老年痴呆症研究取得进展
Advances in research into Alzheimer's disease: transporter proteins at the blood CSF barrier and vitamin D may help prevent amyloid(淀粉体) β build up in the brain Advancing age is a major risk factor for Alzheimer's disease and is associated with build- up of the peptide(缩氨酸) amyloid β in the brain. New research published in BioMed Central's open access journal Fluids and Barriers of the CNS shows that removal of amyloid β from the brain depends on vitamin D and also on an age-related alteration1 in the production of transporter proteins which move amyloid β in and out of the brain.
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Low levels of vitamin D are thought to be involved in age-related decline in memory and cognition and are also associated with Alzheimer's disease. Researchers from Tohoku University, Japan, looked at the mechanism2 behind this and found that vitamin D injections improved the removal of amyloid β from the brain of mice.
Prof Tetsuya Terasaki said, "Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway. These results lead the way towards new therapeutic3 targets in the search for prevention of Alzheimer's disease." #
The transport of amyloid β across the BBB is known to be orchestrated(精心安排) by transporter proteins such as LRP-1 and P-gp, which move amyloid β out of the brain, and RAGE, which controls influx4. Looking at the transport of amyloid β from blood to cerebrospinal fluid (CSF脑脊髓液), and from CSF to blood, researchers from Rhode Island Hospital and The Warren Alpert Medical School, found that LRP-1 and P-gp at the blood-cerebrospinal fluid barrier (BCSFB脑脊髓屏障), increased with age so increasing removal of amyloid β from the CSF and brain. #
Prof Gerald Silverberg said, "While increased production of transporter proteins at the blood CSF barrier may help amyloid β removal from the older brain, production of these proteins eventually fails. This failure may be an important event in brain function as we age and for people with Alzheimer's disease."
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