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      Neuroprotective Role of Phytochemicals

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          Abstract

          Neurodegenerative diseases are normally distinguished as disorders with loss of neurons. Various compounds are being tested to treat neurodegenerative diseases (NDs) but they possess solitary symptomatic advantages with numerous side effects. Accumulative studies have been conducted to validate the benefit of phytochemicals to treat neurodegenerative diseases including Alzheimer’s disease (AD) and Parkinson’s disease (PD). In this present review we explored the potential efficacy of phytochemicals such as epigallocatechin-3-galate, berberin, curcumin, resveratrol, quercetin and limonoids against the most common NDs, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). The beneficial potentials of these phytochemicals have been demonstrated by evidence-based but more extensive investigation needs to be conducted for reducing the progression of AD and PD.

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          EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity.

          Jan Bieschke, Jenny Russ, Ralf P Friedrich … (2010)
          Protein misfolding and formation of beta-sheet-rich amyloid fibrils or aggregates is related to cellular toxicity and decay in various human disorders including Alzheimer's and Parkinson's disease. Recently, we demonstrated that the polyphenol (-)-epi-gallocatechine gallate (EGCG) inhibits alpha-synuclein and amyloid-beta fibrillogenesis. It associates with natively unfolded polypeptides and promotes the self-assembly of unstructured oligomers of a new type. Whether EGCG disassembles preformed amyloid fibrils, however, remained unclear. Here, we show that EGCG has the ability to convert large, mature alpha-synuclein and amyloid-beta fibrils into smaller, amorphous protein aggregates that are nontoxic to mammalian cells. Mechanistic studies revealed that the compound directly binds to beta-sheet-rich aggregates and mediates the conformational change without their disassembly into monomers or small diffusible oligomers. These findings suggest that EGCG is a potent remodeling agent of mature amyloid fibrils.
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            The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse.

            Giselle P. Lim, Teresa Chu, Fusheng Yang … (2001)
            Inflammation in Alzheimer's disease (AD) patients is characterized by increased cytokines and activated microglia. Epidemiological studies suggest reduced AD risk associates with long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Whereas chronic ibuprofen suppressed inflammation and plaque-related pathology in an Alzheimer transgenic APPSw mouse model (Tg2576), excessive use of NSAIDs targeting cyclooxygenase I can cause gastrointestinal, liver, and renal toxicity. One alternative NSAID is curcumin, derived from the curry spice turmeric. Curcumin has an extensive history as a food additive and herbal medicine in India and is also a potent polyphenolic antioxidant. To evaluate whether it could affect Alzheimer-like pathology in the APPSw mice, we tested a low (160 ppm) and a high dose of dietary curcumin (5000 ppm) on inflammation, oxidative damage, and plaque pathology. Low and high doses of curcumin significantly lowered oxidized proteins and interleukin-1beta, a proinflammatory cytokine elevated in the brains of these mice. With low-dose but not high-dose curcumin treatment, the astrocytic marker GFAP was reduced, and insoluble beta-amyloid (Abeta), soluble Abeta, and plaque burden were significantly decreased by 43-50%. However, levels of amyloid precursor (APP) in the membrane fraction were not reduced. Microgliosis was also suppressed in neuronal layers but not adjacent to plaques. In view of its efficacy and apparent low toxicity, this Indian spice component shows promise for the prevention of Alzheimer's disease.
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              Antioxidant and anti-inflammatory activities of quercetin and its derivatives

              Marija M. Lesjak, Ivana N Beara, Natasa Simin … (2018)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Molecules
                Journal ID (iso-abbrev): Molecules
                Journal ID (publisher-id): molecules
                Title: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry
                Publisher: MDPI
                ISSN (Electronic): 1420-3049
                Publication date (Electronic): 27 September 2018
                Publication date Collection: October 2018
                Volume: 23
                Issue: 10
                Electronic Location Identifier: 2485
                Affiliations
                [1 ]Toxicology and Biomedicine Research Group, Faculty of Applied Sciences, Ton Duc Thang University, Ho Chi Minh City 700000, Vietnam
                [2 ]Graduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan; rathinabaski@ 123456gmail.com
                [3 ]Division of Radiation Oncology, Department of Oncology, National Taiwan University Hospital, Taipei 10617, Taiwan; bharathi.log@ 123456gmail.com
                [4 ]Department of Pathology, Anatomy and Cell biology, Thomas Jefferson University, Philadelphia, PA 19107, USA; varadha86@ 123456gmail.com
                [5 ]Department of Life Science and Institute of Biotechnology, National Dong Hwa University, Hualien 97401, Taiwan
                Author notes
                [* ]Correspondence: bharath.kumar.velmurugan@ 123456tdtu.edu.vn (B.K.V.); cfweng@ 123456gms.ndhu.edu.tw (C.-F.W.); Tel.: +84-028-377-55-058 (B.K.V.); +886-3-890-3649 (C.-F.W.)
                Author information
                https://orcid.org/0000-0002-4786-9913
                https://orcid.org/0000-0002-2676-7379
                Article
                Publisher ID: molecules-23-02485
                DOI: 10.3390/molecules23102485
                PMC ID: 6222499
                PubMed ID: 30262792
                SO-VID: 2c093988-0348-44bd-aaca-14e8f4e0a106
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 13 September 2018
                Date accepted : 26 September 2018
                Categories
                Subject: Review

                Keywords: phytochemicals,neurogenerative disease,curcumin,egcg,resveratrol,limonoids
                Data availability:
                Keywords: phytochemicals, neurogenerative disease, curcumin, egcg, resveratrol, limonoids

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