Abelson Kinases Mediate the Depression of Spontaneous Synaptic Activity Induced by Amyloid Beta 1–42 Peptides

Amyloid beta (Aβ) peptides represent one of the most studied etiological factors of Alzheimer’s disease. Nevertheless, the effects elicited by different molecular forms of amyloid beta peptides widely vary between the studies, mostly depending on experimental conditions. Despite the enormous amount...

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Veröffentlicht in:	Cellular and molecular neurobiology 2021-04, Vol.41 (3), p.431-448
Hauptverfasser:	Reichenstein, M., Borovok, N., Sheinin, A., Brider, T., Michaelevski, I.
Format:	Artikel
Sprache:	eng
Schlagworte:	Actin Alzheimer's disease Amino acids Amyloid beta-Peptides - toxicity Animals Biochemical analysis Biomedical and Life Sciences Biomedicine Cell activation Cell Biology Central nervous system Cytoskeleton Enzyme Activation - drug effects Excitatory postsynaptic potentials Excitatory Postsynaptic Potentials - drug effects Hippocampus Hydantoins - pharmacology Imatinib Mesylate - pharmacology Kinases Neurobiology Neurodegenerative diseases Neurosciences Neurotoxicity Neurotransmitter Agents - metabolism Original Research Peptide Fragments - toxicity Peptides Phosphorylation Protein Kinase Inhibitors - pharmacology Protein-tyrosine kinase receptors Proto-Oncogene Proteins c-abl - antagonists & inhibitors Proto-Oncogene Proteins c-abl - metabolism Pyrimidines - pharmacology Rats Rats, Sprague-Dawley RNA, Small Interfering - metabolism Synapses - drug effects Synapses - metabolism Synaptic transmission Synaptic Transmission - drug effects Tau protein
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