in women and testosterone in men are risk factors for AD. Both estrogens and androgens exert a wide range of protective actions that improve multiple aspects of neural health, suggesting that hormone therapies have the potential to combat AD pathogenesis. However, translation of experimental findings into effective therapies has proven challenging. One emerging treatment option is the development of novel hormone mimetics termed selective estrogen and androgen receptor modulators. Continued research of sex hormones and their roles in the aging brain is expected to yield valuable approaches to reducing the risk of AD.