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Caffeine and Alzheimer’s Disease

Hillary Roberts

21 February 2011



What is Alzheimer’s Disease?

            Alzheimer’s disease (AD) is a disease of the brain that “causes problems with memory, thinking, and behavior” ( As a form of dementia, Alzheimer’s affects the brain’s ability to retain memories, think, and reason properly. The disease normally occurs in people over the age of 60, although it has been known to happen as early as 40 years. When a person is afflicted with Alzheimer’s, their symptoms progressively worsen, until they are no longer able to communicate. Although scientists have not determined a cause for Alzheimer’s, genetic and lifestyle factors have been considered as possible causes. (

There is no current cure for Alzheimer’s, however there are several treatments for slowing the symptoms and improving the quality of life of the patients. One of these treatment methods is different medication for the different stages of degeneration, such as cholinesterase inhibitors that treat problems with memory, language, and judgment in the early to moderate stages. They can delay symptoms for up to 6 to 12 months depending on the patient.


Besides treatments after diagnosis, there have been studies on different methods to prevent Alzheimer’s disease. One of the ways that has been suggested is the consumption of caffeine (

What is Caffeine?

            Typically consumed in the form of coffee, soft drinks, chocolate, and certain medicines, caffeine makes the consumer more alert and gives an energy boost by stimulating the central nervous system ( The caffeine is absorbed by the body and travels through the bloodstream. The effects of it can be felt up to six hours. Side effects can be both negative and positive. While caffeine intake can cause dehydration, panic attacks, and emotional fatigue, it can also increase alertness and protect against heart disease as well as Parkinson’s disease (

Caffeine is naturally formed in many plants and can also be artificially produced. It lacks odor and has a naturally bitter taste. It is used in many different foods and drinks because of its stimulant properties. The amount of caffeine in a product depends on many different factors including the brewing method, steeping time, and the particle size. Caffeine has been thought to be associated with different health problems, including a variety of cancers, osteoporosis, and miscarriages (

Research and Studies

            So far, when studies have been done on the effect of caffeine on Alzheimer’s disease they have been retrospective. That is, they must be done by looking into the past and asking questions about routines. The problem that occurs with this type of study is the honesty of the answers given by the subjects.

            A case-control study done by Maia et al. (2002), tested to see if caffeine intake protects against Alzheimer’s disease. In a questionnaire about caffeine intake, researchers calculated the estimated intake depending on the amount of caffeine in different caffeinated products. There were also questions involving tobacco and alcohol consumption. This study reported an inverse association between caffeine intake and Alzheimer’s disease. Those patients with Alzheimer’s disease had an average daily intake of about 73.9 mg of caffeine during the 20 years prior to diagnosis (Maia et al., 2002). Meanwhile, the controls had about 198.7 mg during the same 20 years as their matched pair in the study. One possible reason for this association may be a genetic factor that both protects from Alzheimer’s disease and causes a person to favor caffeinated foods and beverages. The other explanation could be that consuming caffeine truly does protect against Alzheimer’s disease (Maia et al., 2002).

            In a review done by Eskelinen et al. (2010), it was determined that moderate caffeine intake, coffee in particular, is associated with a decreased risk in the diagnosis of Alzheimer’s disease. This review included nine longitudinal studies and the CAIDE study (Cardiovascular risk factors, Aging and Dementia). The results from the longitudinal studies were inconsistent.  One study would provide information supporting the effect of caffeine consumption on the prevention of Alzheimer’s, and the other would show no relationship between the two. The CAIDE study showed that consuming “three to five cups of coffee per day at midlife was associated with a decreased risk of dementia” (Eskelinen et al., 2010). As in Maia’s study, there were multiple explanations for this correlation. Drinking coffee may be associated with a lifestyle that brings about the protective factor or there may be medical conditions that cause dementia and only allow a person to consume very small amounts of coffee (Eskelinen et al., 2010).

A review written in the American Journal of Alzheimer’s Disease and Other Dementias concluded that the “evidence for a protective effect from caffeine on cognitive functioning… is promising” (Rosso et al., 2008). The studies in vitro and on animals have provided evidence supporting this conclusion and when the studies were performed on humans similar associations were made. The human studies expressed that there was improved functioning on cognitive aspects of the brain with long-term caffeine consumption. One particular cross-sectional study that included 1528 patients discovered a correlation in caffeine consumption and cognitive function in women, but not men. Although there is not a specific conclusion that states that there is absolutely a positive effect of caffeine on Alzheimer’s disease, Rosso et al. (2008) concluded that it may one day be discovered with more experiments.


             An experiment performed on a rabbit model explored how caffeine can block the disruption of blood barriers in the brain. The blood brain barrier (BBB) helps to protect the brain and is located between the central nervous system and the systemic circulation. The disruption of the BBB is a common occurrence in acute and chronic neurodegenerative diseases such as Alzheimer’s disease, and can cause “changes in cholesterol homeostasis and high dietary cholesterol” (Chen et al., 2008).  The experiment was carried out on New Zealand white rabbits divided into different groups, each group receiving a different diet. The caffeine consumed was able to block the cholesterol-induced leakages of the BBB. When comparing the groups, the results suggest, “the chronic ingestion of caffeine protects against high cholesterol diet-induced disruption of the BBB” (Chen et al., 2008).

            This experiment shows that caffeine affects the different parts of the brain that protect the cognitive functions. It protects against different breakdowns in the brain that lead to neurodegenerative diseases.


            From the studies that were explored in this paper, it has been concluded that there is an association between caffeine consumption and the protection and/or delay of Alzheimer’s disease. The studies provided evidence that there are correlations in the amount of caffeine consumed in later years of life and the onset and diagnosis of Alzheimer’s disease as well as several other neurodegenerative diseases. Although it would not be wise to consume caffeine in large doses every day for a long period of time, consuming moderate levels of caffeine could protect a person from the onset of Alzheimer’s disease.




















            Chen, Xuesong, Gawryluk, Jeremy W, Wagener, John F, Ghribi, Othman, & Geiger, Jonathon D. (2008). Caffeine blocks disruption of blood brain barrier in a rabbit model of alzheimer's disease. Journal of Neuroinflammation, 5(12), Retrieved from doi: 10.1186/1742-2094-5-12

Eskelinen, Marjo H., & Kivipelto, Miia. (2010). Caffeine as a protective factor in dementia and alzheimer's disease. Journal of Alzheimer's Disease, 20(1), Retrieved from doi: 10.3233/JAD-2010-1404

Maia, L., & De Mendonça, A. (2002). Does caffeine intake protect from alzheimer's disease?. European Journal of Neurology. Retrieved February 15, 2011, from

Rosso, Andi, Mossey, Jana, & Lippa, Carol F. (2008). Review: caffeine: neuroprotective functions in cognition and alzheimer's disease. American Journal of Alzheimer's Disease and Other Dementias, 23(5), Retrieved from doi: 10.1177/1533317508320083




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