For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
40
views
46
references
 Top references
cited by
9
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      110
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Apple Procyanidins Suppress Amyloid β-Protein Aggregation

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Procyanidins (PCs) are major components of the apple polyphenols (APs). We previously reported that treatment with PC extended the mean lifespan of Caenorhabditis elegans (Sunagawa et al., 2011). In order to estimate the neuroprotective effects of PC, we investigated the antiaggregative activity of PC on amyloid β -protein (A β ) aggregation, which is a pathological hallmark of Alzheimer's disease. We herein report that PC significantly suppressed A β 42 aggregation and dissociated A β 42 aggregates in a dose-dependent manner, indicating that PC is a potent suppressor of A β aggregation. Furthermore, PC significantly inhibited A β 42 neurotoxicity and stimulated proliferation in PC-12 cells. These results suggested that the PC and AP acted as neuroprotective factors against toxic A β aggregates.

          Related collections

          Most cited references46

          • Record: found
          • Abstract: found
          • Article: not found

          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.
          Article 0 comments Cited 215 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Ectopic expression of VvMybPA2 promotes proanthocyanidin biosynthesis in grapevine and suggests additional targets in the pathway.

            Nancy Terrier, Veronique Cheynier, Laurent Torregrosa … (2009)
            Grapevine (Vitis vinifera) proanthocyanidins contribute to plant defense mechanisms against biotic stress and also play a critical role in organoleptic properties of wine. In grapevine berry, these compounds are mainly accumulated in exocarps and seeds in the very early stages of development. A previous study has already identified VvMybPA1 as the first transcription factor involved in the regulation of the proanthocyanidin pathway during seed development in grapevine. A novel Myb factor, VvMybPA2, which is described in this study, is in contrast mainly expressed in the exocarp of young berries and in the leaves. This transcription factor shows very high protein sequence homology with other plant Myb factors, which regulate flavonoid biosynthesis. Ectopic expression of either VvMybPA1 or VvMybPA2 in grapevine hairy roots induced qualitative and quantitative changes of the proanthocyanidin profiles. High-throughput transcriptomic analyses of transformed grapevine organs identified a large set of putative targets of the VvMybPA1 and VvMybPA2 transcription factors. Both genes significantly activated enzymes of the flavonoid pathway, including anthocyanidin reductase and leucoanthocyanidin reductase 1, the specific terminal steps in the biosynthesis of epicatechin and catechin, respectively, but not leucoanthocyanidin reductase 2. The functional annotation of the genes whose expression was modified revealed putative new actors of the proanthocyanidin pathway, such as glucosyltransferases and transporters.
            Article 0 comments Cited 148 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Phenolic compounds prevent Alzheimer's pathology through different effects on the amyloid-beta aggregation pathway.

              Tsuyoshi Hamaguchi, Kenjiro Ono, Atsushi Murase … (2009)
              Inhibition of amyloid-beta (Abeta) aggregation is an attractive therapeutic strategy for Alzheimer's disease (AD). Certain phenolic compounds have been reported to have anti-Abeta aggregation effects in vitro. This study systematically investigated the effects of phenolic compounds on AD model transgenic mice (Tg2576). Mice were fed five phenolic compounds (curcumin, ferulic acid, myricetin, nordihydroguaiaretic acid (NDGA), and rosmarinic acid (RA)) for 10 months from the age of 5 months. Immunohistochemically, in both the NDGA- and RA-treated groups, Abeta deposition was significantly decreased in the brain (P < 0.05). In the RA-treated group, the level of Tris-buffered saline (TBS)-soluble Abeta monomers was increased (P < 0.01), whereas that of oligomers, as probed with the A11 antibody (A11-positive oligomers), was decreased (P < 0.001). However, in the NDGA-treated group, the abundance of A11-positive oligomers was increased (P < 0.05) without any change in the levels of TBS-soluble or TBS-insoluble Abeta. In the curcumin- and myricetin-treated groups, changes in the Abeta profile were similar to those in the RA-treated group, but Abeta plaque deposition was not significantly decreased. In the ferulic acid-treated group, there was no significant difference in the Abeta profile. These results showed that oral administration of phenolic compounds prevented the development of AD pathology by affecting different Abeta aggregation pathways in vivo. Clinical trials with these compounds are necessary to confirm the anti-AD effects and safety in humans.
              Article 0 comments Cited 115 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Biochem Res Int
                Journal ID (publisher-id): BCRI
                Title: Biochemistry Research International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-2247
                ISSN (Electronic): 2090-2255
                Publication date (Print): 2011
                Publication date (Electronic): 2 August 2011
                Volume: 2011
                Electronic Location Identifier: 784698
                Affiliations
                1Molecular Gerontology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo 173-0015, Japan
                2JAC Co., Ltd., 1-2-7 Higashiyama, Meguro-ku, Tokyo 153-0043, Japan
                3Asahi Breweries, Ltd., 1-1-21 Midori, Moriya-shi, Ibaraki 302-0106, Japan
                4Ageing Control Medicine, Juntendo University Graduate School of Medicine, 3-1-3-10-201 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
                Author notes
                *Takahiko Shimizu: shimizut@ 123456tmig.or.jp

                Academic Editor: Sanford I. Bernstein

                Article
                DOI: 10.1155/2011/784698
                PMC ID: 3150145
                PubMed ID: 21826271
                SO-VID: d612fa9a-9abb-4c97-9e36-b1fac04f0ecf
                Copyright © Copyright © 2011 Toshihiko Toda et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 28 December 2010
                Date revision received : 11 May 2011
                Date accepted : 27 May 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Biochemistry
                Data availability:
                ScienceOpen disciplines: Biochemistry

                Comments

                Comment on this article

                scite_

                Similar content110

                See all similar

                Cited by8

                See all cited by

                Most referenced authors471

                See all reference authors