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Archive for the ‘Alzheimer’s’ Category

bacteria and virusThe UK’s Daily Mail (8/18, Dobson) reports that researchers say some mental illnesses or conditions “might have links to viruses or bacteria.” For example, “streptococci bacteria, which [cause] many sore throats,” may “play a role in the development of OCD” when, “in some people, the antibodies produced to attack the bacteria home in on the brain, causing changes in behavior.” Another study indicated that “children born to mothers who had a herpes infection during pregnancy were six times more likely to get schizophrenia.” Now, some researchers even theorize that “herpes simplex, the cold sore virus, is a major cause of the protein plaques found in the brains of Alzheimer’s sufferers.” Professor Ruth Itzhaki, of Manchester University, explained, “It’s thought the virus enters the brain in the elderly as their immune systems decline and is the activated by events, such as stress. This causes severe damage in brain cells, most of which disintegrate, releasing amyloid aggregates which develop into amyloid plaques.”

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sleepyThe UK’s Daily Mail (8/13) reports that, according to a study published in the Sept. issue of the European Journal of Neurology, elderly people “who sleep for more than eight hours a day are twice as likely to develop Alzheimer’s.” Moreover, “the danger affects both those who enjoy regular lie-ins in the morning and those who take naps in the afternoon.” For the study, researchers from Spain’s University Hospital of Madrid looked at “3,286 men and women aged 65 or over,” each of whom “was asked about their health and lifestyle, such as how many hours of sleep they averaged over a 24-hour period, including afternoon naps.” After following participants “for more than three years, during which 140 went on to develop Alzheimer’s or another form of dementia,” the investigators found that “those who averaged more than eight or nine hours of sleep a day were twice as likely to have developed dementia.”

The UK’s Daily Telegraph (8/12, Hagan) reported that the reason for the study’s findings remain “unclear, but researchers believe excessive sleep could be an early sign of” dementia. It is “also possible that staying in bed is a sign of depression, a known risk factor for dementia in the elderly.” The study authors “are urging doctors to be on the lookout for long sleep as a warning that a patient is at risk.”

 According to the New York Daily News (8/13, Hazlett), Dr. Susanne Sorenson, of the UK’s Alzheimer’s Society, called for “more research…to investigate the results of the study.” Dr. Sorenson stated, “There is no apparent physiological link, and it is unlikely that sleeping more than normal is a direct risk factor for dementia; it may simply be an early sign of a yet undiagnosed condition.”

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 The San Diego Tribune (8/10, LaFee http://tinyurl.com/alzheimers-gene-therapy) reports that “researchers at the University of California-San Diego” are “seeking qualified study volunteers” in preparation for launching “the second-phase clinical trial (http://tinyurl.com/NGF-alzheimers-phaseII-study) of a promising gene therapy for Alzheimer’s disease.” In previous “animal and human safety trials, a gene therapy” medication “called CERE-110 was injected into patients’ brains, initially via modified skin cells, later using a harmless viral carrier. CERE-110 carries a gene that promotes long-term production of nerve growth factor (NGF), a natural molecule that helps brain cells live and function longer.” The new “phase 2 trial will be conducted at 12 US sites” and will “involve…volunteers between the ages of 50 and 80 with mild to moderate Alzheimer’s symptoms.” During the “randomized,” blind study, “half of the participants” will receive “CERE-110, and the other half” will get “a placebo.” After completion of the study “in 2012…participants in the placebo group will be eligible to be treated with CERE-110,” should the phase II results be promising.

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mcFollowing a HealthDay story, Medscape (7/27, Gandey) reported that, according to a study published in the July 22/29 issue of the Journal of the American Medical Association, “several cerebrospinal-fluid biomarkers have shown accuracy in identifying patients with mild cognitive impairment who went on to develop Alzheimer’s disease (AD).” For the study, researchers from Sweden’s Sahlgrenska University “identified biomarker cutoff levels in patients with AD and controls,” then “evaluated patients with cognitive impairment from 12 centers in the United States and Europe.” In their study of “750 patients with mild cognitive impairment , 529 with AD, and 304 controls,” the team “followed patients with mild cognitive impairment for at least two years or until symptoms had progressed to clinical dementia.” The investigators found that “patients who developed AD had lower median levels of Aß42, higher levels of tau phosphorylated at position threonine, and higher total tau protein levels than patients who did not develop AD.” An accompanying editorial suggested that the study represented “a major step forward.”

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WebMD (7/16, Laino) reported that, according to a study presented at an international conference on Alzheimer’s, taking the nonsteroidal anti-inflamalzmatory medication (NSAID) “naproxen cuts the risk of developing Alzheimer’s disease by two-thirds. Celebrex [celecoxib] also appeared to help brain function, though that finding could have been due to chance.” For the study, researchers from the University of Washington-Seattle performed a “follow-up analysis” of data and participants in the “large Alzheimer’s Disease Anti-inflammatory Prevention Trial, in which healthy people were randomly assigned to take naproxen, Celebrex, or a placebo,” with the goal of determining “if taking NSAIDs could prevent Alzheimer’s.” The investigators discovered that “many of the people taking NSAIDs who developed Alzheimer’s disease early on had undiagnosed mild cognitive impairment, or memory loss, when they entered the study.” Therefore, the authors concluded that while “NSAIDs are harmful to people who already have signs and symptoms of mental decline,” for those “with healthy brains, NSAIDs appear to protect against the development of Alzheimer’s disease.”

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alzWebMD (7/14, Laino) reported that, according to a study presented at an international conference on Alzheimer’s, the “Dietary Approaches to Stop Hypertension (DASH) diet,” a “low-fat, high-fiber diet recommended for lowering blood pressure, may help prevent memory loss and sharpen mental skills.” For the study, researchers at Utah State University analyzed data on “3,831 people 65 and older with no signs of dementia.” At study start, participants “filled out a 142-item food questionnaire asking what they ate and how often they ate it. Based on their adherence to the components of the DASH diet, the participants were divided into five groups, or quintiles.” The investigators found that “those in the highest quintile had the best cognitive functioning at the beginning of the study and the least decline in mental skills over time.” The authors said that “the best foods at curbing mental decline” included “vegetables, whole grains, low-fat dairy products, and nuts and legumes.”

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BBC News (7/5) reported that, according to a mouse study published in the July 5 online edition of the Journal of Alzheimer’s Disease, “drinking five cups of coffee a day could reverse memory problems seen in Alzheimer’s disease.” For the study, researchers from the University of Florida studied “55 mialzce…bred to develop symptoms of Alzheimer’s disease (AD)” and found that “caffeine hampered the production of the” beta-amyloid “protein plaques which are the hallmark of” AD. The team used “behavioral tests to confirm the mice were exhibiting signs of memory impairment when they were aged 18 to 19 months, the equivalent to humans being about 70,” then “gave half the mice caffeine in their drinking water. The rest were given plain water.” The animals received “the equivalent of five 8 oz. (227 grams) cups of coffee a day — about 500 milligrams of caffeine.”
        The UK’s Telegraph (7/5) explained that “at the end of the two-month study, the caffeine-drinking mice performed far better on tests of memory and thinking than mice given only water.” In fact, “their memories were as sharp as those of healthy older mice without dementia.” For humans, the “equivalent dose for their body weight would be consuming 500 milligrams of caffeine a day, equivalent to five cups of ordinary coffee,” which is “the same amount of caffeine can be obtained by drinking two cups of strong coffee, 14 cups of tea, or 20 cola drinks.”
        HealthDay (7/5, McKeever) pointed out that, according to the study’s authors, “consuming 500 milligrams of caffeine a day would not cause ill effects for most people,” but “people with high blood pressure or who are pregnant need to limit their caffeine intake.” Notably, the study authors “also found that caffeine did not improve the memory of normal mice as it did for the Alzheimer’s mice.” They concluded, “This suggests that caffeine will not increase memory performance above normal levels. Rather, it appears to benefit those destined to develop Alzheimer’s disease.”

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lovaHealthDay (6/30, West) reported that, according to a study published in the June issue of the Journal of Alzheimer’s Disease, “treatment with a cholesterol-lowering” medication “might protect against Alzheimer’s disease.” For the study, researchers from the University of Groningen, the Netherlands, “conducted animal experiments in which they administered lovastatin (Altoprev, Mevacor) to overstimulated nerve cells.” The team found that “lovastatin did indeed prevent cell death and, just as important, blocked the loss of memory that accompanies excitotoxicity.” Previous research has demonstrated that “statins seem to stimulate the protective capacity of tumor necrosis factor, a key player in the brain’s immune response.” Furthermore, “some researchers have speculated that high cholesterol might be a risk factor for Alzheimer’s, suggesting that lowering cholesterol could be beneficial.”

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alzHealthDay (6/24, Preidt) reported that, according to a study published in the July issue of The Lancet Neurology, “biomarkers for Alzheimer’s disease can be detected in the cerebrospinal fluid in the very early stages of the disease.” For the study, researchers from Sweden’s University of Gothenburg “analyzed cerebrospinal fluid (CSF) samples from 168 patients and found the typical pattern of biomarkers known as the ‘CSF AD profile’ present in patients with mild memory problems, which is earlier than the illness could be detected by current tests.” In fact, “patients who had the typical changes in biomarker profile of the cerebrospinal fluid had a risk of deterioration that was 27 times higher than the control group,” the investigators found. In addition, the authors “found a relationship between the CFS AD profile and other typical signs of Alzheimer’s, including the presence of the gene APOE e4 and deterioration of the area of the brain that controls memory.”

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namMedscape (6/18, Jeffrey) reported that, according to a study presented at a Parkinson’s disease conference and published online June 9 in The Lancet Neurology, “patients with dementia associated with Parkinson’s disease (PDD) or dementia with Lewy bodies (DLB) may benefit from treatment with memantine,” a medication that is “already approved for use in moderate to severe Alzheimer’s disease.” Researchers from the Norwegian Center for Movement Disorders at Stavanger University Hospital conducted a “parallel-group, 24-week randomized and placebo-controlled pilot study that included 75 patients with PDD and DLB from four centers in Sweden, Norway, and the United Kingdom.” Patients “were randomized to receive either 20 mg per day of memantine or placebo.” At study end, the team found “a significant difference between groups…on the CGIC, with a mean difference of 0.7 points (95 percent CI, 0.04 – 1.39; P = .03).”

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