oa Editorial [Hot Topic: Nutraceuticals and Prevention of Neurodegeneration (Executive Guest Editors: Thea Magrone and Emilio Jirillo)]

The incidence of neurodegenerative disease is increasing mostly in western countries due to the many cofactors involved. Among them, environmental factors (contaminants, pollution, climatic changes), antigenic pressure (microbial infections), life style disorders (smoke, alcohol, diet) as well as alteration of intestinal microbiota seem to represent the major etiopathogenic determinants of neurodegeneration. Nutraceuticals or functional foods have recently been object of intensive investigation for their capacity to prevent or attenuate the onset of many chronic diseases, even including neurodegenerative disease. Therefore, in the present special issue of Current Pharmaceutical Design, entitled “Nutraceuticals and Prevention of Neurodegeneration”, an update of the mechanisms of action of the major nutraceuticals active in the prevention of the neurodegenerative process will be provided. Andrade and Assuncao [1] will point out the beneficial effects of green tea (GT) whose polyphenols have been shown to be brainaccessible. In particular, in a model of aging rats the effects of GT on the glutathione system as well as the activation of cyclic AMP response element binding protein and the increase of brain-derived neurotrophic factor (BDNF) and of the anti-apoptotic protein B-cell lymphoma will be elucidated. Authors conclude that GT polyphenols seem to play an important role in reversal of loss of neuronal plasticity and recovery of neuronal damage in the elderly. Ho and associates [2] will adopt an integrative approach to introduce nutraceuticals able to prevent age-related neurodegeneration. Both small molecules such as polyphenols and big entities, e.g., oligosaccharides and polysaccharides seem to antagonize neurodegeneration in Alzheimer's disease (AD), Age-related Macular Degeneration and Parkinson's disease (PD). The indirect effects of these molecules on peripheral disease-related risk factors will also be discussed. Li and associates [3] will illustrate the effects of resveratrol (RSV), a non-flavonoid polyphenol, on AD. RSV has been shown to promote non-amyloidogenic cleavage of the amyloid precursor protein, enhance the clearance of amyloid beta-peptides, thus reducing the degree of neuronal damage. Some concerns related to bioavailability, biotransformation, synergism with other dietary factors as well as noxious effects due to RSV pro-oxidant capacity will also be taken into consideration. Magrone and associates [4] will emphasize the common pathogenic denominator which characterizes both PD and AD. Exaggerated activation of the systemic and cerebral immune system exerted by bacterial lipopolysaccharides and amyloid beta may account for the release of reactive oxygen species and proinflammatory cytokines. In this scenario, authors point out the properties of certain nutraceuticals such as vitamin D and polyphenols to prevent or attenuate neuroinflammation in both PD and AD. Marzulli and associates [5] will clarify the mechanisms of action of polyphenols from fermented grape marc (FGM). FGM from Koshu and Negroamaro grape Vitis vinifera when tested on peripheral blood mononuclear cells from normal donors generate two major effects: i. the induction of FoxP3 (a biomarker of T regulatory cells); ii the reduction of Granzyme B. Because of these anti-inflammatory effects FGM may represent a valid therapeutic measure to mitigating neuroinflammation in both AD and PD. Ozawa and associates [6] will provide evidence for the neuroprotective effects of lutein in the retina. Lutein is a carotenoid not synthesized in mammals and, therefore, must be obtained from the diet. In lutein-treated murine ocular disease models, oxidative stress is dramatically reduced. Furthermore, degradation of rhodopsin and synaptophysin, depletion of BDNF and DNA damage are also prevented by lutein treatment. Kim and Oh [7] will discuss on the use of traditional herb medicines to prevent or treat neurological disorders. In particular, they have the potential to be developed into optimal pharmaceuticals and nutraceuticals for their multifunction and multi target characteristics. In particular, inhibition of acethylcolinesterase activity, antioxidant and anti-inflammatory capacities seem to represent a common denominator among the biologic properties of many plants. Gadad and associates [8] will present the effects of a novel synthesized compound, Curcumin-glucoside (Curc-gluc). In particular, Curcgluc can inhibit alpha-synuclein aggregation which is centrally involved in PD. Then, Curc-gluc is able to solubilize the oligomeric form disintegrating preformed fibrils, thus preventing further fibrillization of alpha-synuclein. Its exploitation in the course of PD is discussed. Peluso and associates [9] will point out the emerging role of interleukin (IL)-17 in the pathogenesis of neurodegeneration. In particular, they have studied the circulating levels of IL-17 after ingestion of a High Fat Meal (HFM) in healthy overweight individuals. The association of the HFM to fruit juice drink in comparison with placebo reduced the secretion of IL-17. Therefore, this dietary supplementation for its capacity to reduce serum IL-17 may represent a preventive measure for diet-related disease such as AD and PD. Mythri and Srinivas Bharath [10] will describe the neuroprotective potential of curcumin, a polyphenol present in turmeric (Curcuma longa). This compound is able to cross the blood-brain-barrier, thus exerting antioxidant and anti-inflammatory activities at the central nervous system level. The therapeutic potential of curcumin in PD is discussed.