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Green Tea and Memory

Colin Compas 9/20/06

 

Introduction

The lay public and health care professionals have long searched for a single miracle cure for many or all of the medical problems that face humanity.  So far no single cure has been found nor is one likely to be discovered; however, one supplement that seems to have health benefits in a wide range of areas is green tea and green tea extract.  Green tea is thought to have health benefits such as lowering cholesterol, reducing the risk of heart disease, cancer prevention, weight loss, increased immune system response, and improved memory (Daniells, 2006).  Many of these claims have not been well substantiated and are based on limited, if any, scientific evidence.  One of these claims, however, has been studied in some detail and that is the claim of improved memory.  Interest in this benefit of green tea has increased as the American population ages and the rate of age-related dementia increases along with it.  Alzheimer's disease and Parkinson's disease are two common types of dementia that have been examined as part of the effort to study the effect of green tea on memory loss.  Because its effects may be relatively subtle, it is difficult to quantitatively measure the possible benefits of green tea on brain function in relatively healthy people. However, by studying people suffering from neurodegenerative disorders the effects of green tea may be more readily visible.  A focus of considerable research has been to examine the possible effects of green tea in helping to slow the effects of age related dementia (eg. Kim 2004, Levites 2001). 

Internet Claims

            There are many claims on the internet for the “magical” properties of green tea relating to memory loss.  Many postings for green tea supplements list improved memory as one of the benefits, however, they rarely give any of the scientific evidence to support their claim.  For example, a simple quote such as, "A new generation of dietary Text Box:  
Figure 1. http://news.bbc.co.uk/2/low/health/4261558.stm
supplements containing pure EGCG may lead to the greatest benefit for treating Alzheimer's disease," (http://news.bbc.co.uk/2/low/health/4261558.stm) by a physician is often all that is given to substantiate the claim.  In another article the authors state, "Green tea catechins may improve reference and working-memory related learning ability" (Daniells, 2006).  Green tea could prove enticing for someone looking for some way to improve memory because along with improved memory that could be able to, "treat headaches, body ache, poor digestion, and improve well-being and life expectancy" (http://www.bodybuildingforyou.com/health-supplements/green-tea-extract.htm).  Green tea also claims to offer all of these benefits without serious side effects.   

How Green Tea Works

            The two main components of green tea that are thought to work on improving memory are polyphenols and a particular type of polyphenol called flavonoids.  Polyphenols are substances found in plants that are often responsible for their coloring.  It is the antioxidative properties of polyphenols that are seen to be an advantage in preventing memory loss.  Flavonoids, as seen in FiText Box:  
Figure 2. Typical flavonoid structure (http://en.wikipedia.org/wiki/Flavonoid)
gure 2, are a secondary plant metabolite that is also seen to have antioxidative properties.  The most active polyphenol in green tea is (-)-epigalochatechin-3-gallate (EGCG).  EGCG inhibits neuronal loss in two ways.  It decreases the production of Beta-amyloid (Aβ), which forms proteins that can develop into plaques in the brains of Alzheimer's patients (Okello, 2004).  It also decreases neuronal loss due to polyphenol (-)-epigallocatechin-3-gallate (MPTP), which is a potent neurotoxin that specifically affects dopamine production and receptors.  The antioxidative properties of polyphenels are also what is believed to cause many of the other health benefits of green tea because nearly all of the conditions that green tea is able to help are caused by free radicals in the body which come as a result of oxidative stress (Levites 2001). 

            The brain is particularly susceptible to free radical damage because of its high metabolic rate.  The high use of oxygen during the metabolic processes leads to the generation of a large number of free radicals, which are molecules that have unpaired electrons.  When these molecules with unpaired electrons try to bond to other molecules, it causes a bond in the second molecule to break in order to create an electron pair.  This series of events can cause a chain reaction that can eventually lead to cell damage.  The body's natural defense against free radicals comes from antioxidants, which donate an electron to end the chain reaction.  The most common forms of antioxidants in the body are vitamins E and C.  Green tea has proven to be a source many additional antioxidants and this is why it is beneficial in stopping cell degeneration.  One of the reasons that green tea is so beneficial in stopping this degeneration in neuronal cells is that EGCG has been shown to be present in the brain, meaning that it is able to enact its antioxidative affects on the free radicals causing damage in the brain.

 

Conditions Affecting Memory

            The reason that neuronal loss is seen to be so prevalent in elderly people is that free radicals tend to build up over time and therefore have a greater effect as people age.  This is the reason that at 65 years of age about 1.5% of the population suffers from some type of dementia with the rate doubling every 4 years until 30% of the population that is 80 years old suffer from dementia (Kuriyama, 2006).  One of the most common types of dementia is Alzheimer's disease which affects about 4.5 million Americans.  Alzheimer's disease is defined as a progressive brain disorder that gradually destroys a person’s memory and ability to learn, reason, make judgments, communicate and carry out daily activities (alz.org).  The causes of Alzheimer's are not well defined but are a combination of age, family history, and genetics.  One reason that green tea was originally looked at in the treatment of Alzheimer's is because there is a much lower prevalence of the disease in Asia, where green tea is the most popular drink.  Green tea may inhibit the development of Alzheimer's by increasing the amount of acetylcholine (ACh), an important neurotransmitter, in synapses by inhibiting cholinesterases (AChE), which breaks down ACh.

            Parkinson's disease is another neurodegenerative disease for which green tea is thought to have beneficial effects.  Parkinson's disease occurs when neurons in the substantia nigra of the brain die or become impaired (parkinson.org).  The cells of this area of the brain normally produce dopamine which is a neurotransmitter that allows for the smooth coordinated function of the body's muscles.  Symptoms of Parkinson's disease appear when nearly 80% of these cells are damaged.  Symptoms of Parkinson's disease include tremors, slowness of movement, and difficulty with balance.  Green tea is able to help alleviate some of the symptoms of Parkinson's by inhibiting MPTP which is the neurotoxin that affects dopamine in the brain.

           

Scientific Literature

The first scientific studies of green tea as a prevention of age related memory loss came as a result of the knowledge that the memory loss was the result of free radical buildup in the brain (Levites 2001).  It was known that antioxidants could prevent damage by free radicals and green tea was known to be a good source of antioxidants.  It is difficult to study normal memory loss due to aging because it is a very slow process and difficult to quantify.  It is even more difficult to study this process in mice because the life span of a mouse is short enough that there is little free radical buildup in the brain leading to memory loss.  For this reason it proved easier to study the affects of neuronal degradation by looking at a mice model for Parkinson's disease.  Also, this would open the possibility for treatments found in animal research to be applied to treating this debilitating disease in humans.  In Levites et al. (2001) they showed the effectiveness of MGCG on slowing the neurodegenerative process of MPTP.  They looked at different groups of mice who were given MPTP, EGCG and a combination of MPTP and EGCG and examined subsequent neuronal loss as a result of the neurotoxin.  They found that EGCG was effective in inhibiting the neuronal loss.  They believe that this is the result of the catechol-containing compounds, found in green tea, which are known to inhibit free radicals.  By inhibiting the free radicals they found that they could inhibit neuronal loss in the mouse model for Parkinson's disease.

            In a follow up study by Levites et al. (2002) the first potential side effects of green tea were seen.  Green tea only exhibits antioxidative properties at relatively low concentrations and at high concentrations can actually prove to be pro-oxidative (Levites, 2002).  This finding was concurrent with other studies of antioxidants that showed the same properties.  This means that there is a correct dosage that should be taken in order to experience the beneficial effects of green tea as an antioxidant.  It was later shown that an average of two cups of tea per day provide the correct amount of polyphenols and flavonoids necessary to prevent neural degeneration (Mandel, 2004).

Figure 3. Inhibition of AChE by green tea, black tea, and coffee based on concentration of each. (Okello, 2004)

 

            Following studies on the effects of green tea on Parkinson's disease, Kim et al. (2004) looked at the role that green tea could play in inhibiting the progression of Alzheimer's disease.  It was already known that ACh and AChE played a role in the development of Alzheimer's and drugs had already been developed to increase ACh or decrease AChE in order to slow the progression of Alzheimer's but many of these drugs proved ineffective and had many side effects.  Following procedures similar to those used in studies of green tea in mice with Parkinson's, Kim et al. looked at the effects of green tea in a mouse model for Alzheimer's.  They found that green tea inhibited AChE and improved overall cognitive ability in the mouse model.  These findings were furthered by Okello et al. as shown in Figure 3 (Okello, 2004).  This graph shows the relationship between concentration and inhibition of AChE for green tea, black tea, and coffee.  The graph shows that the greatest inhibition results from the green tea.  They also showed similar findings to Levites et al. showing that there is a limit in the concentration that is effective in inhibiting AChE.  The findings of Okello et al. went further in showing that EGCG also inhibits the production of Aβ, which may be responsible for plaque deposits in the brains of Alzheimer's patients.  This could prove very beneficial because synthetic inhibitors of Aβ have proven ineffective due to their high molecular weights.

            It has been shown that green tea is effective in slowing neural loss due to free radicals and oxidative stress, but Mandel et al. (2004) have gone further in looking at the specific pathways that the antioxidants in green tea are taking in order to prevent the degeneration.  They have found that the radical scavenger properties of green tea may not be the sole explanation of the neuroprotective behavior of green tea (Mandel, 2004).  They have found that the benefits may also come from the pharmacological effects of catechins and there derivatives.  Mandel et al. found that the neuroprotective effect of EGCG is actually due to the down regulation of certain genes rather than the up regulation of the antigens of those genes.  Concurrent with other studies they found that this effect was reversed at high concentrations of EGCG.  They found that the flavonoids activate a signal pathway that has a neuroprotective affect rather than acting directly on preserving neural cells themselves. 

            The drawback in many of these studies is that they have been performed either in vitro or in a mouse model.  These models often prove applicable to human patients but it cannot be proven until studies in people are performed.  The problem with human studies of this type is challenge in controlling other variables that may be involved and the time scale necessary for the observance of symptoms due to cognitive loss.  To address some of the limitations of prior research, Kuriyama et al. (2006) attempted to look at a large subset of Japanese population in order to determine the effects of green tea in people.  Three different groups were selected based on the amount of green tea they drank.  The groups were those who drank less than three cups a week, those who drank four to six cups a week, and those who drank two or more cups per day.  It was found that with each increase in green tea consumption there was a corresponding decrease in prevalence of cognitive impairment (Kuriyama, 2006).  While this is a limited demographic that could have many other confounding variables, it is encouraging that many of the finding in vitro and in mice may be applicable to human populations.

Conclusion

            In summary, many claims have been made on the internet about the health benefits of green tea, including its prevention of memory loss.  These claims are often made without reference to adequate scientific research. However, there is now research that may support the claim that green tea helps prevent cognitive loss due to aging and age related dementia.  Many of the studies that have recently been conducted rely on evidence from in vitro and in mouse models, so further human studies are needed.  With that said, the findings of the positive effects of the antioxidative properties of green tea are encouraging and may likely prove to be an effective and side effect free method for treating and perhaps preventing age related memory loss.


References

 

Alzheimer's Association. www.alz.org.  viewed:09-19-06.

 

BBC News / Health http://news.bbc.co.uk/2/low/health/4261558.stm viewed:9-19-06

 

Bodybuildingforyou http://www.bodybuildingforyou.com/health-supplements/green-tea-extract.htm viewed:9-19-06

 

Daniells, Stephen. More Evidence of Green Tea's Brain Benefits. www.nutraingredients.com 03-24-2006.

 

Kim H, Kim M, Kim S, Chong J.  Effects of Green Tea and Polyphenol on Cognitive and Acetylcholinesterase Activities.  Biosci. Biotechnol. Biochem. 2004;68:1977-1979.

 

Kuriyama S, Hozawa A, et al. Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya Project. The American Journal of Clinical Nutrition 2006;83:355-61.

 

Levites Y, Weinreb, et al. Green tea polyphenol (-)-epigallocatechin-3-gallate prevents N-methyl-4-phenyl-1,2,3,6-tetrahyropyridine-induced dopaminergic neurodegeneration. Journal of Neurochemistry 2001;78:1073-1082.

 

Levites Y, Amit T, et al. Involvement of Protein Kinase C Activation and Cell Survival/Cell Cycle Genes in Green Tea Polyphenol (-)-Epigallocatechin 3-Gallate Neuroprotective Action.  The Journal of Biological Chemistry 2002;277:30574-30580.

 

Mandel S, Weinreb O, et al. Cell signaling pathways in the neuroprotective actions of the green tea polyphenol (-)-epigallocatechin-3-gallate: implications for neurodegenerative diseases. Journal of Neurochemistry 2004;88:1555-1569.

 

Meydani M.  Nutrition Interventions in Aging and Age-Associated Disease.  Annals New York Academy of Sciences 2001;928:226-235.

 

National Parkinson Foundation. www.parkinson.org viewed:09-19-06.

 

Okello E, Savelev S, Perry E.  In vitro Anti-β-secretase and Dual Anticholinesterase Activiteis of Camellia sinesis L. (tea) Relevant to Treatment of Dementia.  Phytotherapy Research 2004;18:624-627.

 

Unno K, Takabayashi F, Kishido T, Oku N.  Suppressive effect of green tea catechins on morphologic and functional regression of the brain in aged mice with accelerated senescence (SAMP10).  Experimental Gerontology 2004;39:1027-1034.

 

Unno K, Takabayashi F, et al. Daily consumption of green tea catechin delays memory regression in aged mice. Biogerontology 2006;10:152-160.

 

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