Publications relating to dementia and blood pressure have been reviewed by the paper’s author Dr Sven Kurbel of the Osijek Medical Faculty in Croatia. The cognitive problems suffered by some Alzheimer’s patients have previously been put down to low blood pressure (arterial hypotension). The hypothesis put forward by Dr Kurbel is that the opposite is true. He suggests that as the patient’s memory fails, they forget the causes of anxiety and worry that was causing high blood pressure: failing memory causes hypotension, not vice versa.

Hypertension itself is a cause of disease, including strokes, so paradoxically, Dr. Kurbel’s hypothesis suggests, treatments which alleviate memory loss could affect other causes of illness. If this hypothesis is correct it could have a significant effect on the treatment of conditions such as metabolic syndrome, which involves increased weight and high blood pressure. Dr. Kurbel concludes that “An important question is would reduction of stressful memories and of stress exposure in everyday life help diminish the risk of getting hypertension or metabolic syndrome in the years to come.”

If confirmed by further studies, this will affect how doctors treat the elderly, helping to target drugs more effectively and reduce risks of stokes and heart attack It also suggests that heart disease could be substantially reduced in old people simply by making them happier about themselves and their lives.

Dr. William Bains, editor of Bioscience Hypotheses, said “This is a fascinating piece of lateral thinking, one with real health implications, and just the sort of stimulating, practical idea that we hoped Bioscience Hypotheses would be able to publish for other scientists to think about”.

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Aisen is director of the Alzheimer’s Disease Cooperative Study (ADCS), a multi-center network spanning the United States and Canada, which conducted the clinical trial to determine if reduction of an amino acid called homocysteine would reduce the risk of Alzheimer’s disease or slow its progression. Homocysteine is known to be involved in neurological disease, including Alzheimer’s, and its metabolism is affected by B vitamins. Therefore, it was thought that B vitamin supplements might offer a new therapeutic approach in treating Alzheimer’ disease.

“Prior studies using B vitamin supplementation to reduce homocysteine levels in patients with Alzheimer’s weren’t large enough, or of long enough duration to effectively assess their impact on cognitive decline,” said Aisen. “This study of several hundred individuals over the course of 18 months showed no impact on cognition, although it resulted in lower levels of homocysteine in these patients.”

The study included supplementation with folic acid and vitamins B6 and B12 for 18 months in 409 individuals with mild to moderate Alzheimer’s disease. Participants were randomly assigned to two groups of unequal size; to increase enrollment, 60 percent were treated with high-dose supplements and the remaining 40 percent treated with identical dosages of placebo. A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Cognitive abilities were measured via testing with the Alzheimer Disease Assessment Scale (ADAS-cog).

The researchers found that the ADAS-cog score did not differ significantly between treatment groups, but that symptoms of depression were more common in the high-dose supplement group.

“Our study does not support the treatment of individuals with mild to moderate Alzheimer’s disease and normal vitamin levels with B vitamin supplements,” the authors conclude.

The ADCS, a consortium of more than 50 research institutions in the United States and Canada, is headquartered at UC-San Diego and funded by the National Institute on Aging (NIA), part of the National Institutes of Health.
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The study, led by NC State psychology Ph.D. student Alyssa A. Gamaldo, shows that older African-Americans who reported having trouble falling asleep tended to do much worse on memory tests than those study participants who did not have trouble falling asleep. Gamaldo says that the difference was particularly apparent in tests related to “working memory,” which is the ability to multitask or do two things at once. The study examined 174 subjects between the ages of 65 and 90.

Gamaldo says the findings raise additional questions, which will have to be addressed in future research. For example, Gamaldo says, “it is not clear if lack of sleep is the issue. Is it the quantity of sleep, the quality of sleep, or something else altogether?”

The study raises questions for future research on both sleep and cognitive functioning in the elderly. The findings indicate that sleep may need to be accounted for as a confounding variable in cognition studies targeting seniors. In addition, the findings show that sleep research may need to increase its focus on older adults in order to fully explore the impacts of sleep problems on cognition in seniors.

“If we can better understand how sleep quantity, as well as quality, influences general cognitive functioning, perhaps we could better maintain memory throughout life – including later in life,” Gamaldo says.
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Researcher Marian L. Evatt, M.D., M.S. (Emory University School of Medicine, Atlanta) and colleagues write that, “Vitamin D is important for maintaining many physiologic functions, and vitamin D deficiency is associated with increased risk of disease.” Further, risk factors for vitamin D insufficiency – such as advancing age, obesity, avoidance of sun exposure, residence in northerly latitudes, and darker skin – are commonly observed in patients with chronic neurodegenerative diseases like Parkinson’s and Alzheimer’s diseases.

To investigate the relationship between vitamin D levels and neurodegenerative diseases, Evatt and colleagues studied 100 patients with Parkinson’s disease, 97 Alzheimer’s disease patients, and 99 healthy individuals. Participants were matched for age, sex, race, genotype and geographic location.

The researchers found that, “Significantly more patients with Parkinson’s disease (55 percent) had insufficient vitamin D than did controls (36 percent) or patients with Alzheimer’s disease (41 percent).” Parkinson’s disease patients had an average of 31.9 nanograms per milliliter vitamin D concentration, and Alzheimer’s disease patients and healthy group individuals had concentrations of 34.8 and 37 nanograms per milliliter, respectively – significantly high concentrations of vitamin D than the Parkinson’s patients.

“These findings support the previously suggested need for further studies to assess what contribution a low 25(OH)D [a measure of blood vitamin D levels] concentration adds to the risk of developing Parkinson’s disease (vs. other neurodegenerative disorders) and to determine whether correction of vitamin D insufficiency and deficiency will improve motor or non-motor symptoms in Parkinson’s disease,” conclude Evatt and colleagues.

They add: “Finally, the finding of a high incidence of vitamin D deficiency in the Parkinson’s disease and other cohorts highlights the importance of routinely checking the level of 25(OH)D, particularly in elderly patients, since deficiency is strongly correlated with a higher incidence of osteoporosis, falls and hip fractures and has been associated with a higher incidence of several forms of cancer and autoimmune disorders.”
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“There are many things like heredity that are outside our control, but there are also concrete steps we can take to maintain optimal brain health,” says Marwan Sabbagh, MD, FAAN, a leading Alzheimer’s researcher and physician who has written extensively on the disease. “The time to think about this is long before memory problems start.”

Dr. Sabbagh has looked exhaustively at published research on Alzheimer’s disease and brain health, and he has identified a number of important factors in maintaining cognitive wellness. Among the modifiable risk factors for Alzheimer’s are hypertension (high blood pressure), high cholesterol, high homocysteine levels, diabetes-elevated insulin levels, and obesity, especially during midlife.

There is also evidence that dietary modifications can help maintain cognitive wellness. Combing through published research on the topic, Dr. Sabbagh has identified a group of nutrients that have strong evidence of protective effects.

“The use of these nutrients to support cognitive wellness is well documented in the scientific literature,” says Dr. Sabbagh. “The JAMA article underscores the need to consider supplementation long before disease starts.”

To help American consumers make good supplement choices, Dr. Sabbagh worked with AmeriSciences, a leading science-based nutraceutical company, to develop a formulation that includes ingredients with strong scientific merit. AmeriSciences’ Cognivite Complete was specially formulated under Dr. Sabbagh’s guidance to provide nutritional support to help combat declining mental function and memory loss associated with aging. Dr. Sabbagh’s expertise in this area led AmeriSciences to recently appoint him to chair the company’s Scientific Advisory Board.

Cognivite Complete’s ingredients include: Gingko biloba; docosahexaenoic acid (DHA); turmeric root (curcumin); and phosphatidylserine. Gingko biloba helps maintain normal blood flow to the brain and is rich in flavonoid antioxidants, which may offer protection against neuron damage. Turmeric root, a common spice in Asia and a constituent of many curries, has been shown to exhibit a variety of protective effects in the brain, from stimulation of normal anti-inflammatory functions to the reduction of natural oxidative damage. DHA, an omega-3 fatty acid, is a vital component of the cell membranes of the brain. Studies suggest that it may help overall cognitive maintenance. Phosphatidylserine is a fat derivative (phospholipid) found in soybeans and other foods, which is involved in brain signal activity and is an important part of neuronal membranes.

According to Dr. Sabbagh’s research, a modest decline in cognitive health is an expected part of the aging process; however, this decline can be exacerbated by factors such as poor nutritional habits and stress. Through lifestyle modifications and a consistent nutritional regimen that includes supplementation, Dr. Sabbagh believes people can help preserve normal brain function and ensure cognitive wellness.

Dr. Sabbagh serves as Chief Medical-Scientific Officer and Director of Clinical Research at the Sun Health Research Institute, Sun City, Arizona.
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Publications relating to dementia and blood pressure have been reviewed by the paper’s author Dr Sven Kurbel of the Osijek Medical Faculty in Croatia. The cognitive problems suffered by some Alzheimer’s patients have previously been put down to low blood pressure (arterial hypotension). The hypothesis put forward by Dr Kurbel is that the opposite is true. He suggests that as the patient’s memory fails, they forget the causes of anxiety and worry that was causing high blood pressure: failing memory causes hypotension, not vice versa.

Hypertension itself is a cause of disease, including strokes, so paradoxically, Dr. Kurbel’s hypothesis suggests, treatments which alleviate memory loss could affect other causes of illness. If this hypothesis is correct it could have a significant effect on the treatment of conditions such as metabolic syndrome, which involves increased weight and high blood pressure. Dr. Kurbel concludes that “An important question is would reduction of stressful memories and of stress exposure in everyday life help diminish the risk of getting hypertension or metabolic syndrome in the years to come.”

If confirmed by further studies, this will affect how doctors treat the elderly, helping to target drugs more effectively and reduce risks of stokes and heart attack It also suggests that heart disease could be substantially reduced in old people simply by making them happier about themselves and their lives.

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http://www.livonnetwork.com
http://www.homehealthcareclassifieds.com
yo can post your blogs http://www.legacyblogs.com

The study, led by NC State psychology Ph.D. student Alyssa A. Gamaldo, shows that older African-Americans who reported having trouble falling asleep tended to do much worse on memory tests than those study participants who did not have trouble falling asleep. Gamaldo says that the difference was particularly apparent in tests related to “working memory,” which is the ability to multitask or do two things at once. The study examined 174 subjects between the ages of 65 and 90.

Gamaldo says the findings raise additional questions, which will have to be addressed in future research. For example, Gamaldo says, “it is not clear if lack of sleep is the issue. Is it the quantity of sleep, the quality of sleep, or something else altogether?”

The study raises questions for future research on both sleep and cognitive functioning in the elderly. The findings indicate that sleep may need to be accounted for as a confounding variable in cognition studies targeting seniors. In addition, the findings show that sleep research may need to increase its focus on older adults in order to fully explore the impacts of sleep problems on cognition in seniors.
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Aisen is director of the Alzheimer’s Disease Cooperative Study (ADCS), a multi-center network spanning the United States and Canada, which conducted the clinical trial to determine if reduction of an amino acid called homocysteine would reduce the risk of Alzheimer’s disease or slow its progression. Homocysteine is known to be involved in neurological disease, including Alzheimer’s, and its metabolism is affected by B vitamins. Therefore, it was thought that B vitamin supplements might offer a new therapeutic approach in treating Alzheimer’ disease.

“Prior studies using B vitamin supplementation to reduce homocysteine levels in patients with Alzheimer’s weren’t large enough, or of long enough duration to effectively assess their impact on cognitive decline,” said Aisen. “This study of several hundred individuals over the course of 18 months showed no impact on cognition, although it resulted in lower levels of homocysteine in these patients.”

The study included supplementation with folic acid and vitamins B6 and B12 for 18 months in 409 individuals with mild to moderate Alzheimer’s disease. Participants were randomly assigned to two groups of unequal size; to increase enrollment, 60 percent were treated with high-dose supplements and the remaining 40 percent treated with identical dosages of placebo. A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Cognitive abilities were measured via testing with the Alzheimer Disease Assessment Scale (ADAS-cog).

The researchers found that the ADAS-cog score did not differ significantly between treatment groups, but that symptoms of depression were more common in the high-dose supplement group.

“Our study does not support the treatment of individuals with mild to moderate Alzheimer’s disease and normal vitamin levels with B vitamin supplements,” the authors conclude.

The ADCS, a consortium of more than 50 research institutions in the United States and Canada, is headquartered at UC-San Diego and funded by the National Institute on Aging (NIA), part of the National Institutes of Health.
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“While there is much we don’t yet know about Alzheimer’s disease, tremendous progress has been made since 1983,” said James Wessler, President and CEO of the Alzheimer’s Association MA/NH Chapter. “In November we focus on raising awareness of Alzheimer’s disease and shedding light on the importance of finding breakthroughs in diagnosis, prevention, treatments and, eventually, a cure.” The Alzheimer’s Association will be offering educational programs throughout the state during the month of November. To find out what activities are planned in your area visit the Alzheimer’s Association

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A person with early onset Alzheimer’s may actually be in any stage of the disease – early, middle or late. Each stage is characterized by different symptoms. Symptoms range from mild confusion in the beginning of the disease to the inability to swallow, talk, and move on one’s own in the late stage. While more than 5 million people in the US have Alzheimer’s, an estimated 500,000 people in their 30s, 40s and 50s have it or a related dementia.

This first effort by the Alzheimer’s Association to provide a telephone-based support is open to anyone with a sibling who has early onset Alzheimer’s. Since the early onset disease has been shown to have genetic links, siblings are not only directly affected by the illness within their family; they are also at risk themselves. The continuing support group will run for eight sessions, by phone. Attendance will be limited in order to allow discussion.

“It’s a kind of double jeopardy that is especially difficult emotionally,” said Betsy Percoski, Vice President of Communications and Public Affairs at the Association’s MA/NH Chapter. “And when multiple siblings develop Alzheimer’s the toll is enormous. We are reaching out to them in a way that we hope will make information and resources more accessible.”

To kick off the call-in support group, the Alzheimer’s Association is hosting a free tele-education event on Wednesday, October 22nd at 7 p.m. The guest speaker will be Dr. Richard Mayeux, MD, Professor of Neurology and Epidemiology at Columbia University, Director of the Sergievsky Center, which is devoted to the epidemiological investigation of neurological diseases, and the Co-Director of the Taub Institute for Research on Alzheimer’s and the Aging Brain at Columbia University Medical Center. Dr. Mayeux will talk about genetics and risk of Alzheimer’s disease and his work with siblings of people with young onset Alzheimer’s. He will also take questions.

The phone event is free, but space is limited and a pass code is required to participate, so preregistration is required. For those interested, call the Alzheimer’s Association at 800-272-3900 to reserve a space and receive the toll-free number and a pass code to call in to the talk.
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