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Recent insights into the molecular mechanisms that regulate spine morphogenesis offer potential ways to manipulate dendritic spines in vivo and to explore their physiological roles in the brain

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Taken together, these findings suggest thatcontrary to initial assumptionscomplex II may contribute to ferroptosis not by protecting cells via ubiquinol (CoQ 10 H 2 ) production but by promoting mitochondrial ROS accumulation

Furthermore, A is able to promote the hyperphosphorlyation of Tau in both the cytosolic and synaptic compartments, which has been suggested as a potential explanation of the prion-like seeding hypothesis of Tau transmission inter-neuronally, accounting for the phosphorylated Tau detected in the CSF of AD patients (Wu et al., 2018