Pharmacological Neurorescue in a Paclitaxel-Induced Chemobrain Model

Conversely, these behavioral deficits were rescued with lithium pretreatment, suggesting that lithium administration following paclitaxel exposure can exert a protective effect against chemobrain-associated memory impairment. [...]upon performing Golgi–Cox staining of the brain hemispheres and subsequent Sholl analysis of the dentate gyrus granule cells, the results were found to be similar to the findings in the previous behavioral experiments of the paclitaxel-induced, short-term, and memory impairment model. Furthermore, this study proved a valuable finding that the neuron complexity tended to be stable after an initial burst of cognitive disorder in the progression of chemobrain. [...]lithium rescue of cognitive function in the paclitaxel-exposed model was mainly accomplished via hippocampal neuron complexity enhancement (Pease-Raissi et al., 2017). Another limitation to this study was that the researchers did not detect other cytokines that can mediate PKCα in the paclitaxel-induced chemobrain model, such as growth factors and transcription factors. [...]in the future studies, additional chemobrain-associated biomarkers at various time points should be evaluated to provide further evidence to illuminate the role of InsP3R calcium pathway responses in the pathophysiology of chemobrain. [...]a comprehensive targeting of multiple factors should be considered in the context of diseases in further studies, as this would be the most effective in the long-term restoration of paclitaxel-induced cognitive impairment.