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Posts Tagged ‘Alzheimer’s’

alzheimer's HealthDay (10/12, Preidt) reported that, according to a study published in the Oct. issue of the Archives of Neurology, “the ability to perceive relationships between objects (visuospatial skills) may decline years before a person is diagnosed with Alzheimer’s disease.” In a study population of 444 people, researchers from the University of Kansas “used data from…cognitive assessments to chart declines in various areas before participants were diagnosed with dementia. They found an inflection point (sudden change to a steeper slope of decline) in visuospatial abilities three years before clinical diagnosis of dementia.” After that, “declines in overall cognition occurred the next year, while inflection points for verbal and working memory weren’t seen until one year before diagnosis.”   The UK’s Telegraph (10/13, Devlin) quotes the authors as saying that “research into early detection of cognitive disorders using only episodic memory tasks, such as word lists or paragraph recall, may not be sensitive to either all of the earliest manifestations of disease or the most rapidly changing domain.”

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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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On its front page, the New York Times (4/6, A1, Carey) reports that researchers at the SUNY Downstate Medical Center, in Brooklyn, NY, have found an experimental medication that appears to block “the activity of a substance that the brain apparently needs to retain much of its learned information. And, if enhanced, the substance could help ward off dementias and other memory problems.” To date, the team has worked only with animals, but “scientists say this memory system is likely to work almost identically in people.” Previous research has indicated that the “brain appears to retain a memory by growing thicker, or more efficient, communication lines between” its cells. The Brooklyn team found that a substance called PKMzeta appears to be responsible for this communication. When animals are “injected directly into their brain with a drug called ZIP that interferes with PKMzeta,” they appear to forget memories, even strong ones of pain or disgust. To date, “researchers have already tried to blunt painful memories and addictive urges using existing drugs; blocking PKMzeta could potentially be far more effective.”

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Researchers say nicotine patch may help improve memory in patients with MCI. Medscape (3/11, Cassels) reported, “Transdermal nicotine treatment may help improve memory in patients with amnestic mild cognitive impairment (MCI),” according to a new study. The “large, double-blind, multicenter pilot study” which was presented at a psychiatric association’s meeting recently suggests “that nicotine patches improve attention, memory, and speed, with several other measures showing strong trends toward improvement.” For the study, which was funded by the National Institute on Aging (NIA), researchers “recruited 74 nonsmoking subjects who met the criteria for amnestic MCI.” Subjects were “randomized to receive either a double-blind nicotine or placebo patch for the first 6 months of the study, followed by a 6-month crossover phase in which all subjects received active treatment.” The researchers said, “We found that over a 6-month period, 23 percent of those in the treatment group vs 9 percent of subjects in the placebo group were improved on the global assessment. This just missed statistical significance, but we believe this is because the study was slightly underpowered to detect statistical significance.”

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HealthDay (2/25, McKeever) reported that a study published in the Feb. 24 edition of Cerebral Cortex suggests that “memories and emotions that people associate with familiar songs can be traced to the medial prefrontal cortex, a part of the brain where the wiring for memories and thoughts about music appears to be linked.” The finding might “explain why people with Alzheimer’s disease display strong emotional response to songs. This section of the brain is among the last to be affected by the neurological disease.” For the study, researchers “had 13 university students listen to excerpts of popular songs from their childhood while recording their brain activity using functional magnetic resonance imaging, or fMRI.” The team found that the music that “evoked the strongest memories” and “brought about the most emotion responses” in the students also were the “ones that the fMRI scans revealed as causing the most activity in the medial prefrontal cortex.” Researchers hope the “finding could be a jumping off point for developing a musical therapy to help people with Alzheimer’s.”

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HealthDay (2/8, McKeever) reported that, according to a study published in the Feb. 8 issue of Nature Medicine, “a naturally occurring brain protein” called brain-derived neurotrophic factor (BDNF) “appears able to slow or stop Alzheimer’s disease in recent studies done on animal models.” Working with rodents and monkeys, researchers from the University of California-San Diego School of Medicine found that when they “injected BDNF in lab animals that either were aged, had entorhinal cortex damage, or were genetically altered to have Alzheimer’s-like symptoms,” the “animals had improved memory and cognitive skills, and…cell degeneration and death was prevented or reversed.” In addition, “the animals receiving the treatment…began producing more BDNF on their own and exhibited better brain cell signaling and neuronal function, whereas the untreated animals degenerated further.” The authors posited that “since BDNF appeared both safe and effective on animal models, it could hold hope for treating Alzheimer’s disease in humans.”

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