Chemotherapy-induced cognitive impairments: White matter pathologies

•The relationship between chemotherapy, white matter pathologies and cognitive decline is discussed.•Chemotherapy causes myelin pallor, edema, gliosis, swollen axons, necrosis and leukoencephalopathy.•Chemotherapy induced white matter damage is associated with low IQ scores and poor attention.•Degen...

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Bibliographic Details
Published inCancer treatment reviews Vol. 61; pp. 6 - 14
Main Authors Matsos, A., Loomes, M., Zhou, I., Macmillan, E., Sabel, I., Rotziokos, E., Beckwith, W., Johnston, I.N.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 01.12.2017
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Summary:•The relationship between chemotherapy, white matter pathologies and cognitive decline is discussed.•Chemotherapy causes myelin pallor, edema, gliosis, swollen axons, necrosis and leukoencephalopathy.•Chemotherapy induced white matter damage is associated with low IQ scores and poor attention.•Degeneration of oligodendrocyte precursor cells, demyelination and inflammation may cause chemobrain.•Treatments include anti-inflammatory drugs, exercise intervention, antidepressants and lithium. Whilst chemotherapeutic agents show promising results in the amelioration of cancerous tumors, patients often experience cognitive disturbances associated with chemotherapy long after treatment has ceased. Research has suggested that the structural integrity of white matter fibres in the brain are susceptible to the harmful effects of chemotherapy. Post-chemotherapy, white matter tracts often display altered morphology with a reduction in glial cells such as oligodendrocytes. Demyelination, gliosis and leukoencephalopathy during or post chemotherapy is associated with changes in processing speed and IQ. Thus, understanding the relationship between chemotherapy, white matter damage and cognition is warranted. This review presents evidence for chemotherapy induced white matter damage highlighting the importance of implementing behavioral and pharmological strategies to prevent or reverse such acute toxicity in the brain.
ISSN:0305-7372
1532-1967
DOI:10.1016/j.ctrv.2017.09.010