File Name: vascular and neurogenic rejuvenation in aging mice by modulation of asm .zip
Cell Stress, Vol. Keywords: apoptosis, autophagy, lysosome-dependent cell death, necroptosis, ischemia, vasculature.
Eur J Endocrinol. Cancers Basel. Aging Dis. Epub Sep Afterdischarges elicited by cortical electric stimulation in humans: When do they occur and what do they mean?
Age is associated with altered immune functions that may affect the brain. In this review, we explore novel mechanisms by which the aging immune system alters central nervous system functions and neuroimmune responses, with a focus on brain barriers. Understanding how age alters BBB functions and responses to pathological insults could provide important insight on the role of the BBB in the progression of cognitive decline and neurodegenerative disease. Advances in modern medicine, nutrition, hygiene, and safety standards have doubled the life expectancy of humans worldwide over the last century and a half [ 1 ]. Therefore, it is imperative that the scientific and medical communities investigate approaches that will minimize age-associated disease and maximize quality of life.
Vascular and Neurogenic Rejuvenation in Aging Mice by Modulation of ASM. sources, via Unpaywall: honeycreekpres.org
Electronic address:. Toggle navigation. Login Categories Journals. Publications by authors named "Minseok Kang".
Aging involves a decline in neural function that contributes to cognitive impairment and disease. However, the mechanisms underlying the transition from a young-and-healthy to aged-and-dysfunctional brain are not well understood. Here, we report breakdown of the vascular blood-brain barrier BBB in aging humans and rodents, which begins as early as middle age and progresses to the end of the life span.
Sundaram SM, Schwaninger M. Trends Endocrinol Metab. Epub ahead of print.
Although many studies have reported that the breakdown of the blood-brain barrier BBB represents one of the major pathological changes in aging, the mechanism underlying this process remains relatively unexplored. In this study, we described that acid sphingomyelinase ASM derived from endothelial cells plays a critical role in BBB disruption in aging. ASM levels were elevated in the brain endothelium and plasma of aged humans and mice, resulting in BBB leakage through an increase in caveolae-mediated transcytosis. Mice overexpressing brain endothelial cell-specific ASM exhibited acceleration of BBB impairment and neuronal dysfunction. However, genetic inhibition and endothelial specific knock-down of ASM in mice improved BBB disruption and neurocognitive impairment during aging.
By cleaving sphingomyelin into ceramide, which is an essential component of plasma membrane microdomains, acid sphingomyelinase Asm pivotally controls cell signaling. Acid sphingomyelinase Asm , which catalyzes the hydrolysis of sphingomyelin to ceramide, is a key enzyme in sphingolipid metabolism. Localized in lysosomes, Asm is translocated to the plasma membrane within a few seconds to minutes upon stress stimuli [ 1 , 2 , 3 ]. In plasma membranes, ceramide clusters into membrane platforms that critically control the activity of signal pathways modifying cell survival and death [ 1 , 2 , 4 , 5 ]. Importantly, the pharmacological inhibition or genetic depletion of Asm in mice conferred protection against cystic fibrosis, lung infection and sepsis [ 15 , 16 ], whereas Asm-dependent and -independent ceramide formation was found to be required for radiation-induced tumor apoptosis [ 10 , 17 ]. Hence, the deactivation of Asm represents a potent strategy for the prevention of cell injury in a wide range of pathologies.
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Он не мог понять, почему Мидж всегда права. Он не заметил отражения, мелькнувшего за оконным стеклом рядом с. Крупная фигура возникла в дверях директорского кабинета. - Иису… - Слова застряли у Бринкерхоффа в глотке.
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