Imbalance in the response of pre- and post-synaptic components to amyloidopathy

Alzheimer’s disease (AD)-associated synaptic dysfunction drives the progression of pathology from its earliest stages. Amyloid β (Aβ) species, both soluble and in plaque deposits, have been causally related to the progressive, structural and functional impairments observed in AD. It is, however, sti...

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Veröffentlicht in:	Scientific reports 2019-10, Vol.9 (1), p.14837-11, Article 14837
Hauptverfasser:	Stephen, Terri-Leigh, Tamagnini, Francesco, Piegsa, Judith, Sung, Katherine, Harvey, Joshua, Oliver-Evans, Alice, Murray, Tracey K., Ahmed, Zeshan, Hutton, Michael L., Randall, Andrew, O’Neill, Michael J., Jackson, Johanna S.
Format:	Artikel
Sprache:	eng
Schlagworte:	13/51 14/34 14/69 631/378/1689/1283 631/378/2597/2600 64/60 Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - metabolism Animals Disease Models, Animal Disease Progression Female Humanities and Social Sciences Humans Mice Mice, Transgenic multidisciplinary Mutation Pathology Plaque, Amyloid - pathology Post-Synaptic Density - pathology Presynaptic Terminals - pathology Science Science (multidisciplinary) Senile plaques Structure-function relationships Synapses Synaptic density
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