Alzheimer’s disease (AD) is a rapidly growing public health concern causing severe challenges to the health care system. Affecting the lives of more than 5 million Americans, it is characterized by brain-related morphological changes coupled with decrements in performance on tasks involving cognitive function such as those assessing memory and problem-solving abilities. Fortunately, current scientific research provides evidence that this trend towards rapid cognitive decline in older adults is not immutable, but rather can be attenuated through a simple adjustment to regular engagement in aerobic exercise.
To date, numerous studies have associated regular cardiovascular exercise to changes in brain function and structure. In particular, aerobic exercise has been shown to have a direct effect on the hippocampus (HC), one of the earliest regions of the brain to be affected in AD, which plays an important role in learning and memory. Scientific research on animal models has demonstrated increased adult hippocampal neurogenesis (AHN), or the birth of new neurons, in the dentate gyrus (DG) subregion of the hippocampus as a response to increases in aerobic exercise. Such findings have led to the hypothesis that aerobic exercise can improve cognitive performance, more specifically hippocampal-dependent learning and memory, through the formation of new hippocampal neurons.
Similarly, in human studies, previous research has shown that significant improvements in cardiovascular fitness are positively correlated with increased hippocampal volume. Structural increases in hippocampal volume are thought to be mediated by increased angiogenesis, or the generation of new blood vessels, which in turn are correlated with significant improvements in spatial memory, a task determined by memory function.
The benefits of aerobic exercise, nonetheless, are not limited to the hippocampus. As people age, atrophy of the brain is also inclusive of the prefrontal cortex, a region implicated in planning and decision making. Scientific literature has shown, that similar to the hippocampus, increases in aerobic exercise, directly result to increases in grey matter volume in the prefrontal lobe and increases in white matter volume in the genu of the corpus callosum. Such structural changes in the prefrontal lobe are correlated with enhanced decision making on cognitive tasks, an essential component of executive function.
For the purposes of this study, an effective method of evaluating whether changes in brain structure due to higher cardiorespiratory fitness have an association with cognitive function was through the administration of the Digital Clock Drawing Test (dCDT). The dCDT is a recently developed cognitive test based on the traditional Clock Drawing Test (CDT) that uses a digital pen and allows for the measurement of several parameters such as “Ink time” and “Think time.” Recent scientific studies report that such parameters may have a potential enhanced sensitivity to detecting cognitive change as compared to the traditional CDT. Therefore, the dCDT has come forward as an advantageous approach for testing cognitive skills in aging individuals such as those assessing executive and motor function, and semantic memory, as it happens in real time.
DCDT parameters such as total time to complete the clock drawing, total ink time, total think time, total ink length, and clock size have been shown to differ significantly among subjects of varying degrees of cognitive impairment such as AD, mild cognitive impairment (MCI), and healthy, non-demented controls. Patients who were clinically diagnosed as cognitively impaired spent a greater amount of time thinking and drawing on both the command and copy clocks conditions as compared to healthy, non-demented individuals. Similarly, patients affected by greater cognitive impairments, such as AD, tended to draw smaller clocks in terms of height and width of the clock face that required less total ink length to complete the clock drawing, when compared to healthy controls and MCI participants. Findings showed that AD patients appeared to be working longer (greater time of completion) though producing less output (smaller clock and shorted ink length) as compared to non-impaired individuals. Variations of graphomotor latencies in the dCDT performance, therefore, are associated with individual’s cognitive capacities.
The goal of this study is to investigate the associations between cardiorespiratory fitness based on VO2 max testing and cognitive constructs such as memory, executive function, and gross motor processing speeds as measured by graphomotor latencies and drawing patterns using the dCDT in healthy, non-demented older adults. I hypothesize that greater cardiorespiratory fitness will be negatively associated with graphomotor timed latencies in various parameters of the dCDT, given that exercise has known effects on the brain regions responsible for executive function and memory.
To test these hypotheses, cardiorespiratory fitness and dCDT data from 12 sedentary older adults between the ages of 55 and 85 years from a larger study in the Brain Plasticity and Neuroimaging Laboratory at Boston University were collected and analyzed. A multiple regression analysis was used to predict the dCDT measures from individual’s cardiorespiratory fitness using estimated VO2 max levels.
Results showed that cardiorespiratory fitness in older adults is inversely associated with graphomotor times in both the command and copy test conditions as predicted by our hypothesis. In particular, greater cardiorespiratory fitness was associated with shorter total ink time for both clock drawing testing conditions. These results held when controlled for age, sex, and education; higher cardiorespiratory fit older adults performed better (a shorter time is needed to achieve the same outcome) on tasks requiring greater cognitive constructs such as memory, executive function, and motor processing speeds.
Therefore, it can be concluded that cardiorespiratory fitness may be a neurodegenerative protector in aging adults supporting its beneficial role as a therapeutic agent for cognitive decline in older adults.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/31218 |
| Date | 11 July 2018 |
| Creators | De Siqueira, Nicolle |
| Contributors | Schon, Karin, Au, Rhoda |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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