Three common vitamins—folic acid, B12, and B6—may be able to slow the progression of Alzheimer’s disease, according to the results of a pilot study led by Paul S. Aisen, MD, of Georgetown University. Researchers have discovered that high-dose vitamins reduce homocysteine in individuals with Alzheimer’s disease. “In our vitamin pilot study we have demonstrated that we are able to reduce levels of homocysteine using a vitamin regimen both safe and inexpensive. Now we are conducting a therapeutic trial to determine whether use of the vitamins folic acid, B12, and B6 to lower homocysteine level has a favorable impact on the course of the disease,” said Dr. Aisen. The multicenter vitamin study has begun recruiting patients across the country. The study was published in the March/April American Journal of Geriatric Psychiatry.

In nine patients who died of sporadic Creutzfeldt-Jakob disease, autopsy studies identified deposition of pathologic infectious prion protein (PrPSc) in the olfactory cilia and along the olfactory pathway, but not in the respiratory mucosa. No PrPSc was detected in any of the tissue samples from 11 controls. Reporting their findings in the February 20 New England Journal of Medicine, a group of Italian researchers concluded that the identification of prion protein in the neuroepithelium of the olfactory mucosa suggests that olfactory biopsy may provide diagnostic information in living patients. Currently, diagnosis requires examination of brain tissue.

The brains of children with dyslexia can be rewired—after undergoing intensive training—to function more like those in healthy readers, stated researchers in the March 4 Proceedings of the National Academy of Sciences. fMRI scans of the children with dyslexia who participated in the behavioral remediation showed increased activation in the left temporo-parietal cortex, left inferior frontal gyrus, right hemisphere frontal and temporal regions, and the anterior cingulate gyrus. These results suggest that a partial remediation of language-processing deficits, resulting in improved reading, ameliorates disrupted function in brain regions associated with phonological processing and produces additional compensatory activation in other brain regions.

The first reliable diagnostic test for myotonic muscular dystrophy type 2 (DM2) has been developed by researchers at the University of Minnesota Medical School’s Muscular Dystrophy Center. The findings, published in the February 26 Neurology, have led to the accurate determination of the disease’s clinical and molecular features and have indicated that DM2 is much more common than previously thought. After evaluating the genetic features of 379 individuals from DM2 families, researchers determined that the disease occurs in many families of Northern European ancestry. The investigators also noted that the clinical and molecular parallels between DM2 and myotonic dystrophy type 1 “indicate that the multisystemic features common to both diseases are caused by CUG or CCUG expansions expressed at the RNA level.”

The cost of treating multiple sclerosis is high, but it decreases with prolonged treatment, according to research in the March 8 BMJ. Researchers evaluated the cost-effectiveness of four drugs currently licensed for the treatment of multiple sclerosis in the United Kingdom (three interferon ßs and glatiramer acetate). They assessed the effect of each drug against conventional management during a 20-year period. The investigators calculated that the cost of each year of life saved or prolonged by using any of the four treatments ranged from approximately $66,469 to $156,800; price had a considerable effect on the cost-effectiveness for each drug. They emphasized, however, that uncertainty surrounding these estimates is substantial, largely due to the unpredictability of the disease and the difficulty in capturing all aspects of its impact on patients.

The modest sleep loss that results from going to bed an hour later than usual can compromise children’s alertness and brain functioning, reported a study in the March/April Child Development. Researchers studied the effects of adding or subtracting one hour of sleep on 77 children in the fourth and sixth grades. For the first two nights of the five-night study, the children adhered to their normal sleep pattern; for the last three nights, they either extended or reduced their sleep time by one hour. At the start and end of the study, the investigators gave the children several tests of neurobehavioral functioning. They found that sleep-deprived children’s performance on a reaction-time test suffered, and their performance on recall and responsiveness tests remained stable, while the children with the extra hour of sleep improved their performance on these tests.

A high-fat diet protects newborn brain cells from damage caused by prolonged seizures, according to a study in the February 28 online edition of Annals of Neurology. Researchers investigating the underlying protective mechanisms responsible for the immature brain’s remarkable resistance to seizure-induced excitotoxic cell death have found very high levels of mitochondrial uncoupling protein 2 (UCP2) in the brains of newborn rats. Further, they found that, unlike in the adult, seizures do not increase the formation of reactive oxygen species or result in mitochondrial dysfunction in the neonatal brain, presumably due to the high levels of UCP2, the production of which is increased by fatty acids.

People who describe themselves as highly stressed have a higher risk of fatal stroke than those who say they are stress free, according to a report in the March 14 rapid access Stroke. Investigators used data from the Copenhagen City Heart Study, which asked participants to report their stress intensity; in 13 years of follow-up, 22% of the participants had a fatal stroke. The risk of fatal stroke was 89% higher for those who reported a high level of stress compared with those who reported never having stress. The investigators speculated that the link may be due to the stressed people having cardiovascular risk factors; they tended to smoke, be less physically active, drink more alcohol, and be treated for high blood pressure.

Individuals who believe they can function well on six or fewer hours of sleep every night may be accumulating a sleep debt that could interfere with their normal cognitive abilities, stated a study in the March 15 Sleep. Investigators observed the effects of either four or six hours of nightly sleep on healthy volunteers during a two-week period. They compared the results of the participants’ accumulating performance deficits—determined by psychomotor vigilance and other cognitive tests—with similar test results obtained from participants who had gone without sleep for more than three nights. The first group of participants experienced increasing lapses in psychomotor vigilance, resulting in a decline of performance that matched that of those who went without sleep for 88 hours. Researchers found that chronically sleep-deprived individuals reported feeling only “slightly sleepy,” even when their performance was at its worst during standard psychological testing.

For older people with high blood pressure, a sharp increase in blood pressure in the morning is associated with an increased stroke risk independent of ambulatory blood pressure, nocturnal blood pressure falls, and silent infarct, according to a study in the March 18 Circulation. Researchers observed 519 patients (mean age, 72) with high blood pressure and divided them into two groups—the morning surge group (patients with a morning blood pressure increase of 55 mm Hg or greater) and the non–morning surge group (patients whose morning blood pressure increase was less than 55 mm Hg). The investigators found that participants in the morning surge group were more likely to have multiple silent strokes than were those in the non–morning surge group. They also determined that the relative risk of stroke for people with a morning surge was nearly three times higher than for those without the surge.

The malfunctioning of astrocytes may be responsible for the accumulation of amyloid protein in the brains of patients with Alzheimer’s disease, according to a report in the April Nature Medicine. Researchers noted that astrocytes ingest and degrade ß-amyloid after examining cultured brain tissue, observing that the astrocytes reduced the amount of ß-amyloid by 40% during a 24-hour period. The investigators suggested that while treatments to boost astrocyte activity in Alzheimer’s disease may be therapeutic, there are other astrocyte functions that may contribute to the disease. “Some people think that if the cells don’t migrate to plaques, the astrocytes may not release inflammatory molecules that damage the surrounding brain tissue,” stated Jens Husemann, MD, a researcher from Columbia University in New York City.

NR

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