Blood Pressure May Heighten Effects Of Alzheimer's

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Having hypertension, or high blood pressure, reduces blood flow in the brains of adults with Alzheimer's disease, according to a new study presented at the annual meeting of the Radiological Society of North America (RSNA).

"While hypertension is not a cause of Alzheimer's disease, our study shows that it is another hit on the brain that increases its vulnerability to the effects of the disease," said study co-author Cyrus Raji, scientist and M.D. and Ph.D. candidate at the University of Pittsburgh where the study was conducted.

Hypertension is a condition in which the blood circulates through the arteries with too much force. According to the National Heart, Lung and Blood Institute, approximately 50 million Americans have hypertension. People with hypertension are at elevated risk for heart attack, stroke and aneurysm. Recently, there has been mounting evidence tying cardiovascular health to brain health.

"This study demonstrates that good vascular health is also good for the brain," said co-author Oscar Lopez, M.D., professor of neurology and psychiatry at the University of Pittsburgh. "Even in people with Alzheimer's disease, it is important to detect and aggressively treat hypertension and also to focus on disease prevention."

For the study, the researchers used arterial spin-labeled magnetic resonance imaging (MRI), which can measure blood flow in the brain, to image 68 older adults. Arterial spin-labeled MRI is a novel, noninvasive technique that requires no external contrast agent.

The patient group included 48 normal individuals, including 38 with hypertension and 10 without; 20 Alzheimer's patients, including 10 with hypertension and 10 without; and 20 adults with mild cognitive impairment, 10 with hypertension and 10 without. Mild cognitive impairment, which affects brain functions such as language, attention and reasoning, is a transition stage between normal aging deficits in the brain and greater levels of dementia.

The MRI results showed that in all patient groups blood flow in the brain was substantially decreased in patients with hypertension compared to those without. Cerebral blood flow was lowest among the Alzheimer's patients with hypertension, but the normal group with hypertension showed significantly lower cerebral blood flow than the normal group without hypertension.

"These results suggest that by changing blood flow to the brain, hypertension -- treated or untreated -- may contribute to the pathology of Alzheimer's," Raji said. http://www.worldhealth.net

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Progesterone and Alzheimer's Disease

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The first study on progesterone and Alzheimer's disease has found no clear preventive benefit for the widely prescribed hormone in an animal model. Progesterone is given with estrogen in hormone replacement therapy. Previous studies have suggested that estrogen offers women some protection against Alzheimer's disease. The study's authors, led by gerontologist Christian Pike of the University of Southern California, asked if the same could be true of progesterone.

In a study highlighted in this week's issue of the Journal of Neuroscience, Pike's group reports that progesterone has only limited benefit for mice with Alzheimer's symptoms when taken alone. When taken with estrogen, progesterone actually inhibits some of the other hormone's beneficial effects, the study found.

The problem is not necessarily progesterone itself, Pike said. It could be the constant daily dosage, which fails to replicate the pre-menopausal body's natural cycles of hormone production. "This is probably not the best way to be delivering progesterone," Pike said. "Giving a constant dose of progesterone appears to antagonize a lot of the beneficial effects of estrogen." Pike's group tested progesterone on female mice whose hormone production had been blocked to simulate menopause. The mice, which were genetically predisposed to develop an Alzheimer's-like disease, showed symptoms within months.

Treatment with estrogen reversed the symptoms, Pike's group reported. Treatment with progesterone did not. When the two hormones were given together, progesterone appeared to hinder estrogen's main beneficial function: preventing the buildup of beta amyloid protein, the key risk factor in Alzheimer's. "Estrogen no longer decreases the amount of beta amyloid" when progesterone is present, Pike said.

Progesterone's effects were not all bad, Pike added. The hormone appeared to inhibit tau hyperphosphorylation, another chemical process implicated in Alzheimer's. Progesterone also is known to counteract the increased risk of endometrial cancer from estrogen therapy, which is one reason most women receive both hormones.

Pike said his group's study should provide guidance for the design of human trials studying hormone therapy and Alzheimer's. He added that future studies might need to focus both on the dosage and the formulation of progestins -- the synthetic versions of progesterone given to humans -- as well on the starting age for hormone therapy. Prior to the study, "we really had no idea what the progestins were doing," Pike said. The study was funded by the National Institute on Aging under a large grant to USC's Roberta Brinton, (Progesterone in Brain Aging and Alzheimer's Disease), who is leading a university-wide effort to study the effects of hormone therapy on women's health.

Doctors prescribe hormone therapy to counter some of the harmful consequences of menopause, such as losses in bone density. But other large studies have shown that hormone therapy also increases the risk of breast cancer. http://www.worldhealth.net

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New brain connections and improves cognitive function

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MIT researchers have shown that a cocktail containing three compounds normally in the blood stream promotes growth of new brain connections and improves cognitive function in rodents. The treatment is now being tested in Alzheimer's patients and could hold promise for other brain diseases and injuries.

The mixture, which includes a type of omega-3 fatty acid, is part of a new approach to attacking Alzheimer's. That approach focuses on correcting the loss of synapses, or connections between neurons, which characterizes the disease. For the past 30 years, researchers have tried targeting the clumps of misfolded proteins, known as amyloid beta plaques, found in the brains of Alzheimer's patients. However, that approach has not yielded any effective treatments for the disease, which affects an estimated four million to five million Americans.

"It's been very frustrating," said Richard Wurtman, the Cecil H. Green Distinguished Professor of Neuropharmacology and senior author of a paper on the new work published in the November issue of Brain Research. "Nobody has demonstrated that if you prevent formation of the amyloid, people get better." In December, a group of Alzheimer's researchers, including Wurtman, will participate in a symposium with the goal of developing a public policy to promote new approaches to Alzheimer's research. Organizers of the symposium believe that the current system of dementia research is "broken" and needs to be fixed.

Alzheimer's researchers agree that the cognitive decline seen in Alzheimer's patients is caused by loss of brain synapses. Wurtman and others theorize that restoring some of those synapses could provide an effective treatment, analogous to giving L-dopa to Parkinson's patients. Such treatments don't cure the disease but can restore significant brain function, said Wurtman. Synapses, where information is passed between neurons, play a critical role in learning and memory. Messages travel from a presynaptic neuron to a postsynaptic cell. In the Brain Research paper, the MIT team reported that rodents given a cocktail of DHA (a type of omega-3 fatty acid), uridine and choline showed a greatly increased concentration of dendritic spines, which receive messages in the postsynaptic neuron. That indicates that synapse regeneration has occurred, which is unusual, Wurtman said. Synapse regrowth could also prove an effective treatment for other brain diseases, such as Parkinson's, or for brain injuries, he said.

The researchers found that rodents who received the treatment performed much better on tests of cognitive ability (specifically, navigating a water maze). Sarah Holguin, an MIT graduate student in brain and cognitive sciences, presented those results at the Society for Neuroscience annual meeting earlier this month. Some of the rats in the studies received all three compounds and some received only one. The improvements in synapse growth and cognitive ability were greatest in the rats given all three.

Omega-3 fatty acids are not produced in the body but are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Choline can be synthesized in the body and obtained through the diet; it is found in meats, nuts and eggs. Uridine cannot be obtained from food sources, but is a component of human breast milk and can be produced in the body. The cocktail of compounds is now in clinical studies in Europe. http://www.worldhealth.net

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The door to new treatments for Alzheimer's

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For unknown reasons a protein called amyloid beta aggregates into toxic plaques in the brain, killing neurons. These plaques are one of the hallmarks of Alzheimer's disease. Now two new animal studies show for the first time that the deadly transformation of amyloid beta into plaques can be prevented through an interaction between amyloid beta and another protein called cystatin C.

Although much work needs to be done, these new findings may open the door to new treatments for Alzheimer's disease that mimic the effects of cystatin C, says Efrat Levy, Ph.D., Associate Professor in the Departments of Psychiatry and Pharmacology at New York University School of Medicine, and the lead author of the study. "We are really excited by these findings because recent studies show that cystatin C is protective against a variety of insults that cause cell death in the brain. Our potential therapeutic approach focuses on keeping amyloid beta in a water soluble form, preventing its accumulation in the brain, and thus slowing, halting, or reversing disease progression," says Dr. Levy, who is also Director of the Laboratory of Molecular Pathology of Cerebral Amyloidosis at the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, New York.

With support from the Alzheimer's Association, Dr. Levy's laboratory has already begun studies to develop a drug that will mimic the ability of cystatin C to bind to a non-pathological form of amyloid beta and thereby prevent its accumulation into plaques in the brain.

Alzheimer's is estimated to affect 5 million Americans and there are no medicines that can delay or prevent the disease. Many laboratories worldwide are pursuing ways to prevent the clumping of amyloid beta as possible therapies for the disease. It isn't known whether the protein actually causes Alzheimer's, but amyloid beta is one of the proteins implicated in the disease process.

The two studies appear in the on-line November 18, 2007, edition of the journal Nature Genetics and will be published in its December 2007 issue.

The first study was performed by Dr. Levy in collaboration with other investigators at the Nathan S. Kline Institute for Psychiatric Research and New York University School of Medicine. The second study was performed by Dr. Levy and colleagues in the laboratory of Dr. Mathias Jucker at the Hertie-Institute for Clinical Brain Research in Tubingen, Germany.

Both studies used mice that were genetically engineered to produce human cystatin C as well as abundant amounts of amyloid beta plaques in their brains. The cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice and inhibited the aggregation and deposition of amyloid beta plaques in the brain.

The research shows that cystatin C binds soluble amyloid beta also in the human brain, and suggests that this binding inhibits its aggregation into insoluble plaques in humans, says Dr. Levy. Cystatin C production and body fluid levels vary among healthy individuals and can be influenced by certain hormones, aging, and certain pathological conditions, she says. Furthermore, it was recently demonstrated that a genetic variation in the cystatin C gene in human populations is linked to a greater risk of developing Alzheimer's disease during aging.

These findings suggest, says Dr .Levy, that even subtle modifications of cystatin C protein levels could affect amyloid beta accumulation and deposition in the brain, thereby modifying disease progression.

Cystatin C is found in all body fluids and tissues of mammals. It is a jack-of-all-trades, playing a broad role in many functions, including cell proliferation and growth, modulation of the inflammatory response, and bone resorption. The protein also has been implicated in neuronal degeneration and repair of the nervous system. http://www.worldhealth.net

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New Alzheimer's Gene

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A variant of the gene CDC2 could possibly be used as a risk marker for Alzheimer's disease. The gene variant is considerably more common among Alzheimer's patients. This is shown in a dissertation from the Sahlgrenska Academy at Goteborg University in Sweden.

Alzheimer's disease has several different causes. Since many patients have a close relative who also developed the disease, heredity is believed to be one of the most important factors.

"There is a previously identified Alzheimer's gene that indicates an elevated risk of developing the disease, but we want to find more genes with a strong connection to Alzheimer's. The earlier we can predict that a patient risks developing the disease, the better health care providers can prevent and treat it," says the research Annica Sjolander.

In her dissertation, Annica Sjolander studied different variants of a gene called CDC2. DNA analyses of blood samples from both patients and healthy individuals showed that one gene variant was considerably more common among patients with Alzheimer's disease.

"This is the first discovery of a connection between this specific gene and Alzheimer's. The findings must be confirmed in several other studies before we can be absolutely certain that it is a new Alzheimer's gene that we have found," explains Annica Sjolander.

In the study this gene variant was found in roughly half of all patients with Alzheimer's, compared with 35 percent of the healthy control group.

The dissertation shows that patients with Alzheimer's disease who were carriers of the gene variant also had higher levels of the protein tau, which is associated with the disease. In patients with the disease the mean level of tau in the spinal marrow fluid is about three times higher than the level in healthy individuals of the same age.

The gene CDC2 is responsible for one of the phases when a cell divides and is only active when cell division is in progress. Other research has shown that CDC2 in Alzheimer's patients is turned on inside nerve cells where cell division does not normally take place.

"No one knows why the gene is activated, but it may be the result of a defect in the gene. It is also possible to speculate that the body is perhaps trying to compensate for lost nerve cells by having nerve cells divide," says Annica Sjolander. http://www.worldhealth.net

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