Pharmacological rescue of cognitive function in a mouse model of chemobrain
After chemotherapy, many cancer survivors suffer from long-lasting cognitive impairment, colloquially known as “chemobrain.” However, the trajectories of cognitive changes and the underlying mechanisms remain unclear. We previously established paclitaxel-induced inositol trisphosphate receptor (InsP...
Gespeichert in:
| Hauptverfasser: | , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
26 June 2021
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| In: |
Molecular neurodegeneration
Year: 2021, Jahrgang: 16, Pages: 1-16 |
| ISSN: | 1750-1326 |
| DOI: | 10.1186/s13024-021-00463-2 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1186/s13024-021-00463-2
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| Verfasserangaben: | Lien D. Nguyen, Tom T. Fischer and Barbara E. Ehrlich |
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| 520 | |a After chemotherapy, many cancer survivors suffer from long-lasting cognitive impairment, colloquially known as “chemobrain.” However, the trajectories of cognitive changes and the underlying mechanisms remain unclear. We previously established paclitaxel-induced inositol trisphosphate receptor (InsP3R)-dependent calcium oscillations as a mechanism for peripheral neuropathy, which was prevented by lithium pretreatment. Here, we investigated if a similar mechanism also underlay paclitaxel-induced chemobrain. | ||
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