In the group of older women, risk was cut by nearly 20 percent whenįolate intake was at least 1 mg. More specifically, among women in the younger group who consumed a minimum of 1 mg of folate daily, hypertension risk was decreased by more than 45 percent, compared to women who consumed less than 0.2 mg every day. When the Harvard team compared medical records to information about folate intake from regularly updated dietary questionnaires, they found a general correlation between a high intake of folate and reduced risk of high blood pressure. In either phase had been diagnosed with hypertension at the outset of the study. The second phase included the records of more than 62,000 women, aged 43 to 70. The first phase examined eight years of medical and dietary records for well over 93,000 women under the age of 44. Researchers collected data from two phases of the Nurses’ Health Study. In a January issue of the Journal of the American Medical Association, researchers at Harvard Medical School report on a study that examines the association between hypertension risk and the intake of folate a B vitamin. Obviously, blood pressure is closely tied to the health of your heart, so it’s no surprise really to find a new study that demonstrates how the intake of a key nutrient that promotes heart health may also alleviate hypertension risk. If you and your doctor discover and address the root problem of hypertension, you’re more likely to successfully treat it. High blood pressure isn’t a disease, in the same way that a high fever isn’t a disease – it’s a sign that something else is wrong. ‘Scheduling’ has no place in your bedroom! New-found energy and enthusiasm, just visit: Continue to astound your spouse or girlfriend with One new powerful supplement can support your sexual strength and driveĪll naturally. Now you can maintain peak performance whenever you desire – with the NEW This review highlights the importance of Ca v1.2 channel overexpression, the accumulation of hyperphosphorylated tau and suppression of autophagy in Alzheimer's disease and modulation of this pathway by isradipine.**************************************************** A better understanding of brain pharmacokinetics of calcium channel blockers will be critical for designing new experiments with appropriate drug doses in any future clinical trials for Alzheimer's disease. Our results further suggest that isradipine became bioavailable, lowered tau burden, and improved autophagy function in the brain.
We have previously shown that administration of isradipine to triple transgenic animal model for Alzheimer's disease was well-tolerated. Our studies have shown that isradipine in vitro attenuates beta amyloid oligomer toxicity by suppressing calcium influx into cytoplasm and by suppressing Ca v1.2 expression. Isradipine is a Federal Drug Administration-approved dihydropyridine calcium channel blocker that binds selectively to Ca v1.2 in the hippocampus. Increased intracellular calcium modulates amyloid precursor protein processing and affects multiple downstream pathways including increased hyperphosphorylated tau and suppression of autophagy. Paradoxically, L-type calcium channel subtype Ca v1.2 also promotes synaptic plasticity and spatial memory. Beta amyloid accumulation leads to dysregulation of intracellular calcium by plasma membrane L-type calcium channels located on neuronal somatodendrites and axons in the hippocampus and cortex. The greatest challenge has been to identify and define downstream mechanisms reliably predictive of clinical symptoms. The drug development effort to modify Alzheimer's disease pathology by intervention at beta amyloid production sites has been largely ineffective or inconclusive. Alzheimer's disease is the most devastating neurodegenerative disorder in the elderly, yet treatment options are severely limited.
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