Fig. 6From: Amyloid-β accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolismAβ exposure affects OXPHOS in astrocytes, but the ATP levels remain unchanged. Seahorse OCR analysis was performed in astrocyte cultures exposed to Aβ and untreated controls at three different time points; 7d, 7d + 6d, and 7d + 12d (A–C). Maximal respiration and spare respiratory (SRC) capacity were significantly decreased in Aβ-exposed astrocytes compared to controls at 7d + 12d (D, E). ATP levels remained unchanged both when analyzed with Seahorse OCR (F) and ATP assay (G). WB analysis showed a clear decrease in COX IV expression in Aβ-exposed astrocytes, both at 7 and at 7 + 6 d (H), suggesting a reduced activity of the electron transport chain in these cultures. Since VDAC-1 levels were stable between controls and Aβ-exposed cultures (I), the COX IV decrease was not a result of reduced number of mitochondria. Immunostainings for COX IV (red) and VDAC-1 (green) in control astrocytes did not reveal a complete overlap of the mitochondrial markers, indicating that there is a mitochondria population in the astrocytes that is COX IV negative (J). Scale bar: A = 20 µmBack to article page