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      The neuroprotective role of melatonin in neurological disorders

      review-article
      Author(s): 1 , 2 ,
      Publication date (Electronic):
      Journal: Journal of Neuroscience Research
      Publisher: John Wiley and Sons Inc.
      Keywords: melatonin, ischemia, alzheimer, parkinson

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          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

          Melatonin is a neurohormone secreted from the pineal gland and has a wide‐ranging regulatory and neuroprotective role. It has been reported that melatonin level is disturbed in some neurological conditions such as stroke, Alzheimer's disease, and Parkinson's disease, which indicates its involvement in the pathophysiology of these diseases. Its properties qualify it to be a promising potential therapeutic neuroprotective agent, with no side effects, for some neurological disorders. This review discusses and localizes the effect of melatonin in the pathophysiology of some diseases.

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          The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

          John Hardy, Dennis Selkoe (2002)
          It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.
          Article 0 comments Cited 1116 times – based on 0 reviews     Review now
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            alpha-Synuclein in filamentous inclusions of Lewy bodies from Parkinson's disease and dementia with lewy bodies.

            M Spillantini, R A Crowther, R. Jakes … (1998)
            Lewy bodies and Lewy neurites are the defining neuropathological characteristics of Parkinson's disease and dementia with Lewy bodies. They are made of abnormal filamentous assemblies of unknown composition. We show here that Lewy bodies and Lewy neurites from Parkinson's disease and dementia with Lewy bodies are stained strongly by antibodies directed against amino-terminal and carboxyl-terminal sequences of alpha-synuclein, showing the presence of full-length or close to full-length alpha-synuclein. The number of alpha-synuclein-stained structures exceeded that immunoreactive for ubiquitin, which is currently the most sensitive marker of Lewy bodies and Lewy neurites. Staining for alpha-synuclein thus will replace staining for ubiquitin as the preferred method for detecting Lewy bodies and Lewy neurites. We have isolated Lewy body filaments by a method used for the extraction of paired helical filaments from Alzheimer's disease brain. By immunoelectron microscopy, extracted filaments were labeled strongly by anti-alpha-synuclein antibodies. The morphologies of the 5- to 10-nm filaments and their staining characteristics suggest that extended alpha-synuclein molecules run parallel to the filament axis and that the filaments are polar structures. These findings indicate that alpha-synuclein forms the major filamentous component of Lewy bodies and Lewy neurites.
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              Pathobiology of ischaemic stroke: an integrated view

              Ulrich Dirnagl, Costantino Iadecola, Michael A. Moskowitz (1999)
              Article 0 comments Cited 260 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                B. S. Alghamdi:
                ORCID: http://orcid.org/0000-0002-9411-3609
                basalghamdi@kau.edu.sa
                Journal
                Journal ID (nlm-ta): J Neurosci Res
                Journal ID (iso-abbrev): J. Neurosci. Res
                Journal ID (doi): 10.1002/(ISSN)1097-4547
                Journal ID (publisher-id): JNR
                Title: Journal of Neuroscience Research
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0360-4012
                ISSN (Electronic): 1097-4547
                Publication date (Electronic): 01 March 2018
                Publication date (Print): July 2018
                Volume: 96
                Issue: 7 ( doiID: 10.1002/jnr.v96.7 )
                Pages: 1136-1149
                Affiliations
                [ 1 ] Department of Physiology, Faculty of Medicine King Abdulaziz University Jeddah KSA
                [ 2 ] Neuroscience Unit, Faculty of Medicine King Abdulaziz University Jeddah KSA
                Author notes
                [*] [* ] Correspondence Badrah Saeed Alghamdi, Department of Physiology, Faculty of Medicine, King Abdulaziz University, Jeddah, KSA. Email: basalghamdi@ 123456kau.edu.sa
                Author information
                http://orcid.org/0000-0002-9411-3609
                Article
                Publisher ID: JNR24220
                DOI: 10.1002/jnr.24220
                PMC ID: 6001545
                PubMed ID: 29498103
                SO-VID: bbf60549-c40a-49ef-933b-73ebc8fa9636
                Copyright © © 2018 The Authors Journal of Neuroscience Research Published by Wiley Periodicals, Inc.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 23 October 2017
                Date revision received : 08 December 2017
                Date accepted : 08 January 2018
                Page count
                Figures: 3, Tables: 0, Pages: 14, Words: 11515
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id jnr24220
                cover-date July 2018
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.1.1 mode:remove_FC converted:14.06.2018

                ScienceOpen disciplines: Neurosciences
                Keywords: melatonin,ischemia,alzheimer,parkinson
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: melatonin, ischemia, alzheimer, parkinson

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