Researchers can detect abnormalities in the brains of healthy adults in their 20s and 30s who are at a genetic risk for developing Alzheimer’s disease—decades before symptoms of the disease appear, according to a presentation made at the 8th International Conference on Alzheimer’s Disease and Related Disorders. A dozen healthy young adults who carry the apolipoprotein E (APOE) epsilon4 allele were compared to 15 young adults who do not carry the allele. Clinical ratings and neuropsychologic tests assessed the participants’ memory and thinking, and positron emission tomography imaging and brain mapping software were used to chart differences in brain activity. Although the young adults carrying the APOE epsilon4 allele performed normally on the memory and thinking tests, researchers found that they had abnormally low brain activity in the same regions of the brain as patients clinically diagnosed with Alzheimer’s disease.

Injections of botulinum toxin A reduce spasticity following a stroke, according to a study in the August 8 New England Journal of Medicine. In a randomized, double-blind study, researchers issued either a one-time injection of 200 to 240 units of botulinum toxin A or a placebo into the wrists or fingers of 122 subjects with post-stroke spasticity. Each subject was asked to choose among personal hygiene, dressing, pain, and limb position as the primary outcome measure. Six weeks following treatment, 62% of the subjects given the botulinum toxin reported improvement in the principal target of treatment, compared with 27% of the placebo group. In addition, 83% of the subjects who received injections of botulinum toxin A had at least a 1-point improvement in the Disability Assessment Scale, compared with 53% of the placebo group.

Researchers have determined that brain damage after coronary artery bypass grafting (CABG) is associated with a transient metabolic neuronal disturbance. Thirty-five patients undergoing elective CABG were included in this study, which appeared in the July Archives of Neurology. Patients underwent neurologic and psychologic examinations before and after CABG, and magnetic resonance protocol was applied before and after surgery. None of the patients revealed a new focal neurologic deficit after surgery. While magnetic resonance imaging showed new ischemic lesions in 26% of the patients, researchers determined the lesions were not related to impaired postoperative test performance. However, following surgery, magnetic resonance spectroscopy showed a significant decrease in the metabolite ratio of N-acetylaspartate–creatine. The extent of deterioration in postoperative neuropsychologic test performance was closely related to the degree of N-acetylaspartate–creatine ratio decrease.

A protein mutation contributes to the development of Huntington’s disease by disrupting the process by which the brain’s nerve cells produce energy, according to a study in the August Nature Neuroscience. By isolating mitochondria from patients with Huntington’s disease and from genetically engineered mice, researchers showed that Huntington’s disease appears to interfere with nerve cell metabolism by disrupting the way the cells process calcium, resulting in excessively high calcium levels that damage the nerve cells. Investigators also found that they could reproduce the abnormalities they saw in the mitochondria by directly applying proteins containing the mutation to mitochondria from healthy subjects, suggesting that the direct interaction of the mutation with mitochondria may be centrally involved with causing the disease.

Subtle defects in the processing of a single protein that provides structure to muscle cells can lead to several forms of muscular dystrophy. Researchers reported in the July 25 Nature that defects in enzymes responsible for the processing of the structural protein dystroglycan are the underlying cause of several rare forms of the disease. The investigators studied the proteins involved in several muscular dystrophies, and discovered that while the core dystroglycan protein is present on cell surfaces, it is missing distinctive sugar molecules on the protein. This process, called glycosylation, is an important finishing step in the processing of many proteins. Researchers hypothesize that several genes defective in these forms of muscular dystrophy are involved in the biochemical pathway that leads to glycosylation of dystroglycan.

African-Americans with Alzheimer’s disease have high levels of homocysteine and low levels of B12, reported researchers at the 8th International Conference on Alzheimer’s Disease and Related Disorders. The investigators collected blood samples from 256 African- Americans who showed no signs of cognitive impairment and 58 African- Americans who had a clinical diagnosis of Alzheimer’s disease. All study participants were older than 50. When comparing the two groups, the researchers found homocysteine levels were significantly higher in the individuals with Alzheimer’s disease and levels of B12 were significantly lower. In addition, researchers found that both groups had significantly higher levels of folic acid in their blood, which could eventually translate into a decrease in vascular and neurodegenerative disease.

Depressive symptoms in the elderly may be associated with an increased risk of Alzheimer’s disease, according to a study found in the August 13 Neurology. Participants from the Religious Orders Study who did not have clinical evidence of Alzheimer’s disease underwent annual clinical evaluations that included clinical classification of Alzheimer’s disease, 19 cognitive tests and an evaluation based on the Center for Epidemiologic Studies Depression (CES-D) scale for a period of seven years. At baseline, subjects reported an average of one depressive symptom on the CES-D scale. During the seven years of follow-up, 108 subjects developed Alzheimer’s disease. Researchers determined that the number of depressive symptoms at baseline predicted the development of Alzheimer’s disease, and for each depressive symptom, the risk of developing Alzheimer’s disease increased by approximately 20%.

Nitric oxide can activate enzymes on the outside of nerve cells to trigger their demise during stroke and neurodegenerative diseases, according to an article in the August 16 Science. The enzymes belong to a family known as matrix metalloproteinases (MMPs). When activated in excess, the enzymes destroy the outside of nerve cells, resulting in their death. Using mass spectrometry, researchers found that the MMP enzymes are not only activated by nitric oxide, but also that the MMPs are further affected by oxygen-related molecules to produce permanent and pathologic activity of the enzymes, leading them to destroy the normal environment surrounding the nerve cell.

Though it may have an initial palliative effect on patients with mild traumatic brain injury, researchers have determined that bed rest is no more effective than no bed rest at all. One hundred and seven patients who recently suffered mild traumatic brain injury participated in the study. The subjects were randomly assigned to two groups, with one group advised not to take bed rest and the other group advised to take full bed rest for six days after the trauma. Investigators measured the severity of the patients’ physical and mental health and their posttraumatic complaints at two weeks and three and six months after the trauma. After six months, researchers found that the posttraumatic complaints from the full rest group tended to be more severe, but there were no other significant differences found. The study was published in the August Journal of Neurology, Neurosurgery, and Psychiatry.

Japanese women who report high levels of mental stress have double the risk for stroke-related and heart-related deaths than those reporting low stress levels. In a study found in the August 12 online Circulation, researchers analyzed health screenings and lifestyle questionnaires from 73,424 Japanese men and women between the ages of 40 and 79. In the eight years the study encompassed, there were 778 cardiovascular deaths among the men and 643 among the women. Researchers found that 8,656 women and 6,891 men reported high mental stress. After adjusting for risk factors and psychologic variables, investigators discovered that women in the high stress group had 2.24 times greater risk for stroke and 2.28 times greater risk for coronary heart disease.

Children who are poor readers appear to have a disruption in the part of their brain involved in reading phonetically, according to a study funded by the National Institute of Child Health and Human Development. The study also found that children who read poorly but who do not receive any extra help or training eventually compensate for their disability by using other parts of the brain as backup systems for the impaired brain regions. In the study, which appeared in the July Biological Psychiatry, researchers used functional magnetic resonance imaging to demonstrate differences in brain images between children with dyslexia and non–reading-impaired control children. The disruption in the brain systems for reading was evident when the children performed phonologic tasks, the researchers reported. “Although most of these children eventually do learn to read, they never do so with the same fluency as do good readers. This is probably because the ‘backup’ brain systems … cannot process printed information as easily as can the brain systems primarily involved in reading,” they concluded.

NR

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