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      Synaptopathies: synaptic dysfunction in neurological disorders – A review from students to students

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          Abstract

          Abstract

          Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. Thus, optimal synaptic communication is required for proper brain physiology, and slight perturbations of synapse function can lead to brain disorders. In fact, increasing evidence has demonstrated the relevance of synapse dysfunction as a major determinant of many neurological diseases. This notion has led to the concept of synaptopathies as brain diseases with synapse defects as shared pathogenic features. In this review, which was initiated at the 13th International Society for Neurochemistry Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental disorders (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer and Parkinson disease). We finally discuss the appropriateness and potential implications of gathering synapse diseases under a single term. Understanding common causes and intrinsic differences in disease‐associated synaptic dysfunction could offer novel clues toward synapse‐based therapeutic intervention for neurological and neuropsychiatric disorders.

          In this Review, which was initiated at the 13th International Society for Neurochemistry ( ISN) Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer's and Parkinson's diseases), gathered together under the term of synaptopathies.

          Read the Editorial Highlight for this article on page 783.

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

          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.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Alpha-synuclein in Lewy bodies.

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

              Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families.

              The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). Risk for AD increased from 20% to 90% and mean age at onset decreased from 84 to 68 years with increasing number of APOE-epsilon 4 alleles in 42 families with late onset AD. Thus APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.
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                Author and article information

                Contributors
                seidenc@lin-magdeburg.de
                Journal
                J Neurochem
                J. Neurochem
                10.1111/(ISSN)1471-4159
                JNC
                Journal of Neurochemistry
                John Wiley and Sons Inc. (Hoboken )
                0022-3042
                1471-4159
                08 September 2016
                September 2016
                : 138
                : 6 ( doiID: 10.1111/jnc.2016.138.issue-6 )
                : 785-805
                Affiliations
                [ 1 ] Department of Molecular and Cellular NeurobiologyNencki Institute of Experimental Biology Polish Academy of Sciences WarsawPoland
                [ 2 ]Institute of Medical Biochemistry Leopoldo de Meis Federal University of Rio de Janeiro Rio de JaneiroBrazil
                [ 3 ] Department for Neurochemistry and Molecular BiologyLeibniz Institute for Neurobiology Magdeburg MagdeburgGermany
                [ 4 ]Laboratory of Amyloidosis and Neurodegeneration Fundación Instituto Leloir‐IIBBA‐CONICET Buenos AiresArgentina
                [ 5 ] Department of BiochemistryInstitute of Post Graduate Medical Education & Research Kolkata West BengalIndia
                [ 6 ]Systems Biology Program Cellular and Systems Neurobiology Centre for Genomic Regulation The Barcelona Institute of Science and Technology BarcelonaSpain
                [ 7 ]Universitat Pompeu Fabra BarcelonaSpain
                [ 8 ] Department of Physiology and BiophysicsVirginia Commonwealth University Richmond VAUnited States of America
                [ 9 ]Laboratorio de Neurotoxicología Departamento de ToxicologíaCentro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional México D.F. 07000Mexico
                [ 10 ]Florey Institute of Neuroscience and Mental Health University of Melbourne VictoriaAustralia
                [ 11 ] Department of Human AnatomyCross River University of Technology Okuku Campus Cross RiverNigeria
                [ 12 ] The Department of Biological ChemistryThe Edmond and Lily Safra Center for Brain Sciences The Alexander Grass Center for Bioengineering The Hebrew University of Jerusalem Israel
                [ 13 ] Laboratory of Molecular Neuro‐OncologyTexas Children's Hospital Baylor College of Medicine Houston TXUnited States of America
                [ 14 ] Department of Drug Design and PharmacologyFaculty of Health and Medical Sciences University of CopenhagenDenmark
                [ 15 ] Department of PharmacologyUCL School of Pharmacy 29‐39 Brunswick Square London WC1N 1AXUK
                [ 16 ]Brain Function Research Group School of Physiology Faculty of Health Sciences University of the Witwatersrand JohannesburgSouth Africa
                [ 17 ] Department of BiochemistryMidnapore Medical College West Bengal University of Health Sciences West BengalIndia
                [ 18 ]Institute for Clinical Neurobiology Julius‐Maximilians‐University of Wuerzburg WuerzburgGermany
                [ 19 ]Department of Neurosciences Uconn Health Center Farmington CTUnited States of America
                [ 20 ]CNR Institute of Neuroscience MilanItaly
                [ 21 ] Department of Lymphoma/MyelomaThe University of Texas MD Anderson Cancer Center Houston TXUnited States of America
                [ 22 ]Center for Behavioral Brain Sciences (CBBS) Magdeburg MagdeburgGermany
                Author notes
                [*] [* ]Address correspondence and reprint requests to Constanze Seidenbecher, Department for Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology Magdeburg, Magdeburg, Germany. E‐mail: seidenc@ 123456lin-magdeburg.de
                [†]

                These authors contributed equally to this work.

                Article
                JNC13713
                10.1111/jnc.13713
                5095804
                27333343
                cfefb9e3-e34b-4b9f-8826-1229dc3a6116
                © 2016 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 29 April 2016
                : 03 June 2016
                : 06 June 2016
                Page count
                Figures: 2, Tables: 0, Pages: 21, Words: 19025
                Funding
                Funded by: International Society for Neurochemistry (ISN)
                Categories
                Review
                Highlighted Article
                Review
                Custom metadata
                2.0
                jnc13713
                September 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.6 mode:remove_FC converted:04.11.2016

                Neurosciences
                alzheimer disease,autism,down syndrome,epilepsy,hyperekplexia,synapses
                Neurosciences
                alzheimer disease, autism, down syndrome, epilepsy, hyperekplexia, synapses

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