TY  - JOUR
A1  - Lepeta, Katarzyna
A1  - Lourenco, Mychael V.
A1  - Schweitzer, Barbara C.
A1  - Martino Adami, Pamela V.
A1  - Banerjee, Priyanjalee
A1  - Catuara-Solarz, Silvina
A1  - de la Fuente Revenga, Mario
A1  - Marc Guillem, Alain
A1  - Haider, Mouna
A1  - Ijomone, Omamuyovwi M.
A1  - Nadorp, Bettina
A1  - Qi, Lin
A1  - Perera, Nirma D.
A1  - Refsgaard, Louise K.
A1  - Reid, Kimberley M.
A1  - Sabbar, Mariam
A1  - Sahoo, Arghyadip
A1  - Schaefer, Natascha
A1  - Sheean, Rebecca K.
A1  - Suska, Anna
A1  - Verma, Rajkumar
A1  - Vicidomini, Cinzia
A1  - Wright, Dean
A1  - Zhang, Xing-Ding
A1  - Seidenbecher, Constanze
T1  - Synaptopathies: synaptic dysfunction in neurological disorders - a review from students to students
JF  - Journal of Neurochemistry
N2  - 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 .
KW  - Amyloid-beta oligomers;
KW  - Central nervous system
KW  - P75 Neurotrophin receptor
KW  - Cellular prion protein
KW  - Temporal-lobe epilepsy
KW  - Familial Alzheimers-disease
KW  - Inhibitory glycine receptor
KW  - Autism spectrum disorders
KW  - Alpha-synuclein oligomers
KW  - Dentate granule cells
KW  - Alzheimer disease
KW  - autism
KW  - Down syndrome
KW  - epilepsy
KW  - hyperekplexia
KW  - synapses
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-187509
VL  - 138
IS  - 6
ER  -