Fig. 5From: Interleukin-1β mediates alterations in mitochondrial fusion/fission proteins and memory impairment induced by amyloid-β oligomersSchematic representation of the effects of AβOs inducing synapse loss, memory impairment, and abnormal mitochondrial dysfunction via IL-1β signaling. AβOs lead to increase brain levels of IL-1β, leading to perturbations in mitochondrial proteins, including an increase of Drp1 levels and decrease of MFN-1, MFN-2, and OPA-1, causing synapse loss and memory impairment. Anakinra, an IL-1 antagonist, decreases IL-1β expression leading to restoration of normal levels of mitochondrial proteins. Mdivi-1, a fission inhibitor, inhibits Drp1 increased, as well reduced IL-1β expression, suggesting a negative feedback loop between mitochondrial dynamics proteins and IL-1β activityBack to article page