Breast cancer continues to be the number one cause of cancer in women over age 50, with a median age at diagnosis of 61 years. (ACS, 2013). Treatment advances have led to a significant increase in the number of breast cancer survivors; survival rates now range from 88% at 5 years to 78% after 15 years post diagnosis (ACS, 2013). A significant number of these women, 35% of early stage breast cancer (Stages I/II) and 61% of later stage breast cancer patients (Stages III/IV), receive chemotherapy (The National Cancer Database, 2008).
Cognitive disturbances, often referred to as “chemobrain” are common among breast cancer survivors. Where most experience cognitive disturbances during treatment, many improve upon treatment termination, up to a fourth may experience persistent cognitive decline 1-year post treatment. Many describe these issues as related to declines in memory.
In older patients, the likelihood of cognitive disturbances are even greater (Ahles, 2010) because they often have lower cerebral blood flow, and have additional comorbidities, including undetected neurodegenerative diseases.
The purposes of this descriptive exploratory study are twofold: (1) examine how factors, both biological and functional, relate to cognitive function, in older breast cancer survivors who report persistent cognitive impairment, 12-36 months after completing their chemotherapy regimen and (2) characterize and compare the genetic and phenotypical profiles of breast cancer survivors to the profiles found in a neurologist verified sample of older adults diagnosed with mild cognitive impairment (MCI), pre MCI, and no MCI.
Twenty older breast cancer survivors (10 with and 10 without measurable impairment, age 50 years and older) will complete a 4 day journal and complete questionnaires describing the impact of their treatment regimen on their ability to think and the strategies they use to adapt to their perceived deficits. Afterwards, they will come to the Neurocognitive Assessment Laboratory and undergo a comprehensive neurocognitive battery, including behavioral and electroencephalographic measures of memory functions, sleep, and cerebral oxygenation. Blood draws for inflammation, oxidative stress and neuroprotective factors (neuroglobin, antioxidant activity and brain derived neurotrophic factors) and genetic polymorphism (APOE, neuroglobin) will also be measured in order to compare these variables to equivalent data collected from adults without cancer.
Data will be analyzed using thematic content analysis for the journals, schematic plots and t-tests for the measures of proinflammatory risk, neuroprotective factors and memory consolidation. Cross tabulation and chi-square will be used to compare genetic risk between samples. Each marker will be analyzed in a two-way ANOVA, sample by cognitive status, where the interaction will be used to test the differential relationship of the marker and cognitive status by cancer status
Results will be used to develop a larger, prospective study aimed at refining the recognition of women at greater risk for persistent cognitive decline and factors to ameliorate that risk. In addition to this, information gained from this study will facilitate the development of interventions to help women cope, adapt and even improve their cognitive functioning while on treatment.
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