Chemotherapy Might Cause Chemo Brain By Disrupting The Formation Of Brain Nerve Cells - Food for Breast Cancer

I'm always interested in understanding the obvious effects chemotherapy has had on my memory and the way my brain works ... or doesn't work. The situation really has improved but, especially if I'm tired or just generally fatigued/overwhelmed, I struggle. I've also learned to not expect to remember all kinds of things - it doesn't freak me out like it once did. And I've learned ways of adjusting so that, in addition to general improvements, I cope better.

Chemotherapy Might Cause Chemo Brain By Disrupting The Formation Of Brain Nerve Cells - Food for Breast Cancer

A new study presented at the 2011 Era of Hope breast cancer conference has reported that chemotherapy might produce cognitive impairment ("chemobrain”) by disrupting the formation of new nerve cells (neurogenesis) in the brain. Cognitive impairment occurring after chemotherapy has symptoms such as frequent memory lapses, trouble focusing and multitasking, problems recalling details, and difficulty remembering common words or names. While it is clear that certain chemotherapy drugs can produce cognitive deficits, the mechanism is unknown.

Neurogenesis occurs throughout adulthood and is controlled by cell cycle regulators. The hippocampus, a brain region important to memory and learning, is a primary site of neurogenesis. Because some chemotherapy drugs act by inhibiting cell cycle progression, the authors hypothesized that such drugs may produce cognitive impairment by disrupting neurogenesis in the hippocampus.


The CMF chemotherapy combination is used in the treatment of various types of cancer, and the drugs have been shown to interfere with DNA synthesis and cellular replication. To conduct the study, seven week-old female C57/BL6 mice were given intraperitoneal injections once a week for three weeks with either saline (control group) or one of the following drugs: methotrexate (3, 10, or 30 mg/kg); cyclophosphamide (10, 30, or 100 mg/kg); or 5-fluorouracil (10, 30, or 100 mg/kg). One week following the last injection, the mice were divided into groups and used either for behavioral testing or for brain tissue analysis.


Methotrexate was found to decrease neurogenesis in the hippocampus. Mice treated with methotrexate were found to have significant deficits in the performance of two tests of spatial memory which are thought to reflect hippocampal-dependent processes. Treatment with 5-fluorouraci was found to produced nonspecific brain cell toxicity. On the other hand, cyclophosphamide, which does not readily cross the blood-brain-barrier, did not alter neurogenesis or cognitive function. The authors conclude that the study results support the hypothesis that some chemotherapeutic agents produce cognitive impairment by disrupting hippocampal neurogenesis. This finding sets the groundwork for future studies assessing whether drugs that stimulate neurogenesis can prevent or treat cognitive deficits in people who undergo cancer chemotherapy.


Comments regarding the study


Based on anecdotal evidence, it can take two years or more for chemo brain to wear off (the good news is that the brain does heal in the majority of cases and that chemo brain does not appear to set the stage for Alzheimer's disease). We are not aware of any studies specifically addressing how specific foods or food components can influence chemobrain. However, some foods have been found to be neuroprotective in other contexts and might help the brain heal more quickly. The following foods have known neuroprotective activities while at the same time being neutral or chemopreventive with respect to breast cancer:

Bananas

Chocolate, dark

Papayas

Spinach

Strawberries

Turmeric

Sage has been shown to improve memory retention in both Alzheimer's patients and college-age subjects, however long-term heavy use can cause seizures or other neurological symptoms due to sage's thujone content. The soy isoflavones genistein and daidzein, which are sold as supplements, have been shown to be toxic to neuronal cells at high concentrations.