Alzheimer's Research
Alzheimer’s disease is elusive. It is the most common form of dementia but scientists still work tirelessly to understand exactly what the disease is and how it causes the damage that it does; it is a chronic, progressive, terminal disease that deteriorates the brain causing loss of higher cognitive function (Australian Broadcasting Corporation, 2016, 02:50–03:00) (Martone & Piotrowski, 2019). So far, Alzheimer’s disease is understood to develop through the formation of toxic deposits containing beta-amyloid protein which attract another protein called tau. These proteins interact with each other in a way that causes fibrous masses to form inside of brain cells which take over the brain network and cause it to deteriorate. This deterioration of the brain network produces the visible symptoms of cognitive decline; typically starting with functions of the memory (Australian Broadcasting Corporation, 2016, 03:05–03:58). Alzheimer’s disease most commonly asserts itself in people between the ages of sixty and seventy years, but the formation of the fibrous masses as mentioned can begin twenty years before the onset of recognizable symptoms (Australian Broadcasting Corporation, 2016, 03:12–04:25).
The scientific communities’ next step in furthering their understanding of Alzheimer’s disease is identifying causes and prevention methods to inevitably discover a cure. Currently, there a few identified verified genetic factors that heighten a person’s risk for developing Alzheimer’s disease, however, these genetic predispositions are overcome by the 75% influence rate that environmental factors have on rates of risk and progression (Australian Broadcasting Corporation, 2016, 06:06–06:50). This fact implies that there are preventive measures one can take to decrease the likelihood that he or she will develop Alzheimer’s disease or at the very least slow its progression. In the documentary Alzheimer’s: Can We Prevent It? — Catalyst (2016) Australian Professor Cassandra Szoeke, American Neuroscientist Kirk Erickson, Australian Professor Ralph Martins Ao, Australian Researcher Sue Radd, Professor and Neuroscientist Suzanne De La Monte, Associate Professor Clare Anderson and sleep scientists at Melbourne University set out to answer the question of what environmental interventions can be made to prevent Alzheimer disease which, through reverse reasoning, will help me identify some of the likely predispositions of Alzheimer disease.
Professor Szoeke conducted an observational longevity study on four hundred women between the ages of forty-five and fifty-five years and observed them for twenty years. During the twenty-year observation period, Szoeke’ tracked participants physical status such as weight and BMI through standard means of measurement and psychological status using neuropsychiatric tests that are designed to measure psychomotor speed, choice reaction time, attention, recognition memory, working memory, long-term memory, and executive function (Australian Broadcasting Corporation, 2016, 07:00–09:40). The results of her study concluded that the most important factors for preventing Alzheimer’s disease are physical activity, “normal blood pressure and high levels of cholesterol” (Australian Broadcasting Corporation, 2016, 08:15–08:25). Szoeke’s findings are significantly back by quantitative data but her study does not fully meet scientific standards. To attain the scientific gold standard requirement, Szoeke would need to conduct randomized control trials and the results of those trials would need to support her current conclusions. Furthermore, her data is limited in that they only represent the female population and do not provide a clear explanation as to why these factors are the potential preventative measure for Alzheimer’s disease. Therefore, Szoeke’s study is useful as a foundation for future research but serves very little in addressing matters of disease causation or reason of prevention. Luckily, Dr. Kirk Erikson conducted a study that validated and elaborated on Szoeke’s findings.
In 2001 Erickson conducted a study to solidify physical activity as a prevention method for Alzheimer’s disease, distinguish what type of physical activity worked best and as a prevention method, and test the effect of different types of exercise on memory. To fully meet the scientific gold standard, Erikson used the randomized control trial method involving one hundred fifty inactive men and women. Each trial participant was assigned to one of two activity intensity groups. One group involved moderately intense physical activity such as walking or aerobics, and the other group was the control group assigned to doing light-intensity physical activity such as stretching. Over the course of one year, trial participants worked in their assigned groups three times each week and underwent thorough MRI scans to monitor changes in the hippocampus: the central unit involved in memory processes. Erickson found that the activity of the control group had no impact on hippocampal development as expected. On the contrary, the moderate-intensity activity group saw a 2% reversal of natural hippocampal degeneration; essentially canceled out the effects of natural aging equivalent to two years (Australian Broadcasting Corporation, 09:46–12:26). Erickson’s study meets the scientific gold standard and supports the theory of physical activity being a preventive measure for Alzheimer disease because physical activity has the potential to reverse brain deterioration specifically in the hippocampal region which is the brain structure that serves in functions of memory, learning, motivation, and emotion regulation; all of which are impacted negatively by the deterioration caused by Alzheimer disease.
With the solidification that Alzheimer’s disease can be prevented with moderate physical activity, scientists began looking into dietary impacts on cognition concerning Alzheimer’s disease prevention. The Australian Imaging and Biomarkers and Lifestyle (AIBL) Study is a commonly recognized study that does just that. The AIBL study consisted of five hundred participants and was conducted over the course of 8 years to investigate the cognitive change effects of a Western diet versus a Mediterranean diet by simply having half the participants maintain a Mediterranean diet and the other half maintain a Western diet while keeping a record of participants cognitive abilities. The findings of the AIBL study concluded that a Mediterranean diet decreases one’s risk for Alzheimer’s disease by increasing participants’ cognitive executive ability and a Western diet decreases visuospatial ability potentially placing them at a higher risk for Alzheimer disease progression (Australian Broadcasting Corporation, 2016, 14:05–15:00). These findings also suggest that omega-three, fish, and antioxidants (primary components of the Mediterranean diet) improve cognitive function and that refined sugars (a primary component of the Western Diet) inhibit brain function putting a person at higher risk for Alzheimer’s disease. The AIBL, like Soeke’s study, does not meet the scientific gold standard but it does provide useful information for furthering the research on the effects of diet on cognition. Information that researcher and dietician Sue Radd considers to be the next frontier of dietary research; a frontier that Professor De La Monte has started exploring, bringing the scientific and medical communities closer to understanding the causes of Alzheimer’s disease (Australian Broadcasting Corporation, 2016, 15:20–20:00).
Professor De La Monte has conducted multiple lab research scenarios that focus on the effects of refined sugar and how insulin affects the brain. For one of her lab experiments, De La Monte blocked the insulin receptors in the brains of a group of lab rats and left another group untampered with to serve as the control. Then rats were placed in a large bucket with water deep enough for the rats to not be able to stand in without the use of a platform that had also been placed in the bucket. The platform was slightly shorter than the level of the water in the bucket and the water was made cloudy so the rats could not see the platform, thus they would have to rely on memory to find it each time they were placed in the experiment environment (Australian Broadcasting Corporation, 2016, 20:00–21:00). Through this experimentation method, De La Mont found that the rats who had their insulin receptors inhibited moved slower than the control group, struggled to find and remember the location of the platform, and showed signs of significant disorientation. Furthermore, she found that the insulin inhibited “rats had developed amyloid-like plaques resembling the ones found in people with Alzheimer’s (Australian Broadcasting Corporation, 2016, 21:07–21:12).” Thus, concluding that the progression of Alzheimer’s disease and diminished hippocampal operation was a result of a lack of proper insulin processing in the brain. De La Monte’s findings “fortify” the hypothesis that Alzheimer’s disease is a brain-specific metabolic disease and supports the AIBL study’s implication that a diet low in refined sugars can improve executive function and prevent Alzheimer’s disease (Australian Broadcasting Corporation, 2016, 21:18–21:29).
With the establishment of physical activity and diet as environmental interventions that prevent and lower one’s risk of Alzheimer disease a group of sleep scientists, a Melbourne University began a study to identify the impacts of sleep as well as the combined effects of lifestyle interventions on cognitive function about Alzheimer disease prevention. To uphold the scientific gold standard this study is a randomized control trial. The trial involves the observation and measurement documentation of elder participants who are placed in an “enriched environment” consisting of adequate mental stimulus, social involvement, and a regulated physical need routine (Australian Broadcasting Corporation, 2016, 22:15–23:50). This study is currently ongoing therefore the results are not finalized but the expected outcome is confirmation that a healthy diet and exercise paired with adequate mental stimulus and healthy sleep patterns result in improved cognitive functioning (Australian Broadcasting Corporation, 2016, 24:54 -25:30). This ongoing trial is somewhat useless as the results have not yet been officiated however, this trial’s attention to multiple variables provides insight into the direction future research may be headed.
References
Alzheimer’s. Can we prevent it? — Catalyst. [electronic resource]: (2016). Australian Broadcasting Corporation. Retrieved from http://search.ebscohost.com.proxy.ccis.edu/login.aspx?direct=true&db=cat01798a&AN=slc.b2573915&scope=site
De La Monte, S. M. & Wands, J. R. (2008). Alzheimer’s disease is type 3 diabetes-evidence reviewed. Journal of diabetes science and technology, 2(6), 1101–1113. doi:10.1177/193229680800200619
Erickson, Kirk I., Voss, Michelle W., Prakash, Ruchika., Shaurya, Basak., Chandramallika., Szabo, Amanda., Chaddock, Laura., Kim, Jennifer S., Heo, Susie., Alves, Heloisa., White, Siobhan M., Wojcicki, Thomas R., Mailey, Emily., Vieira, Victoria J., Martin, Stephen A., Pence, Brandt D., Woods, Jeffrey A., McAuley, Edward., Kramer, Arthur F. (2011) Exercise training increases size of hippocampus and improves memory. National Academy of Science USA (108):3017–3022. doi10.1073/pnas.1015950108.
Loughrey, D. G., Lavecchia, S., Brennan, S., Lawlor, B. A., & Kelly, M. E. (2017). The Impact of the Mediterranean Diet on the Cognitive Functioning of Healthy Older Adults: A Systematic Review and Meta-Analysis. Advances in nutrition (Bethesda, Md.), 8(4), 571–586. doi:10.3945/an.117.015495
Martone, R. L., & Piotrowski, N. A., PhD. (2019). Alzheimer’s disease. Magill’s Medical Guide (Online Edition). Retrieved from http://search.ebscohost.com.proxy.ccis.edu/login.aspx?direct=true&db=ers&AN=86193878&scope=site
Szoeke, C., Ames, D., Coulson, M., Campbell, K., Dennerstein, L., Desomnd, P., Masters, C. L., Robertson, J. S., Rowe, C. C. & Yates, P. (2013). The Women’s Healthy Ageing Project: fertile ground for investigation of healthy participants ‘at risk’ for dementia. Int Rev Psychiatry. 25(6): 726–737. DOI: 10.3109/09540261.2013.873394
