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Neville Vassallo

Bio: Neville Vassallo is an academic researcher. The author has contributed to research in topics: Health effects of natural phenols and polyphenols & Antioxidant. The author has an hindex of 1, co-authored 1 publications receiving 20 citations.

Papers
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01 Jan 2008
TL;DR: The present study focused on the effects of polyphenols on the regulation of Hormone-Related Diseases Index and the role of these chemicals in the prevention of diabetes and obesity.
Abstract: Preface Flavonoids and Cardiovascular Disease: Mechanisms Involved in the Cardioprotective Effects of Quercetin Olive Oil Phenolics as Potential Therapeutical Agents Vascular Protective Effects of Flavonoids in Animal Models of Hypertension and Diabetes Protection and Preservation of Vascular Cells and Tissues by Green Tea Polyphenols Neuroprotective Effects of Polyphenols in Alzheimer's Disease: Antioxidant Activities and Beyond Protective Efects of Green Tea-Derived Polyphenols and Stilbenes on Amyloid Neurotoxicity Regulation of Neural Gene Transcription by Flavonoids Polyphenols and Cancer Chemopreventions: Modulation of Signaling Pathways Dietary Phytochemicals in the Chemoprevention of Prostate Cancer Dietary Polyphenols in Modulation of The Immune System Mitochondrial Generation of Reactive Oxygen Species and its Targeting by Antioxidants: A Future Vision for Diabetes and Obesity Phytoestrogens and Related Polyphenols in the Prevention of Hormone-Related Diseases Index

24 citations


Cited by
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Journal ArticleDOI
TL;DR: Alpha‐synuclein binds to Alpha‐ synuclein by biophysical interaction (View Interaction 1, 2) and this binding is regulated by the proton-proton correspondence between Alpha and Synuclein.

249 citations

Journal ArticleDOI
TL;DR: This review summarizes the current knowledge about the major classes of RWP and places into perspective their potential to be considered as nutraceuticals to target neuropathology in AD and PD.
Abstract: Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common age-related neurodegenerative disorders and hence pose remarkable socio-economical burdens to both families and state. Although AD and PD have different clinical and neuropathological features, they share common molecular mechanisms which appear to be triggered by multi-factorial events such as protein aggregation, mitochondrial dysfunction, oxidative stress (OS) and neuroinflammation, ultimately leading to neuronal cell death. Currently, there are no established and validated disease-modifying strategies for either AD or PD. Among the various lifestyle factors that may prevent or slow age-related neurodegenerative diseases, epidemiological studies on moderate consumption of red wine, especially as part of a holistic Mediterranean diet, have attracted increasing interest. Red wine is particularly rich in specific polyphenolic compounds which appear to affect the biological processes of AD and PD, such as quercetin, myricetin, catechins, tannins, anthocyanidins, resveratrol and ferulic acid. Indeed, there is now a consistent body of in vitro and in vivo data on the neuroprotective effects of red wine polyphenols showing that they do not merely possess anti-oxidant properties, but may additionally act upon, in a multi-target manner, the underlying key mechanisms featuring in both AD and PD. Further, it is important that bioavailability issues are addressed in order for neuroprotection to be relevant in a clinical study scenario. This review summarises the current knowledge about the major classes of red wine polyphenols and places into perspective their potential to be considered as nutraceuticals to target neuropathology in AD and PD.

98 citations

Journal ArticleDOI
TL;DR: Common pathways shared by both sporadic and familial PD that remarkably and consistently converge at the level of mitochondrial integrity are outlined, which has incontrovertibly established mitochondria as a valid therapeutic target in neurodegeneration.
Abstract: Summary Parkinson's disease (PD) is an incurable neurodegenerative disorder leading to progressive motor impairment and for which there is no cure. From the first postmortem account describing a lack of mitochondrial complex I in the substantia nigra of PD sufferers, the direct association between mitochondrial dysfunction and death of dopaminergic neurons has ever since been consistently corroborated. In this review, we outline common pathways shared by both sporadic and familial PD that remarkably and consistently converge at the level of mitochondrial integrity. Furthermore, such knowledge has incontrovertibly established mitochondria as a valid therapeutic target in neurodegeneration. We discuss several mitochondria-directed therapies that promote the preservation, rescue, or restoration of dopaminergic neurons and which have been identified in the laboratory and in preclinical studies. Some of these have progressed to clinical trials, albeit the identification of an unequivocal disease-modifying neurotherapeutic is still elusive. The challenge is therefore to improve further, not least by more research on the molecular mechanisms and pathophysiological consequences of mitochondrial dysfunction in PD.

91 citations

Book ChapterDOI
TL;DR: Consistent mechanistic data on the neuroprotective and neuroregenerative effects of tea polyphenols indicate that they do not just possess anti-oxidant or anti-chelating properties but may directly interfere with aggregation of the αS protein and modulate intracellular signalling pathways, both in vitro and in animal models.
Abstract: Parkinson's disease (PD) is a common motor neurodegenerative disorder with multifactorial etiology that is an increasing burden on our aging society. PD is characterized by nigrostriatal degeneration which might involve oxidative stress, α-synuclein (αS) aggregation, dysregulation of redox metal homeostasis and neurotoxicity. Although the exact cause remains unknown, both genetic and environmental factors have been implicated. Among the various environmental factors tea consumption has attracted increasing interest, as besides being one of the most consumed beverages in the world, tea contains specific polyphenols which can play an important role in delaying the onset or halting the progression of PD. Green and black teas are rich sources of polyphenols, the most abundant being epigallocatechin-3-gallate (EGCG) and theaflavins. There is now consistent mechanistic data on the neuroprotective and neuroregenerative effects of tea polyphenols, indicating that they do not just possess anti-oxidant or anti-chelating properties but may directly interfere with aggregation of the αS protein and modulate intracellular signalling pathways, both in vitro and in animal models. EGCG in green tea has been by far the most studied compound and therefore future investigations should address more the effects of other polyphenols, especially theaflavins in black tea. Nevertheless, despite significant data on their potential neuroprotective effects, clinical studies are still very limited and to date only EGCG has reached phase II trials. This review collates the current knowledge of tea polyphenols and puts into perspective their potential to be considered as nutraceuticals that target various pathologies in PD.

66 citations

Journal ArticleDOI
TL;DR: These systems could be proposed as novel transdermal drug delivery systems, since they were found able to control the percutaneous permeation of small drugs across the skin.

53 citations