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294 A. SCALBERT ET AL. exceed 4 and 1.4 mg, respectively, in the Western diet.203 As, previously stressed, for cardiovascular diseases, flavonols, cate- chins, and phytoestrogens considered in epidemiological studies so far published, only account for a minor fraction of the total polyphenols. Here, again, more complete polyphenol food com- position tables or validated exposure biomarkers for other types of polyphenols, such as proanthocyanidins, flavanones, phenolic acids, and anthocyanins, are needed. POLYPHENOLS AND NEURODEGENERATIVE DISEASES Neurodegenerative diseases represent an increasing burden to our aging societies. About 15% of the population over 65 are afflicted by Alzheimer’s disease and 1% by Parkinson’s disease, not including other type of dementia resulting from ischemic injury.204 Such diseases are dependent of oxidative stress, which particularly affects brain tissues,205 and antioxidants may, there- fore, contribute to their prevention.204 Feeding aging rats a diet supplemented with aqueous extracts of spinach, strawberry, or blueberry rich in polyphenols improved their cognitive func- tions and neuronal signal transduction.206,207 Blueberries rich in anthocyanins were particularly effective. These effects were not explained by a sparing of vitamins E and C in the brain;208 a direct implication of polyphenols as antioxidants is, therefore, suspected. Intravenous injection of epicatechin or catechin to mice im- proved the memory impairment induced by cerebral ischemia.209 Polyphenols also protect experimental animals against some neurotoxic drugs whose toxicity is linked to a stimulation of oxidative stress. Dietary supplementation with grape polyphe- nols reduced the neurodegenerative changes induced by chronic ethanol consumption, and improved the synaptic function mea- sured on isolated synaptosomes.210 The oral administration of EGCG restored the dopaminergic neurotransmission in rats injected with N -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a drug used to reproduce a parkinsonian syndrome, and prevented the increase of SOD and catalase induced by this drug.150 The chronic consumption of ferulic acid with the drinking water protected mice from the deleterious effects of an intracerebral injection of β-amyloid peptide, a component of senile plaques postulated to be involved in the pathogenesis of Alzheimer’s disease.211 It prevented the drop of learning and memory performance and the increase in the level of inflam- mation markers in the brain induced by the β-amyloid peptide, possibly via a transitory activation of hippocampal astrocytes. Similar protective effects were observed with curcumin in an Alzheimer transgenic mouse model.212 In vitro experiments showed that catechins improve the sur- vival of cultured neuronal cells when challenged by a β-amyloid peptide, 6-hydroxydopamine, or oxidized LDL.213−215 These ef- fects appear to be mediated by restoration of protein kinase C activity or the inhibition of NF-κB translocation, both mecha- nisms involved in the regulation of cell proliferation and apopto- sis. These effects are dose dependent. At low doses (0.1–10 μM), epigallocatechin gallate protects neuronal cells against oxyda- tive damage and improves cell survival, whereas at higher doses (50 μM), it appears pro-oxidant and toxic.213 Therefore, low polyphenol concentrations would be more effective to prevent neurodegenerative diseases. Little is known about the polyphe- nol concentrations in the brain. The concentrations reached in the brain after feeding rats with genistein are much lower (0.04 nmol/g tissue) than those reached in the plasma (2 μmol/L) and other tissues.216 The poor permeability of the blood-brain barrier to polyphenols was confirmed in other studies with naringin or quercetin.217,218 The glucuronide conjugate of epicatechin was unable to protect cortical neurons against oxidative stress in- duced by H2O2.154 However, the low amounts of polyphenols present in the brain may be only aglycone, as has been shown for genistein, and due to the poor permeability of the blood-brain barrier, to anionic conjugates.216,219 The relationship between polyphenol or wine consumption and neurodegenerative risk has been studied in a few epidemi- ological studies. A moderate wine consumption was negatively associated to the risk of dementia in 3 prospective studies carried out in France, Denmark, and Canada.220−222 Such an association was not observed for beer or spirits in the Danish cohort. This indicates a possible contribution of polyphenols to the preven- tion of dementia. Cognitive impairment was also found to be lower in moderate alcohol drinkers compared to non-drinkers in an Italian cohort, but the probability of cognitive impairment was increased in heavy alcohol drinkers.223 An inverse associa- tion between the intake of flavonols and flavones and the risk of dementia has also been observed in a French cohort.224 POLYPHENOLS AND DIABETES Many plants have been traditionally used in the treatment of diabetes. Polyphenols contained in these plants may explain some of their therapeutic activity.225,226 The acute or chronic ad- ministration of polyphenols to experimental animals influences glycemia. Caffeic acid and isoferulic acid, when administered intravenously to rats, reduce the fasting glycemia and attenuate the increase of plasma glucose in an intravenous glucose toler- ance test.227−229 These effects were observed in a genetic model of insulin-dependent diabetes of rats or in streptozotocin-treated rats, but are less pronounced in normal rats. More interestingly, some hypoglycemic effects were also ob- served with polyphenols administered orally, shortly before con- sumption of the glucose source. A diacylated anthocyanin re- duced the peak of glycemia induced by maltose consumption in normal rats.230 An ill-defined leucodelphinidin (probably a mixture of prodelphinidins) reduced fasting glycemia in rats and lowered the plasma glucose peak in a glucose tolerance test.231 Similar effects were observed with 4-hydroxybenzoic acid.232 Catechin improved the tolerance to glucose induced by starch or sucrose ingestion in rats.233 A fermented tea extract showed hypoglycemic effects in mice.234 These effects were alsoPDF Image | Dietary Polyphenols and the Prevention of Diseases
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