Your coffee could be helping you more than you know. With the passing of time, we are reminded of those who are no longer able to remember. In recent years, roughly fourteen percent of Americans, age seventy-one and over, have been diagnosed with a chronic disease called dementia. Dementia is a disease that effects the brain’s ability to make decisions, remember critical information, and maintain personality. It commonly leads to other brain diseases such as Parkinson’s and Alzheimer’s, being the top two most common neurodegenerative diseases (Spillanti et al, 1998). There are several difficulties that individuals who suffer from the persistent disorder must overcome to make decisions, reason, and express themselves effectively. Every day, millions of families experience the impact of dementia as they assist their loved ones with the completion of basic tasks and with the retention of fundamental information. Oftentimes, these people report that their abilities to recognize their loved ones have diminished because of this disease. A cure for dementia has yet to be discovered despite the first reports of the disease date back as far as the eighteenth century. This unforgiving illness is the subject of a tremendous amount of research that takes place every day in attempt to find a cure that will save millions of lives. The preventative may have been lying in front of our eyes and on our breakfast table all this time.
After years of advancements in research to find a cure for dementia and other related cognitive diseases, such as Parkinson’s and dementia, researchers from Rutgers University finally uncovered a link between the disease and America’s favorite drink: coffee. Before the study, the team of researchers found that EHT, a fatty acid derivative of the neurotransmitter serotonin was effective in protecting the brains of mice. However, they wanted to test whether caffeine would be an effective catalyst, or in other words a substance that can speed up a chemical reaction, for EHT in preventing the accumulation of abnormal proteins. Researchers hypothesized that EHT, which is present in the coating of a coffee bean in addition to caffeine may prevent the accumulation of harmful proteins in the brain, specifically tau and amyloid, which lead to dementia (Yan et al, 2018).
The researchers assigned groups of mice that were given EHT alone, caffeine alone, and a group that got both. Scientists ran several behavioral assessments to summarize brain activity in different regions of the brain and observe the effects of this experiment. The mice were tested based on the number of PP2A present in the brain. PP2A is a protein phosphate that controls major pathways of cells in the cell cycle (Wlodarchak and Xing, 2016). A rotarod and Wire Hang test was used to evaluate motor performance, a Morris Water Maze test measuring spatial learning and memory to analyze hippocampal function, and nesting behavior to reflect nigrostriatal function. Researchers found that caffeine and EHT were not as effective by themselves as they were together. After nine months of treatment, mice that were tested in this study showed a decreased rate of protein build up in the brain after caffeine was added to EHT. This led the researchers to conclude that coffee consumption may slow or stop symptoms of dementia but does not block brain degeneration (Yan et al, 2018).
Researchers in this study were responding to a preceding study conducted on the information surrounding whether caffeine has an impact on overexpressing human wild-type α-synuclein, a disordered protein found in the brain (Rockenstein et al, 2002). The results of this study provided pertinent information about caffeine’s ability to neurologically alter the brain which prompted the researchers at Rutgers University to test certain parts of rat brains to see if there may be a link to Parkinson’s disease and dementia with Lewy bodies. Rutgers University was prompted to conduct this study as wild-type α-synuclein can alter brain function and dementia is caused by degradation of brain cell function. Researchers in the previous study did not draw the connection between caffeine and EHT with any brain diseases, leaving Rutgers researchers the opportunity to further their research.
As a result of the methodology surrounding the experiment, this research has proven to be both efficient and ethical. Researchers used experimental and control groups, leaving no room for doubt regarding the effectiveness of the treatments. They also did not admit to altering any data. One potential concern of the study’s ethicality is related to the usage of rats for experimentation considering rats were induced with EHT and caffeine for the duration of seventy days. However, they mention at the end of the study that the rats were induced safely and with an amount that would have miniscule effects on their overall wellbeing. They did not use a high concentration of any substance, but it would be useful to know how the rat’s health was after the study. This seems to be an ethical and reliable transaction.
This research is groundbreaking. The information gathered is bound to become popular among people who have family that suffered or currently suffer from this disease and have the gene that will someday lead them to develop it as well. This study could also be of interest to people who don’t have a predisposition to develop the disease. This is because they want to be cautious regarding the unknowns of their health in the future. It is imperative for people to know what they can do to better their health, especially with irreversible diseases like these.
Considering the broader implications of this study, it could be argued that if less people develop dementia the work force will be larger, the economy will be stronger, and health care will be more accessible to everyone. This study can be implemented in the everyday lives of humans, changing the face of medicine. It could also provide people with some reassurance about their future health. With more research surrounding the topic, millions of families can be saved. Coffee is the cure.
References
Braak H, Del Tredici K. 2017 March 6 1Neuropathological staging of brain pathology in sporadic Parkinson’s disease: Separating the wheat from the chaff. 7(1). https://content.iospress.com/articles/journal-of-parkinsons-disease/jpd179001
Rockenstein E, Mallory M, Hashimoto M, Song D, Shults CW, Lang I, Masliah E. Jun 2002 Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and thy-1 promoters. 68(5):568-78. https://pubmed.ncbi.nlm.nih.gov/12111846/
Spillanti M, Crowther RA, Jakes R, Hasegawa M, Goedert M. 1998 May 26. Α-synuclein in filamentous inclusions of Lewy bodies from … – PNAS. 95 (11). https://www.pnas.org/doi/10.1073/pnas.95.11.6469
Wlodarchak N and Xing Y. 2016. “PP2A As a Master Regulator of the Cell Cycle.” Critical reviews in biochemistry and molecular biology. U.S. National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905575/.
Yan R, Zhang J, Park H-J, Park E, Oh S, Zheng H, Junn E, Voronkov M, Stock J, Mouradian MM. 2018 Dec. 3. Synergistic neuroprotection by coffee components EICOSANOYL-5 … – PNAS. 115 (51). https://www.pnas.org/doi/10.1073/pnas.1813365115
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