Skip to main content
Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Amyloid-β accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolism

Fig. 6

Aβ 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 (AC). 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 µm

Back to article page