For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
46
views
139
references
 Top references
cited by
23
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      191
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Towards Retinoid Therapy for Alzheimer’s Disease

      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

          Alzheimer’s disease(AD) is associated with a variety of pathophysiological features, including amyloid plaques, inflammation, immunological changes, cell death and regeneration processes, altered neurotransmission, and age-related changes. Retinoic acid receptors (RARs) and retinoids are relevant to all of these. Here we review the pathology, pharmacology, and biochemistry of AD in relation to RARs and retinoids, and we suggest that retinoids are candidate drugs for treatment of AD.

          Related collections

          Most cited references139

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

          Inflammation and Alzheimer's disease.

          H Akiyama, S. Barger, S Barnum … (2000)
          Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
          Article 0 comments Cited 627 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The biological functions of T helper 17 cell effector cytokines in inflammation.

            Wenjun Ouyang, Jay K Kolls, Yan Zheng (2008)
            T helper 17 (Th17) cells belong to a recently identified T helper subset, in addition to the traditional Th1 and Th2 subsets. These cells are characterized as preferential producers of interleukin-17A (IL-17A), IL-17F, IL-21, and IL-22. Th17 cells and their effector cytokines mediate host defensive mechanisms to various infections, especially extracellular bacteria infections, and are involved in the pathogenesis of many autoimmune diseases. The receptors for IL-17 and IL-22 are broadly expressed on various epithelial tissues. The effector cytokines of Th17 cells, therefore, mediate the crucial crosstalk between immune system and tissues, and play indispensable roles in tissue immunity.
            Article 0 comments Cited 420 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Systemic infections and inflammation affect chronic neurodegeneration.

              V. Perry, Colm Cunningham, Clive Holmes (2007)
              It is well known that systemic infections cause flare-ups of disease in individuals with asthma and rheumatoid arthritis, and that relapses in multiple sclerosis can often be associated with upper respiratory-tract infections. Here we review evidence to support our hypothesis that in chronic neurodegenerative diseases such as Alzheimer's disease, with an ongoing innate immune response in the brain, systemic infections and inflammation can cause acute exacerbations of symptoms and drive the progression of neurodegeneration.
              Article 0 comments Cited 316 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Alzheimer Res
                Journal ID (publisher-id): CAR
                Title: Current Alzheimer Research
                Publisher: Bentham Science Publishers Ltd.
                ISSN (Print): 1567-2050
                ISSN (Electronic): 1875-5828
                Publication date (Print): June 2009
                Volume: 6
                Issue: 3
                Pages: 302-311
                Affiliations
                [1 ]Research Foundation ITSUU Laboratory, Molecular and Functional Bioscience, Japan
                [2 ]Institute of Medicinal Molecular Design, Inc., Molecular and Functional Bioscience, Japan
                Author notes
                [* ]Address correspondence to this author at the Research Foundation ITSUU Laboratory, 2-28-10 tamagawa, setagaya-ku, Tokyo 158-0094, Japan; E-mail: kshudo@ 123456itsuu.or.jp
                Article
                Publisher ID: CAR-6-302
                DOI: 10.2174/156720509788486581
                PMC ID: 2765081
                PubMed ID: 19519313
                SO-VID: db741425-a80b-4ee9-bc92-696c5bf16e84
                Copyright © ©2009 Bentham Science Publishers Ltd.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.5/) which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 28 July 2008
                Date revision received : 5 November 2008
                Date accepted : 12 November 2008
                Categories
                Subject: Article

                ScienceOpen disciplines: Neurology
                Keywords: alzheimer’s disease,retinoic acid receptors,immunology,retinoid,inflammation,regulatory t cell,neurodegeneration.
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: alzheimer’s disease, retinoic acid receptors, immunology, retinoid, inflammation, regulatory t cell, neurodegeneration.

                Comments

                Comment on this article

                scite_

                Similar content191

                See all similar

                Cited by21

                See all cited by

                Most referenced authors1,908

                See all reference authors