Synaptopathies: synaptic dysfunction in neurological disorders - a review from students to students
Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-187509
- 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 ofSynapses 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 .…
Autor(en): | Katarzyna Lepeta, Mychael V. Lourenco, Barbara C. Schweitzer, Pamela V. Martino Adami, Priyanjalee Banerjee, Silvina Catuara-Solarz, Mario de la Fuente Revenga, Alain Marc Guillem, Mouna Haider, Omamuyovwi M. Ijomone, Bettina Nadorp, Lin Qi, Nirma D. Perera, Louise K. Refsgaard, Kimberley M. Reid, Mariam Sabbar, Arghyadip Sahoo, Natascha Schaefer, Rebecca K. Sheean, Anna Suska, Rajkumar Verma, Cinzia Vicidomini, Dean Wright, Xing-Ding Zhang, Constanze Seidenbecher |
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URN: | urn:nbn:de:bvb:20-opus-187509 |
Dokumentart: | Artikel / Aufsatz in einer Zeitschrift |
Institute der Universität: | Medizinische Fakultät / Institut für Klinische Neurobiologie |
Sprache der Veröffentlichung: | Englisch |
Titel des übergeordneten Werkes / der Zeitschrift (Englisch): | Journal of Neurochemistry |
Erscheinungsjahr: | 2016 |
Band / Jahrgang: | 138 |
Heft / Ausgabe: | 6 |
Seitenangabe: | 785-805 |
Originalveröffentlichung / Quelle: | Journal of Neurochemistry (2016) 138:6, 785-805. https://doi.org/10.1111/jnc.13713 |
DOI: | https://doi.org/10.1111/jnc.13713 |
Allgemeine fachliche Zuordnung (DDC-Klassifikation): | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Freie Schlagwort(e): | Alpha-synuclein oligomers; Alzheimer disease; Amyloid-beta oligomers;; Autism spectrum disorders; Cellular prion protein; Central nervous system; Dentate granule cells; Down syndrome; Familial Alzheimers-disease; Inhibitory glycine receptor; P75 Neurotrophin receptor; Temporal-lobe epilepsy; autism; epilepsy; hyperekplexia; synapses |
Datum der Freischaltung: | 16.06.2020 |
Lizenz (Deutsch): | CC BY-NC-ND: Creative-Commons-Lizenz: Namensnennung, Nicht kommerziell, Keine Bearbeitungen 4.0 International |