In the journal Cancer Investigation researchers from the University of Rochester Medical Center (URMC) have published a study that hints at one possible source of the phenomenon known as chemobrain, as well as a possible means of at least partially reversing it.
Researchers began with the premise that chemotherapy drugs had some negative effect on the regeneration of brain cells in the hippocampus, the area of the brain involved in memory. Further hypothesizing that the blood-brain barrier played a role, they chose two common chemotherapy drugs that were known to cross that barrier—cyclophosphamide and fluorouracil—and two that were not—paclitaxel and doxorubicin.
Results in mice showed that each of the drugs caused a fairly significant reduction in brain cell regeneration, ranging from the low end (a 15.4% reduction from fluorouracil) to the high end (a 36% reduction from paclitaxel), suggesting that the role of the blood-brain barrier may be immaterial.
Researchers also administered the experimental growth hormone IGF-1 to mice prior to and following cyclophosphamide, both in a multiple-dose regimen and as one single high dose, since IGF-1 has shown to be successful in developing new brain cells. Results suggest that the IGF-1 was indeed successful in increasing new brain cells, but that it was less successful against the multiple-dose regimen than it was against the single high-dose.
As one might expect, these results warrant more research, especially in human models.
Chemobrain is the phenomenon in which cancer survivors who have undergone chemotherapy claim, following treatment, of a loss of some measure of cognitive function. No hard data exists on the source, mode, or effects of chemotherapy on cognitive ability, and the actual number of sufferers is believed to range between 20-80% of chemo survivors.
To read more about the URMC study, click here.
To read more about chemobrain, click here.
By Ross Bonander
