Accumulation of APP C-terminal fragments causes endolysosomal dysfunction through the dysregulation of late endosome to lysosome-ER contact sites

Neuronal endosomal and lysosomal abnormalities are among the early changes observed in Alzheimer’s disease (AD) before plaques appear. However, it is unclear whether distinct endolysosomal defects are temporally organized and how altered γ-secretase function or amyloid precursor protein (APP) metabo...

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Veröffentlicht in:	Developmental cell 2024-06, Vol.59 (12), p.1571-1592.e9
Hauptverfasser:	Bretou, Marine, Sannerud, Ragna, Escamilla-Ayala, Abril, Leroy, Tom, Vrancx, Céline, Van Acker, Zoë P., Perdok, Anika, Vermeire, Wendy, Vorsters, Inge, Van Keymolen, Sophie, Maxson, Michelle, Pavie, Benjamin, Wierda, Keimpe, Eskelinen, Eeva-Liisa, Annaert, Wim
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Protein Precursor - metabolism Amyloid Precursor Protein Secretases - metabolism Animals APP proteolysis APP-CTF Calcium - metabolism Cholesterol - metabolism endolysosomal homeostasis Endoplasmic Reticulum - metabolism Endosomes - metabolism Fibroblasts - metabolism Hippocampus - metabolism Hippocampus - pathology Humans late endosome/lysosome-endoplasmic reticulum contact sites lysosomal Ca2 Lysosomes - metabolism Mice Neurons - metabolism presenilins primary hippocampal neurons Proteolysis Signal Transduction γ-secretase γ-secretase inhibitor
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