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In the field of public health, it is a well-established fact that Alzheimer’s is developing into a health crisis for the elderly in the US. An estimate of over 5 million people in the US are currently victims of this disease, and by mid-century, this number is projected to grow into a whopping 13 million, fueled by the aging of the baby boomer generation. The prevalence of this disease places a huge financial burden upon households and the US medical system: in 2015, the global cost of Alzheimer’s disease is $818 million, which is equivalent to the GDP of the world’s 18th largest economy (Livingston, et al., 2020). With these startling facts and figures in mind, we shall all agree on the significance of recognizing the causes possible cures for this disease. While the field of science has devoted a significant amount of time and funding to the research and development of drugs targeting Alzheimer’s, only five drugs have been approved by the FDA to treat AD over the past hundred years since the first AD patient was diagnosed (citation needed). Moreover, these approved drugs usually provide temporary and incomplete symptomatic relief accompanied with severe side effects, unable to slow the progression of AD. However, a study done by Dr. G.W.Arendash and his team, treating mice suffering cognitive impairment with caffeine, suggested that something as trivial as a cup of everyday coffee might promise to outdo costly drugs and slow down the development of Alzheimer’s.


Before we dive into the aforementioned study, a bit of background knowledge regarding the pathological cause of Alzheimer’s and the known benefits of caffeine might be helpful. Due to the complexity of human brains and the lack of reasonable animal models and research tools, the detailed pathogenesis of AD is still unclear so far. In the scientific community, there are currently a number of hypotheses about AD, and, prompted by studies that showed an increase in the quantity of β-amyloid in the progression of AD patient’s cognitive decline, the majority of scientists approve of the hypothesis that points to the abnormal deposit of β-amyloid as the disease’s cause (Du, et al. 2018). This progress in the community has given birth to treatments and studies that target β-amyloid as the key substance. The study that we will be discussing is not an exception. Now, as you might ask, how did it come about that caffeine was the substance that Dr. G.W.Arendash and his fellow researchers were experimenting with? The answer lies in the fact that, according to numerous epidemiologic studies, caffeine proves to provide unequivocal cognitive benefits to the human brain, increasing its alertness and even, in some cases, lowering the incidence of diseases like the Parkinson’s. Thus, it is safe for Dr. G.W.Arendash and his team to make the assumption that caffeine could provide cognitive benefits for AD patients.


In the study, Dr. G.W.Arendash and his team chose mice carrying APPK670N, M671L gene (hereafter referred to as “APPsw mice”) and non-transgenic mice (hereafter referred to as “NT mice”) as the experiment’s subjects. The former type of mice would display symptoms of cognitive impairment in the progress of the study, and the latter won’t. The researchers then randomly assigned a certain number of APPsw mice to the experiment group, where drinking water containing caffeine is served, mimicking the daily moderate intake of caffeine by human beings. For the NT mice and the remaining APPsw mice, normal tap water was served, for the purpose of creating a controlled group. Over the course of the experiment, all mice underwent a series of tests examining their sensorimotor, anxiolytic, and cognitive functions. The results were not beyond what the researchers had expected: the APPsw mice from the experiment group, namely those that were served drinking water containing caffeine, performed almost as well as their NT peers in the series of cognitive tests. In contrast, APPsw mice that were served normal drinking water performed far less remarkably than the aforementioned two groups of mice. The boost in cognitive functions displayed in APPsw mice served with caffeinated drinking water could only be attributed to caffeine. After the researchers killed the mice and conducted analyses on their brains, they discovered, in the brains of APPsw mice served with caffeinated water, a significant reduction of β-amyloid in the hippocampus. This finding could serve as a potential explanation on the mechanism whereby caffeine boosts APPsw mice’s cognitive performance. (Arendash.G., et al. 2006) More importantly, since, as mentioned earlier in this article, there might exist a correlation between the Alzheimer’s and the abnormal deposit of β-amyloid in the patient’s brain, the finding could also provide an anecdotal basis for the idea that the everyday caffeine intake by human beings could potentially help slow down and even reverse the Alzheimer’s.


Admittedly, instead of jumping to an oversimplified conclusion and announcing to the world “hey, ya’ know what, drinking coffee can cure Alzheimer’s !”, more studies that look into the specific relationship between the Alzheimer’s and caffeine must be conducted to further determine how caffeine could help with treating AD, as Dr. G.W.Arendash and his team pointed out by the end of the paper. With that said, their discovery certainly has far-reaching implications. It promises to prompt the field of medicine and the general public to reimagine the Alzheimer’s and the vast benefits of caffeine: intimidating as the disease is, an unassuming cup of Starbucks every day might be the secret weapon to repel it.



Du, X., Wang, X., Geng, M., 2018. Alzheimer’s disease hypothesis and related therapies. Translational Neurodegeneration, Volume7, Article2, 30 January 2018. [accessed date: 2020 Sep 2nd]; doi: 10.1186/s40035-018-0107-y.


Arendash.G., et al. 2006. Caffeine protects Alzheimer’s mice against cognitive impairment and reduces brain β-Amyloid production. Neuroscience. Volume 142, Issue 4, 3 November 2006, Pages 941-952 [accessed date: 2020 Aug31]; doi: 10.1016/j.neuroscience.2006.07.021.


Livingston. G., Huntley, J., Sommerland, A., Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet, 2020; DOI: 10.1016/S0140-6736(20)30367-6


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