Mini-review: Aplastic myelin following chemotherapy

Solomiia Savchuk; Michelle Monje

doi:10.1016/j.neulet.2022.136861

Mini-review: Aplastic myelin following chemotherapy

Neurosci Lett. 2022 Nov 1:790:136861. doi: 10.1016/j.neulet.2022.136861. Epub 2022 Aug 30.

Authors

Solomiia Savchuk¹, Michelle Monje²

Affiliations

¹ Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA.
² Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA; Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305, USA; Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA; Department of Pathology, Stanford University, Stanford, CA 94305, USA; Department of Pediatrics, Stanford University, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA. Electronic address: mmonje@stanford.edu.

PMID: 36055447
DOI: 10.1016/j.neulet.2022.136861

Abstract

The contribution of chemotherapy to improved outcomes for cancer patients is unquestionable. Yet as its applications broaden, so do the concerns for the long-term implications of chemotherapy on the health of cancer survivors, with chemotherapy-related cognitive impairment as a cause for particular urgency. In this mini review, we explore myelin aplasticity following chemotherapy, discussing the role of myelin plasticity in healthy cognition and failure of myelin plasticity chiefly due microenvironmental aberrations in chemotherapy-related cognitive impairment. Possible therapeutic strategies to mitigate chemotherapy-induced myelin dysfunction are also discussed.

Keywords: Adaptive myelination; CRCI; Cancer neuroscience; Chemotherapy; Myelin; OPC; Oligodendrocyte; White matter.

Publication types

Review
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural

MeSH terms

Antineoplastic Agents* / adverse effects
Cancer Survivors* / psychology
Chemotherapy-Related Cognitive Impairment*
Cognitive Dysfunction* / etiology
Humans
Myelin Sheath
Oligodendroglia

Substances

Antineoplastic Agents