Archive March 2016

Pycnogenol® and Grape Seed Extract for Cognitive Function?

In this study, 44 subjects (55-70 yrs) with high oxidative stress were supplemented with Pycnogenol® daily for 12 months. Another group with comparable oxidative stress was followed as a reference group. Cognitive testing, including IQ Code, cognitive function and SBT were conducted using defined scales. Results after 12 months showed significant improvement in the supplemented group vs the reference group for all tests conducted. Researchers concluded that Pycnogenol® supplementation appears to improve cognitive function and oxidative stress in normal subjects between 55 and 70 years old.(1) Researchers at Mount Sinai School of Medicine and the University of Minnesota evaluated the ability of grape-derived polyphenols to prevent the generation of a specific form of β-amyloid (Aβ) peptide, a substance in the brain known to cause neurotoxicity associated with Alzheimer disease (AD). They administered grape seed extracts to mice genetically determined to develop memory deficits and Aβ neurotoxins similar to those found in AD. They found that the brain content of Aβ*56, a specific form of Aβ previously implicated in the promotion of AD memory loss, was substantially reduced after treatment. Their study corroborates other studies suggesting grape polyphenols may protect against cognitive decline in AD.(2, 3)

1. Belcaro G, et al. The COFU3 Study. Improvement in cognitive function, attention mental performance with Pycnogenol® in healthy subjects (55-70) with high oxidative stress. J Neurosurg Sci 2015;59: 437-46.
2. Lie P, et al. Grape Seed Polyphenolic Extract Specifically Decreases Aβ*56 in the Brains of Tg2576 Mice. Journal of Alzheimer’s Disease, Vol 26, No. 4.
3. Natural chemicals found in grapes may protect against Alzheimer’s disease. ScienceDaily, 18 July 2011

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EGCG to Treat Rheumatoid Arthritis (RA)?

EGCG, a bioactive phytochemical found in green tea, was found to regulate transforming growth factor β-activated kinase 1 (TAK1) in human rheumatoid arthritis synovial fibroblasts (RASF), indicating that TAK1 regulation may be a therapeutic target in RA. EGCG appears to effectively inhibit TAK1 by blocking its phosphorylation. As a mediator of inflammation, TAK1 is integral to the activation of downstream mitogen-activated protein kinases (MAKPs) in response to receptor stimulation by the inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor (TNF). A team of researchers led by Associate Professor Salah-uddin Ahmed of Washington State University College of Pharmacy in Spokane, analyzed the mechanism of TAK1 regulation in a pre-clinical mouse model of human RA. After 10 days of treatment with EGCG, the researchers found a significant reduction in ankle circumference, a measurement used as a surrogate for symptomatic inflammation. Authors stated that they have provided a rationale for targeting RASF TAK1 in RA and identified a unique mechanism through which EGCG inhibits the interaction between signaling molecules important in cytokine signaling, ultimately inhibiting inflammation and tissue destruction in RA.

Singh AK, Umar S, Riegsecker S, et al Regulation of transforming growth factor β-activated kinase activation by epigallocatechin-3-gallate in rheumatoid arthritis synovial fibroblasts: suppression of K63-linked autoubiquitination of tumor necrosis factor receptor-associated factor 6. Arthritis Rheum. 2016;68(2):347-358.

CP Sison (Med Editor) Rheumatoid Arthritis Advisor. March 01, 2016

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Proton Pump Inhibitors (PPIs) Increase Risk of Dementia!

While PPIs are widely used to treat gastrointestinal illnesses, recent evidence suggests they may be related to cognitive decline. A group of German researchers conducted a prospective cohort study to examine the association between the use of PPIs and the risk of incident dementia in the elderly. They used observational data (from 2004-2011) from the largest German statutory health insurer. Their analysis of 73,679 participants (≥ 75 yrs.) concluded in November 2015. The association between PPI use and dementia was analyzed using time-dependent Cox regression, adjusted for potential confounding factors such as age, sex and polypharmacy. Researchers discovered that patients receiving regular PPI medication had a significantly increased risk of incident dementia compared with patients not receiving PPIs. The researchers concluded that the avoidance of PPI medication may prevent the development of dementia. This finding is supported by recent pharmacoepidemiological analyses on primary data, and is in line with mouse models in which the use of PPIs increased the levels of β-amyloid in the brains of mice.

Comm, W, et al. Association of Proton Pump Inhibitors with Risk of Dementia; A Pharmacoepidemikological Claims Data Analysis. JAMA Neurol. doi:10.1001/jamaneurol.2015.4791 Published online Feb 14, 2016.

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