Alzheimer's Disease Summary

external image Alzheimer-May-Caused.jpgAlzheimer’s Disease is a progressive disease that effects the brain and causes disruptions in one’s memory, thinking, and behavior (Alzheimer’s Association, 2010). It is the most common form of dementia accounting for 50-70 percent of dementia cases and is the sixth leading cause of death in the United States. Life expectancy, upon notice of one’s first symptoms, is an average of 8 years with a range from three to twenty years (Alzheimer’s Association, 2010). Memory loss is mild in the early stages of Alzheimer’s Disease, but in its later stages one loses the ability to carry on conversations and respond to his/her environment (Alzheimer’s Association, 2010). Most of what is known about Alzheimer’s Disease has been discovered in the last 15 years (Alzheimer’s Association, 2010). Because of our ability to understand this disease better, more studies are being done to seek out therapies to help prevent and reverse its effects. Among the many treatments being studied is diet. The media tends to latch on to each new study and write articles that are sometimes more “noise” than actual “news.” Below are four critiqued headlines complete with research and offered opinions on whether the information that was presented in each headline is “news” or “noise.”

Important Definitions

  • Alzheimer's Disease- a brain disease that causes problems with memory, thinking and behavior. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. Alzheimer's Association What is Alzheimer's Disease?
  • Neurodegeneration- umbrella term for the progressive loss of structure or function of neurons, including death of neurons. Many neurodegenerative diseases, including Parkinson's, Alzheimer's and Huntington's, occur as a result of neurodegenerative processes.
  • Hyperinsulinemia- excess levels of circulating insulin in the blood.
  • Insulin Resistance- a condition where insulin becomes less effective at lowering blood sugars.
  • Mediterranean Diet- The principal aspects of this diet include high olive oil consumption, high consumption of legumes, high consumption of unrefined cereals, high consumption of fruits, high consumption of vegetables, moderate consumption of dairy products (mostly as cheese and yogurt), moderate to high consumption of fish, low consumption of meat and meat products, and moderate wine consumption.
  • Amyloid-Beta Peptide- a peptide of 36–43 amino acids that appears to be the main constituent of amyloid plaques in the brains of Alzheimer's Diseased patients.
  • Brain synapses- the point of connection usually between two nerve cells. Specifically, a synapse is a specialized junction at which a nerve cell (a neuron) communicates with a target cell. The neuron releases a chemical transmitter (a neurotransmitter) that diffuses across a small gap and activates specific specialized sites called receptors situated on the target cell.
  • Omega 3 fatty acids- a polyunsaturated fatty acid, essential for normal retinal function, that influences various metabolic pathways, resulting in lowered cholesterol and triglyceride levels, inhibited platelet clotting, and reduced inflammatory and immune reactions.
  • DHA- docosahexaenoic acid: an omega-3 fatty acid present in fish oils.
  • Uridine- a crystalline pyrimidine nucleoside C 9 H 12 N 2 O 6 that is composed of uracil attached to ribose, that is derived by hydrolysis from nucleic acids, and that in the form of phosphate derivatives plays an important role in carbohydrate metabolism
  • Choline- a quaternary ammonium cation, C 5 H 14 N + O, one of the B-complex vitamins, found in the lecithin of many plants and animals.
  • Confounding Factors- A confounding factor in a study is a variable which is related to one or more of the variables defined in a study. A confounding factor may mask an actual association or falsely demonstrate an apparent association between the study variables where no real association between them exists. If confounding factors are not measured and considered, bias may result in the conclusion of the study.
  • Apolipoprotein E Genotype- is a class of apolipoprotein found in the chylomicron and IDLs that binds to a specific receptor on liver cells and peripheral cells. It is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. The gene resides on the 19th chromosome and has three allelic forms; one normal and two dysfunctional. One of the dysfunctional alleles, E4 has been implicated in atherosclerosis and Alzheimer's disease, impaired cognitive function, and reduced neurite outgrowth.
  • Tertile- Any of the two points that divide an ordered distribution into three parts, each containing a third of the population.
  • Cohort Study- A cohort study is an analytical study in which individuals with differing exposures to a suspected factor are identified and then observed for the occurrence of certain health effects over some period, commonly years rather than weeks or months. The occurrence rates of the disease of interest are measured and related to estimated exposure levels. Cohort studies can either be performed prospectively or retrospectively from historical records.
  • Prospective Cohort Study- A research study that follows over time groups of individuals who are alike in many ways but differ by a certain characteristic and compares them for a particular outcome.

Links to Nutrition Headlines

Call; Alzheimer's and Diet: Good for The Heart May Be Good for The Brain;
The news article Alzheimer’s and Diet: Good for Heart May Be Good for Brain, Mediterranean-Like Diet May Lower Dementia Risk, Researchers Find by Todd Neale summarizes findings from a cohort study performed in New York that suggests a Mediterranean diet may decrease one's risk for Alzheimer's Disease (AD). In this study, researchers examined associations between adherence to a Mediterranean diet and Alzheimer's Disease (Scarmeas, 2006). In this article Todd Neale brings to light some results of the study in New York. He seems to bring a sense of hope to those who are effected by AD by stating it "may" reduce the risk of dementia using the study's results to back him up. Still he remains neutral on the subject bringing in quotes from other doctors, one of which states that the reason it might be good for the brain is because the diet shares many similarities with a heart healthy diet, and since heart disease increases the risk for Alzheimer's Disease, it would only make since that a diet, like the MeDi, sharing similarities with a heart healthy diet would decrease one's risk for Alzheimer's Disease.

The study in New York, which is what Todd Neale's article is based on, used a newer approach. Instead of focusing on one particular nutrient or mineral, this study focuses on the overall diet pattern (Scarmeas, 2006). To assess adherence to the dietary pattern the use of a scoring system utilized rating adherence on a scale from 0-9 (0 being lowest adherence, 9 being highest adherence). It took place over an average of 4 years with participants being reassessed every 1.5 years. In an effort to remove bias, Scarmeas and his fellow researchers did adjust for many confounding factors including aplipoprotein E genotype. In the findings of this study it was found that there was a 39-40 percent decrease in participants who were in the tertile that followed the MeDi to the greatest extent. Therefore, according to the study done in New York, it shows only an association between the MeDi and a decreased risk for Alzheimer's Disease. (Scarmeas, 2006) Though the data above may seem fairly conclusive, another study done by Catherine Fèart and other researchers (including Nikolaos Scarmeas who headed the study in New York) did a prospective cohort study on elderly individuals 65 years or older in France over a period of 5 years (Fèart, 2009). This article used very similar methods to the one performed in New York with the use of rating adherence the the MeDi, many of the same confounding factors that were adjusted for, and many of the same cognitive tests to measure cognitive/memory decline (Fèart, 2009). The difference comes in their results and conclusions. Although higher adherence to the MeDi was associated with fewer errors on one mental state examination, the results for the other examinations led the researchers to conclude that more research is needed before they could associate higher adherence to the MeDi to Alzheimer's Disease (Fèart, 2009). Another study was done by a different set of researchers investigating the use of olive oil, a known major player in the MeDi, and the risk of Alzheimer's Disease. This multi-center cohort study was conducted in France with four years of follow-up (Berr, 2008). This study used tests like the Isaacs Set Test, Mini Mental-State Examination, and the Benton Visual Retention Test to measure mental declines (Berr, 2008). The results from this study showed and association between intensive olive oil use with a 15 percent reduction in verbal fluency decline and a 17 percent reduction in visual memory decline, though the study states that association with intensive use was significant for visual memory but not for verbal fluency in multivariate analysis (Berr, 2008). The researchers conclude that due to other factors, further research is needed (Berr, 2008).

The article titled Alzheimer’s and Diet: Good for Heart May Be Good for Brain, Mediterranean-Like Diet May Lower Dementia Risk, Researchers Find by Todd Neale is more "news" than "noise." Reasons for this include he did not mislead readers by using words like "can" or "will." Instead he chose the word "may" when describing the relationship found between the MeDi and Alzheimer's Disease in Scarmeas's study. Todd Neale is not claiming causation after reviewing Scarmeas' and teams journal article. He also included quotes from other doctors with their opinions. More research is needed before any definite conclusions can be made, but at least Neale is trying to shed light of hope for those who are experiencing, or who have loved ones who are experiencing, the effects of this disease by providing accurate information from an available study.

Peterson: Fatty Diet Could Cause Alzheimer's;
The news article Fatty Diet Could Cause Alzheimer’s recapitulated the findings of an animal experiment completed at Baylor College of Medicine in Houston, headed by Khojima M and associates (Motoyuki, 2010). The purpose of the experiment was to support current evidence between a high caloric diet and the development of Alzheimer's Disease. In the experimental group, mice were exposed to a high fat diet containing 42% of calories from fat. This was compared to a control group that was feed a standard rodent laboratory diet containing 15% of calories from fat. Caloric intake was measured every two weeks. The mice fed a high fat diet resulted in excess total body weight, fat mass and hyperinsulinemia. When the mice’s brains were studied, increased levels of the short peptide amyloid-beta were easily evident in the mice fed the high fat diet. This short peptide is found in excess in the Alzheimer’s Diseased brain forming characteristic plaques. The experimental evidence does support the concept that caloric intake does indeed increase the likelihood of developing Alzheimer’s Disease. The study also supported a connection between type-2 diabetes and Alzheimer’s Disease.

Hyperinsulinemia and insulin resistance are metabolic abnormalities that are becoming suspect for not only having a role in type II diabetes but also many neurodegenerative diseases like Alzheimer’s and Dementia. The most incriminating evidence that insulin resistance does indeed play a role in Alzheimer’s is that the gene that encodes the insulin-degrading enzyme lies on the same chromosome that is linked to late-onset Alzheimer’s disease. Insulin resistance is often found in overweight and obese individuals and is a component in metabolic syndrome. Overweight and obesity is mainly caused by an imbalance of excess calories consumed versus calories used. In a population based study by Gustaw-Rothenberg and associates, the dietary pattern of the Alzheimer’s diseased patients showed a high calorie diet that was also high in intake of meats, butter, high-fat dairy, eggs and sugar (Gustaw-Rothenberg, 2009). The intake of high fat foods is also correlate with the development of insulin resistance and type II diabetes. In yet another study, by Luchsinger and colleagues, cohorts were followed over about four years, mainly focusing on an allele type but also showed a correlation between high caloric intake, mainly attributed to high fat intake, and Alzheimer’s disease.(Luchsinger, 2002).

I found this headline to be much more ‘news’ than ‘noise’. The writers did a very good job on summarizing the peer-reviewed article from which it was based and made understandable connections. It is phrased well for consumers to understand and not get confused about the results. I do believe more studies are needed to truly understand what the mechanisms of Alzheimer’s are but this is very promising and the article Fatty Diet Could Cause Alzheimer’s at least gets consumers more aware of what risk factors could impact their mental health.

Sherwood; Nutritional drink, imaging show promise for Alzheimer's;
The news article Nutritional drink, imaging show promise for Alzheimer's reports of a study done on a medical drink that has been shown to improve verbal recall test scores and therefore may help with the symptoms of Alzheimer’s disease (225 patients 52-92-years-old were involved in the study) (Scheltens, 2010). The news article is a little misleading on this point because it starts out talking about how Alzheimer’s disease is related to the loss of synapses, which are junctions between two neurons or between a neuron and a muscle in the brain. This leads the reader to believe that this medical drink called Souvanaid does just that when in fact synapse restoration was not even tested at all in the original study. The study used memory recall tests to show that this drink may delay the symptoms of Alzheimer’s, such as memory loss and language distortion. Two groups were studied; one group receiving the active drink everyday and one group receiving a control drink everyday. The medical drink contains three main components that have been shown in other studies to increase brain synapse restoration in rats. These three components are uridine, choline, and the omega-3 fatty acid DHA. The article fails to mention the other components in the drink, such as vitamin E, vitamin C and six other nutrients that have also been associated with improved Alzheimer’s disease. This isn’t a critical issue, but should be noted as they may be contributing to the observed outcome of the study reported.

Some components of Souvenaid (DHA, uridine, and choline) when taken together have been shown to have restoration effects on brain synapses in rats, but these results have not been replicated to provide additional credibility to this result (Wurtman, 2006). Also, the results from this study do not necessarily mean that these nutrients have the same impact in humans from Souvanaid, like the news article portrays. Other components of the medical drink include vitamins C and E. Studies have shown that these two antioxidant vitamins when taken together is associated with decreased risk of Alzheimer’s disease (Zandi, 2004). This supports the theory that taking these everyday, such as in a medical drink like Souvanaid, may decrease symptoms related to Alzheimer’s disease.

This headline from CNN is more “noise” than “news” after looking at the facts. The main reason for my opinion is because, although the medical drink shows much potential, it is still in the preliminary stages of research. More studies must be done to confirm their results. Many news articles, in general, are published on studies that are so preliminary that nothing can really be taken as fact from them but are portrayed as fact to the general public. This is one of the major sources of confusion for the public when it comes to nutrition and health. Although the separate components of the Souvanaid drink have been associated with a decrease in some symptoms of Alzheimer’s disease, studies on the drink itself are limited. Because this is such a preliminary study, more studies must be done to validate results before any conclusions can be drawn. Another thing to consider is the fact that Groupe Danone, the company that would make a profit from selling Souvenaid, is funding the Scheltens study. Because of this, results may be influenced.

Pitcher.Mind and Diet Update:
The article Mind and Diet Update: Processed Food linked to Depression, High Protein to Alzheimer's references a study that suggests a correlation between a high protein diet and incidences of Alzheimer's Disease. The author of the article is very concise in her explanation of the findings of the study and accurately represents the results in their proper context. The study, outlined in Molecular Neurodegeneration, describes a lab based experimental design intended to examine the effects of high protein diets on the brains of mice (Pedrini, 2004.) The mice were divided into 4 groups and each was fed a different diet until 18 weeks of age. One group was given a standard mice chow, another was given a high fat/low carbohydrate mice how, another was given high protein/low carbohydrate chow and the final group was given a high carbohydrate/low fat chow mix. After 18 weeks, the brains of the mice were extracted and studied. Researchers examined AB42 levels, brain weights, body weights and the hippocampus of the mice to determine the effects of each diet on these factors. The brain mass of the mice on the high protein/low carbohydrate diet had decreased considerably compared to the masses of the brains of the other mice. This is significant because it shows a possible correlation between high protein diets and brain deterioration. It is worthwhile to note that the researchers did account for several other factors that could have affected their results, which lends credibility to their research. For example, they were careful to consider how the diets affected the male and female mice differently and any impact this would have had on their results. They also considered the cholesterol content of the different chow mix combinations and the possible impact that would have on the different distribution of macronutrients in the test diets.

There is a great deal of attention being payed to the role of protein in the development of Alzheimer's disease. In a related study published in The Journal of Biological Chemistry (Chisti, 2001) it was found that high protein diets correlated with memory loss in mice. This study lends a great deal of credibility to the effects of protein on memory loss because it was conducted in such a way that they could rule out other contributing factors. For example, cloning was used to produce mice that were controlled for other genetic factors known to play a role in the development of Alzheimer's. Researchers were then able to rule out many other factors suspected of being related to the memory loss and focus in on protein specifically. Another study documented in the Journal of Neurochemistry (Thirumangalakudi, 2008) examined how cholesterol impacts protein deposition levels in the brain. In this study, the researchers approached their testing using the assumption that protein deposits in the brain are related to development of Alzheimer's disease and proceeded from there. It appears that many working in this area of research approach their studies with an accepted conclusion that protein deposits are related to Alzheimer's disease.

It is my opinion that the article Mind and Diet Update is more "news' than it is "noise." The author accurately represented the studies they cited in their article, and they referenced a study that can be backed up by many other studies with similar findings. The relationship between high protein levels in the brain and Alzheimer's is quite widely accepted in the research community. The author keeps the discussion in perspective by pointing out limitations of the referenced studies, such as the fact that they were conducted on mice, not humans. Furthermore, the author even used the words "with all the data we have so far..." I think this is a fair way of summing up the facts of the article they have referenced. It acknowledges that this is an ongoing field of study with many unknown variables. This wording guides the reader to conclude that with the data we have so far, it is fair to proceed under the hypothesis that high protein diets may be related to Alzheimer's disease. I think the article was a responsible representation of the information we have thus far in the area of Alzheimer's and dietary protein research.


Many studies related to Alzheimer’s disease are too preliminary to draw any definite conclusions from yet. The media sometimes portrays study results as fact, which can mislead the general population. For example, research on the relationship between the Mediterranean diet and Alzheimer's Disease is inconclusive, though some results did show decreased cognitive decline. The Mediterranean diet does have similarities with a heart healthy diet, so a reduced risk in Alzheimer's could be a result from reducing the risk of heart disease, which is a risk factor in Alzheimer's Disease. Also, who is funding the study should always be taken into consideration. This is especially true with studies that are testing a product, such as Souvenaid, that may be put on the market someday for profit. Results may be biased and the product may be portrayed as more effective than it really is. More research will need to be done on both the Mediterranean diet and on Souvenaid before any final conclusions can be made.
In contrast, the media represented the news of how a high fat diet affects one's risk of Alzheimer's disease very well. Consumers who read the article Fatty Diet Could Cause Alzheimer’s were given well supported information in a way that they could easily understand. The same was true with the Mind and Diet Update article. Overall, the information was presented in a responsible way. While the studies cited show great promise, the author was careful to point out limitations and acknowledge how much about this complex and mysterious disease is still unknown.
In a news world filled with entertainment mixed with news, it can be difficult to discern real news from just "noise." It is important to review media reports with an awareness that we will need to do our own reasearch to discern the validity of the information given.


Alzheimer’s Association. What is Alzheimer’s. 2010. Available at: Accessed: Nov 22, 2010.

Scarmeas N, Stern Y, Tang MX, Mayeux R, and Luchsinger J A. Mediterranean diet and risk for Alzheimer's disease. Annals of Neurology. 2006; 59:912-921.

Feart C, Sameiri C, Rondeau V, et al. Adherence to a Mediterranean Diet, Cognitive Decline, and Risk of Dementia. JAMA. 2009; 302(6): 638-648.

Berr C, Portet F, Carriere I, et al. Olive Oil and Cognition: Results from a Three-City Study. Dementia and Geriatric Cognitive Disorders. 2008; 28(4): 357-364.

Motoyuki K, Yuxiang S, Lawrence C. Increased food intake leads to obesity and insulin resistance in the Tg2576 Alzheimer’s disease mouse model. Endocrinology. 2010;151:1532-1540.

Gustaw-Rothenberg K. Dietary patterns associated with Alzheimer’s disease: population based study. Int. J. Environ. Res. Public Health. 2009;6:1335-1340.

Luchsinger A, Tang M, Shea S, Mayeux R. Caloric intake and the risk of Alzheimer disease. Arch Neurol. 2002;59:1258-1263.

Scheltens P, Kamphuls PJGH, Verhey FRJ, et al. Efficacy of a medical food in mild Alzheimer's disease: A randomized, controlled trial. Alzheimer's and Dementia. 2010;6(1):1-10.

Wurtman RJ, Ulus IH, Cansey M, et al. Synaptic proteins and phospholipids are increased in gerbil brain by administering uridine plus docosahexaenoic acid orally. Brain Res. 2006;1088:83-92.

Zandi PP, Anthony JC, Khachaturian AS, et al. Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements. Arch Neurol. 2004;61:82-88.

Pedrini S, Thomas C, Brautigam H, et al. Dietary composition modulates brain mass and solubilizable AB levels in a mouse model of aggressive alzheimer’s amyloid pathology. Molecular Neurodegeneration. 2009;4:40

Chisti M, Yang D, Janus C, et al. Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695. Journal of Biological Chemistry. 2001;276:21562-21570.

Thirumangalakudi L, Prakasam A, Zhang R, et al. High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice. Journal of Neurochemistry. 2008;106(1):475-485.