Introduction

General presentation of polyphenols

In plants, polyphenols (or phenolic compounds) play an essential role, in protection from ultraviolet radiation and against aggression by pathogens or predators, contribute to their colour and flavour and facilitate growth and reproduction. To date, more than 8000 natural polyphenols have been identified in plants (Pandey and Rizvi, 2009). They may be grouped into classes according to the shared structural characteristics of their carbon skeletons. The main classes include phenolic acids and derivatives (hydroxybenzoic and hydroxycinnamic), flavonoids ( flavanols, flavonols, flavones,flavanones, isoflavones, chalcones, anthocyanins), tannins(condensed or hydrolysable), stilbenes, lignans, coumarins,lignins (Naczk and Shahidi, 2006). Polyphenols share one common feature: an aromatic ring with at least one hydroxyl substituent. However, they vary greatly in their complexity from phenols to the highly polymerized tannins. They occur predominantly as conjugates with one or more sugars residues generally linked to hydroxyl groups or, less frequently,aromatic carbon atoms (Pandey and Rizvi, 2009). The principle sugar residue is glucose, while others (e.g., galactose,rhamnose, xylose or arabinose) are also encountered (Bravo,1998). When ingested, polyphenols enter the digestive system primarily in form of glycosides, although some aglycones may be present. Before absorption, these compounds must be hydrolysed by endogenous enzymes (Pandey and Rizvi, 2009). This metabolism should be kept in mind when interpreting results, since the forms reaching the blood and tissues are different from those present in food: the most common polyphenols in our diet are not necessarily those showing highest concentration of active metabolites in target tissues (Pandey and Rizvi, 2009).

Biological activities and health implications of polyphenols

In the last decade of 20th century, the major researches focused on antioxidant activity of polyphenols due to their properties to scavenge free radical such as reactive oxygen species or hydroxyl radicals, which are produced in living organisms. Due to their unpaired electron, free radicals are very reactive species and their overproduction can cause damage to all biological macromolecules (DNA, proteins,lipids), resulting in cell alteration. Polyphenols can also act as antioxidants through their capacity to chelate metal ions such as iron. Some of them have antioxidant activity stronger than the reference water soluble vitamin E analogue Trolox, (Fauconneau et al., 1997). There are increasing evidences that polyphenols may protect cell constituents against oxidative damage and limit various disease associated with oxidative stress. Number of in vitro and in vivo studies have demonstrated that polyphenols intake limits the incidence of coronary heart diseases, in particular atherosclerosis in which low density lipoprotein (LDL) oxidation play a key mechanism in the development of this , studies provide evidence for a protective role of a diet rich in polyphenols against chronic diseases including cancers (Anantharaju et al., 2016) and diabetes (Jung et al.,2007). In more recent works, polyphenols may provide protection in neurodegenerative disorders, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) (Figure 1).

AD and PD

Figure 1 Classification of representative natural polyphenols reported in this article as modulating protein aggregates in Alzheimer’s disease and Parkinson’s disease.

AD and PD are the most common neurodegenerative disorders. For demographic reasons, these two diseases affect an increasing percentage of population. The common molecular mechanism observed in these neurodegenerative diseases is the formation of protein aggregates (Hashimoto et al., 2003). The ubiquitin-proteasome system cannot remove these aggregates not only because they are in excessive quantities but also because these proteins are misfolded,have excessive sizes and consequently present resistance to degradation. Indeed, aggregation and accumulation of these misfolded proteins in the central nervous system is due to a result of changes in the native proteins conformation and is consequent to aberrant production or overexpression of specific proteins, leading to progressive neurological impairment and neuronal dysfunction observed in AD (Hashimoto et al., 2003; Gadad et al., 2011) and in PD (Guerrero et al.,2013). Autophagy, as a lysosomal pathway, could play an important role in preventing the accumulation of abnormal proteins (Kroemer and Levine, 2008). However, defects of autophagy and accumulation of protein aggregates are observed in neurodegenerative diseases such as AD (Lee et al.,2010; Gusdon et al., 2012; Francois et al., 2014) and PD (Wu et al., 2011; Lynch-Day et al., 2012).

AD and PD share some neuropathological features with prion diseases and consequently these neurodegenerative diseases are considered as prion-like diseases. They involve proteins able to aggregate, β-amyloid (Aβ) peptide, tau,α-synuclein (α-syn) and synphilin-1, following conformational changes (Toni et al., 2017). Moreover, metal ions can directly bind to them, enhancing aggregates formation.

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