Abstract
Mild Cognitive Impairment (MCI) is a clinical disorder characterized as an intermediate stage of cognitive impairment between normal cognitive aging and more advanced cognitive impairment associated with dementia. MCI causes measurable decline in cognitive abilities including memory and reasoning. Occurrence of MCI has been linked to altered physiological functions, co‐morbid conditions, and adverse events related to therapeutic drugs or toxins. MCI is commonly diagnosed by a physician's clinical judgement based on the following parameters: complete medical history, assessment of independent function and daily activities, input from family members, assessment of mental status (i.e. Mini Mental Status Exam), neurological examinations, and laboratory tests including blood tests and imaging of the brain's structure. The testing required is extensive and often subjective in nature. Currently, there are few biochemical markers thought to correlate with the onset of early‐stage MCI and those that do exist require expensive or invasive techniques to measure accurately. Therefore, using valid animal models representative of cognitive impairment, this study aims to determine the validity of using hematological markers as predictors of early‐stage MCI development.
In this study, we measured the hematological markers in animal models of cognitive impairment compared to their respective control group. Cognitive impairment was observed in a chemotherapeutic (CT) rodent group dosed with doxorubicin (2 mg/kg, IP) and cyclophosphamide (50 mg/kg, IP) once weekly for 4 weeks. Cognitive impairment was also observed in a hyperglycemia rodent group dosed with Streptozotocin (STZ) 55 mg/kg, once, IP. Blood samples were withdrawn, and hematological markers analyzed. There was a significant increase in creatine kinase and lactate dehydrogenase (LDH) in the CT model versus control. Glucose levels were significantly increased in the STZ model versus control. With regard to BUN, there was a significant increase in the STZ model compared to their control group, however there was a decrease in the CT model compared to their control group. Interestingly, triglycerides were significantly elevated in both the STZ and CT treated animal models. Previous studies with human subjects have shown a potential link between the increase in triglyceride levels influencing cognitive impairment. Likewise, our data indicates a possible correlation with an increase in triglycerides to cognitive impairment in animal models. This suggests elevated levels of triglycerides may prove to be a potential, minimally invasive, hematological marker for the increased risk of cognitive deficit in these animal models. However, further studies are necessary to determine the causal relationship between elevated triglyceride levels and early‐stage MCI.
This is from the Experimental Biology 2018 Meeting. There is no full text article associated with this published in The FASEB Journal.