Alzheimer's Disease

Muted emotions misleading in Alzheimer's disease

August, 2010

Indications that blunted emotions are part of Alzheimer’s are a warning not to assume that reduced emotional response is a sign of depression.

A small study suggests that the apathy shown by many Alzheimer's patients may not simply be due to memory or language problems, but to a decreased ability to experience emotions. The seven patients were asked to rate pictures of positive and negative scenes (such as babies and spiders) by putting a mark closer or further to either a happy face or a sad face emoticon. Closeness to the face indicated the strength of the emotion felt. Although most of the time the Alzheimer’s patients placed their mark in the appropriate direction, they did make more inappropriate choices than the control group, and typically also gave less intense judgments.

Both comprehension problems and depression were ruled out. A lower emotional response may result from damage to brain areas that produce neurotransmitters, which typically occurs early in Alzheimer’s. It may be that medication to replace or increase these neurotransmitters would improve emotional experience.

This finding is a warning that apathy should not be automatically taken to mean that the patient is depressed. The researchers, enabled by the small size of the study, tested more thoroughly for depression than is usually the case in large studies. It may be that in these studies, this apathy has often been confounded with depression — which may explain the inconsistencies in the research into depression and Alzheimer’s (see the news item just previous to this).

The finding may also help caregivers understand that any emotional indifference is not ‘personal’.

Reference: 

[1674] Drago, V., Foster P. S., Chanei L., Rembisz J., Meador K., Finney G., et al.
(2010).  Emotional Indifference in Alzheimer's Disease.
J Neuropsychiatry Clin Neurosci. 22(2), 236 - 242.

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Predicting the progression of Alzheimer's

February, 2010

A 15-year study concludes that a simple progression rate calculated at the initial visit can reliably identify slow, intermediate and rapid progression.

By following 597 Alzheimer’s patients over 15 years, researchers have determined that a simple progression rate can be calculated at the initial visit, using symptom onset and present performance, and that this can reliably identify slow, intermediate and rapid progression.

Reference: 

[175] Doody, R. S., Pavlik V., Massman P., Rountree S., Darby E., & Chan W.
(2010).  Predicting progression of Alzheimer's disease.
Alzheimer's Research & Therapy. 2(1), 2 - 2.

Full text available at http://alzres.com/content/2/1/2/

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High-dose vitamin regime may help slow Alzheimer's

March, 2003

A preliminary study suggests that a regime of high doses of folic acid, B12 and B6 reduces levels of homocysteine in people with mild to moderate Alzheimer’s. A larger study, recruiting 400 participants from all over the U.S., is to be undertaken to assess whether such a vitamin regime can slow the progression of Alzheimer's disease. In the meantime, it is not advised that people take high doses of these vitamins, as there are possible side-effects, including peripheral nerve damage.

Reference: 

[723] Bell, K., Sano M., Aisen P. S., Egelko S., Andrews H., Diaz-Arrastia R., et al.
(2003).  A pilot study of vitamins to lower plasma homocysteine levels in Alzheimer disease.
The American Journal of Geriatric Psychiatry: Official Journal of the American Association for Geriatric Psychiatry. 11(2), 246 - 249.

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Why Vitamin E might slow the progress of Alzheimer's

December, 2000

A chemical called methionine (an amino acid found in beta-amyloid) may be the source of the toxic free radicals produced by the amyloid-beta peptide. Recent studies have demonstrated that higher than normal doses of vitamin E may slow the advance of Alzheimer's in some people with late stages of the disease. The current study provides a possible explanation for this link. Vitamin E, an antioxidant, appears to work by destroying free radicals (oxidants) produced by amyloid.

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The study was presented at the 2000 International Chemical Congress of Pacific Basin Societies.

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Diet rich in foods with Vitamin E may reduce Alzheimer’s disease risk

January, 2002

Two studies have come out in favor of a diet rich in foods containing vitamin E to help protect against Alzheimer's disease. One study involved 815 Chicago residents age 65 and older with no initial symptoms of mental decline, who were questioned about their eating habits and followed for an average of about four years. When factors like age and education were taken into account, those eating the most vitamin E-rich foods had a lower risk of developing Alzheimer’s, provided they did not have the ApoE e4 allele. This was not true when vitamin E was taken as a supplement. Intake of vitamin C and beta carotene appeared protective, but not at a statistically significant level. The other study involved 5,395 people in the Netherlands age 55 and older who were followed for an average of six years. Those with high intakes of vitamins E and C were less likely to become afflicted with Alzheimer's, regardless of whether they had the gene variation. This association was most pronounced for current smokers, for whom beta carotene also seemed to be protective. A number of clinical trials are underway to further investigate these links.

Reference: 

Engelhart, M.J., Geerlings, M.I., Ruitenberg, A., van Swieten, J.C., Hofman, A., Witteman, J.C.M. & Breteler, M.M.B. 2002. Dietary Intake of Antioxidants and Risk of Alzheimer Disease. JAMA, 287, 3223-3229. Morris, M.C., Evans, D.A., Bienias, J.L., Tangney, C.C., Bennett, D.A., Aggarwal, N., Wilson, R.S. & Scherr, P.A. 2002. Dietary Intake of Antioxidant Nutrients and the Risk of Incident Alzheimer Disease in a Biracial Community Study. JAMA, 287, 3230-3237.

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Why diet, hormones, exercise might delay Alzheimer’s

February, 2004

A theory that changes in fat metabolism in the membranes of nerve cells play a role in Alzheimer's has been supported in a recent study. The study found significantly higher levels of ceramide and cholesterol in the middle frontal gyrus of Alzheimer's patients. The researchers suggest that alterations in fats (especially cholesterol and ceramide) may contribute to a "neurodegenerative cascade" that destroys neurons in Alzheimer's, and that the accumulation of ceramide and cholesterol is triggered by the oxidative stress brought on by the presence of the toxic beta amyloid peptide. The study also suggests a reason for why antioxidants such as vitamin E might delay the onset of Alzheimer's: treatment with Vitamin E reduced the levels of ceramide and cholesterol, resulting in "a significant decrease in the number of neurons killed by the beta amyloid and oxidative stress.

Reference: 

Cutler, R.G., Kelly, J., Storie, K., Pedersen, W.A., Tammara, A., Hatanpaa, K., Troncoso, J.C. & Mattson, M.P. 2004. Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease. PNAS, 101, 2070-5.

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Using vitamin E and C supplements together may reduce risk of Alzheimer's

January, 2004

A study involving 4,740 elderly (65 years or older) found the greatest reduction in both prevalence and incidence of Alzheimer's in those who used individual vitamin E and C supplements in combination, with or without an additional multivitamin. There was no significant benefit in using vitamin C alone, vitamin E alone, or vitamin C and multivitamins in combination.

Reference: 

Zandi, P.P., Anthony, J.C., Khachaturian, A.S., Stone, S.V., Gustafson, D., Tschanz, J.T., Norton, M.C., Welsh-Bohmer, K.A. & Breitner, J.C.S. 2004. Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements: The Cache County Study. Archives of Neurology, 61, 82-88.

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Dietary supplements offer new hope for Alzheimer's patients

April, 2006

A "cocktail" of dietary supplements (omega-3 fatty acids, uridine and choline) has been found to dramatically increase the amount of membranes that form brain cell synapses in gerbils. The treatment is now in human clinical trials. It is hoped that such treatment may significantly delay Alzheimer's disease. The treatment offers a different approach from the traditional tactic of targeting amyloid plaques and tangles. Choline can be found in meats, nuts and eggs, and omega-3 fatty acids are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Uridine, which is found in RNA and produced by the liver and kidney, is not obtained from the diet, although it is found in human breast milk.

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Circadian clock may be critical for remembering what you learn

October, 2008

We know circadian rhythm affects learning and memory in that we find it easier to learn at certain times of day than others, but now a study involving Siberian hamsters has revealed that having a functioning circadian system is in itself critical to being able to remember. The finding has implications for disorders such as Down syndrome and Alzheimer's disease. The critical factor appears to be the amount of the neurotransmitter GABA, which acts to inhibit brain activity. The circadian clock controls the daily cycle of sleep and wakefulness by inhibiting different parts of the brain by releasing GABA. It seems that if it’s not working right, if the hippocampus is overly inhibited by too much GABA, then the circuits responsible for memory storage don't function properly. The effect could be fixed by giving a GABA antagonist, which blocks GABA from binding to synapses. Recent mouse studies have also demonstrated that mice with symptoms of Down syndrome and Alzheimer's also show improved learning and memory when given the same GABA antagonist. The findings may also have implications for general age-related cognitive decline, because age brings about a degradation in the circadian system. It’s also worth noting that the hamsters' circadian systems were put out of commission by manipulating the hamsters' exposure to light, in a technique that was compared to "sending them west three time zones." The effect was independent of sleep duration.

Reference: 

[688] Ruby, N. F., Hwang C. E., Wessells C., Fernandez F., Zhang P., Sapolsky R., et al.
(2008).  Hippocampal-dependent learning requires a functional circadian system.
Proceedings of the National Academy of Sciences. 105(40), 15593 - 15598.

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