Nutritional Outlook

Nutritional Outlook, September 2013

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Cognitive Health site for other polyphenolic compounds has been proposed to be on the brain plasma membrane. Tis binding contributes to the activation of various downstream enzymes, indicating the ability of favonoids to initiate the synthesis of a number of synapserelated proteins that can afect structural changes involved in memory acquisition and storage. Neurodegenerative processes are also favorably impacted by this protein synthesis, as the activation of proteins, including phosphatidylinositide 3-kinases (a family of enzymes involved in cellular growth and survival), may lead to the enhancement of downstream gene expression that infuences neuroprotective efects. Flavonoids have been further shown to facilitate the activation of processes that increase neuron communication, new nerve cell growth, and synaptic plasticity (the ability of the nerve connection to change and adapt in response to neural stimuli). Flavonoids have also been shown to inhibit infammatory events and cell death. Te cumulative benefts of these efects may include overall prevention of neural degeneration and premature brain aging, and enhanced memory and cognitive function (Free Radical Biology & Medicine, 2012). tor for vascular remodeling. Increased blood fow to brain tissues serves to stabilize the structure and function of newly synthesized neurons (Cell, 2008). Toxins and Infammation Brain infammation, as a result of toxic exposures in neural tissues, is an important factor in Parkinson's disease, Alzheimer's disease, and other neurodegenerative conditions. And growing evidence suggests that favonoids play an important role in reducing this damage. Blueberry favonoids were recently shown to inhibit pro-infammatory factors in mice microglia cells (immune cells innate to the central nervous system), such as tumor necrosis factor-alpha (Journal of Agricultural and Food Chemistry, 2013). Green tea polyphenols have shown an ability to reduce damage in neural tissue via the chelation, or removal, of free iron, a pro-infammatory mineral (Genes & Nutrition, 2009). Another mechanism employed by favonoids to address the efects of toxins and infammation in brain tissue is the uniquely suited as efectors of structural and physiological changes in brain tissue. Human Evidence: Flavonoids and Cognitive Health Several studies in humans highlight the association between the consumption of polyphenol-rich foods and a delay in the onset of Alzheimer's disease. One such study found that frequent consumption of fruits and vegetables reduced the risk of dementia and Alzheimer's disease (Neurology, 2007). Additional research prospectively examined favonoid consumption in a cohort of individuals over a ten-year period and found that higher favonoid consumption resulted in superior cognitive outcomes (American Journal of Epidemiology, 2007). Furthermore, Kristopher Beking and Amandio Vieira from Simon Fraser University in British Columbia, Canada, undertook an evaluation of global data on favonoid intake and dementia from 23 developed countries. Te results of their evaluation suggest that higher dietary favonoid consumption, especially of favonols (including quercetin and others), is associated with lower rates of dementia in the population at-large (Public Health Nutrition, 2010). Elizabeth Devore's group from Harvard Medical School and the German Center for Neurodegenerative Diseases in Bonn, Germany, found that greater intakes of blueberries and strawberries, as well as greater anthocyanidin and total favonoid consumption, were associated with slower rates of cognitive decline in more than 16,000 participants aged 70 and older from the Nurses' Health Study. Te results of their analysis indicated that higher berry intake delayed cognitive aging by up to 2.5 years (Annals of Neurology, 2012). In terms of interventional studies, research on Ginkgo biloba continues to show positive benefts for cognitive function. While the GuidAge trial (The Lancet Neurology, 2012) on standardized ginkgo extract in 2854 individuals age 70 and older with memory complaints did not show a preventive efect on the development of Flavonoids promote endothelial function, regulate blood pressure, and decrease infammation—all of which facilitate better cerebral blood fow. Vascular Effects Te health of the vascular system is a key factor in brain health because a number of cardiovascular risk factors are strongly associated with various forms of dementia. Flavonoids promote endothelial function, regulate blood pressure, and decrease infammation—all of which facilitate better cerebral blood fow (Free Radical Biology & Medicine, 2012). Studies have shown that enhanced cerebral blood fow leads to increased generation of neurons in the hippocampus. Following the induction of ischemia in mice, treatment with citrus favonoids was found to enhance neurogenesis in the hippocampus via increased expression of cellular growth factors in brain tissue (Neuroscience Letters, 2012). Flavonoids have also been found to enhance the production of nitric oxide in endothelial tissue, a key fac38 magenta cyan yellow black enhancement of endogenous antioxidants. As an example, the favonoid epicatechin was found to increase glutathione production in astrocytes (Journal of Neurochemistry, 2008), star-shaped cells that are also the most abundant cell type in the human brain, facilitating nervous system repair and neurotransmitter uptake and release, among other critical functions. Fisetin, a favonoid found in strawberries and other fruits, was recently investigated for its ability to counter aluminum chloride toxicity in mice. Aluminum chloride induced several pro-infammatory efects on brain tissue, and oral administration of fsetin was shown to reduce infammatory markers and exert neuroprotective efects (Neuromolecular Medicine, 2013). Te benefts of favonoids and the breadth of their interaction with neurons extends far beyond any direct antioxidant efect that may be conferred by them. Te complexity of these interactions makes favonoids SEPTEMBER 2013 ■ NUTRITIONAL OUTLOOK ES315728_NO1309_038.pgs 09.04.2013 04:17 UBM

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