PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation

Excess of Aβ42 peptide is considered a hallmark of the disease. Here we express the human Aβ42 peptide to assay the neuroprotective effects of PI3K in adult . The neuronal expression of the human peptide elicits progressive toxicity in the adult fly. The pathological traits include reduced axonal tr...

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Veröffentlicht in:	Molecular biology of the cell 2020-02, Vol.31 (4), p.244-260
Hauptverfasser:	Arnés, Mercedes, Romero, Ninovska, Casas-Tintó, Sergio, Acebes, Ángel, Ferrús, Alberto
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - chemically induced Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - chemistry Amyloid beta-Peptides - pharmacology Animals Animals, Genetically Modified Axonal Transport - drug effects Brain - drug effects Brain - metabolism Brain - pathology Carrier Proteins - genetics Carrier Proteins - metabolism Cell Line, Tumor Disease Models, Animal Drosophila melanogaster - genetics Drosophila melanogaster - metabolism Drosophila Proteins - genetics Drosophila Proteins - metabolism Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Longevity - drug effects Neurons - drug effects Neurons - metabolism Neurons - pathology Olfactory Perception - drug effects Peptide Fragments - chemistry Peptide Fragments - pharmacology Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Plaque, Amyloid - chemically induced Plaque, Amyloid - genetics Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Protein Aggregates R-SNARE Proteins - genetics R-SNARE Proteins - metabolism Synapses - drug effects Synapses - metabolism
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