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Acknowledgements This work was financially supported by the NSFC (T2422030 (WL), 82172081 (J.Q.) and 32471462 (J.Q.)), CAMS Initiative for Innovative Medicine (2021-I2M-1-043 (W.L.)), the Science and Technology Program of Tianjin, China (22JCYBJC01000 (W.L.) and 22JCQNJC01640 (J.Q.)), and the Fundamental Research Funds for the Central Universities (2021-RC350-006 (W.L.))

It has been observed that the apoptotic process in paclitaxel induced-painful neuropathy is due to the permeability transition pore opening, with the consequent cytochrome c release and Ca 2+ homeostasis dysregulation (Areti et al., in vivo could also reverse or attenuate the above-mentioned symptoms, but with deleterious effects on motor coordination in the case of complex I inhibition at 3 and 24 h after paclitaxel administration

Although current antipsychotic therapies can alleviate certain manifestations of the disease, particularly those associated with dopaminergic hyperactivity, they often provide limited benefit for negative and cognitive symptoms and do not correct the underlying biological heterogeneity of schizophrenia

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