Does Dreaming Enhance Memory?
Numerous studies show that a period of sleep following learning enhances memory, apparently through the replay of brain activity that occurred during task performance. Robert Stickgold and his colleagues had subjects learn to navigate a virtual maze on a computer; then one group took a 90-minute nap while the other subjects remained awake. The researchers monitored EEG, eye movements, and muscle activity and woke the subjects if they entered REM sleep. Consistent with previous findings, when subjects were retested 5 hours after training the subjects who napped improved significantly more than those who remained awake. What is different about this study is that the napping subjects who reported dreaming about the maze task improved markedly more than those who didn't, with their gains accounting for most of the nap group's superiority; thinking about the maze while awake did not boost performance in the waking subjects. Subjects who dreamed about the maze were more likely to have been poorer performers during learning; however, their improvement was still greater after statistical correction for initial performance, so the greater improvement of the napping group can't be explained simply because they had more room for improvement. Current Biology, Vol 20, 850-855.
Motivation Affects Sleep/Memory Relationship
In a second study, subjects learned various declarative and procedural tasks (word associates, object location, finger tapping) before either sleeping or remaining awake; however, in this case some subjects were told they would be tested for recall later and others weren't. Sleep enhanced later improvement only if the subjects had been told about the retesting. Further, the informed group showed greater slow-wave activity during sleep, and the amount of slow-wave activity was strongly correlated with the degree of improvement. Apparently the motivation to remember helps select memories for replay and enhancement during sleep; presumably this would occur whether the motivation involved an intent to remember or the experience was in some way important, for example, evoking emotion. Journal of Neuroscience, Vol 31, 1563-1569.
Learning From Mistakes Begins Around Age 12
The way we learn changes as we age; one of the most significant ways is our ability to profit from our mistakes, and this information is important for understanding behavior and for educational design. Researchers in the Netherlands used fMRI to monitor brain activity in 8-9 year olds, 11-13 year olds, and 18-25 year olds while they performed a learning task on a computer; feedback consisted of a + after correct responses and an x after incorrect trials. The dorsolateral prefrontal cortex and the superior parietal cortex responded more to positive feedback in 8-9 year olds, but more strongly to negative feedback in 18-25 year olds. Response was equal in these areas in 11-13 year olds, suggesting that the transition occurs during this time. The anterior cingulate cortex was more active following negative feedback in both older groups but not in the younger group. The anterior cingulate cortex apparently is involved in conflict monitoring and directing cognitive responses to conflict (Science, Vol 303, 1023-1026.), so it is interesting that the transition in this area precedes the transition in the prefrontal area, which is important in dealing with the consequences of behavior. Journal of Neuroscience, Vol 28, 9495-9503.
Number of Late-Onset Alzheimer's Genes Doubles
Thanks to the efforts of the Alzheimer Disease Genetics Consortium, 5 new genes associated with late-onset Alzheimmer's disease have been identified, doubling the known number of genes. The two studies that identified the genes took the unusual step of replicating their initial results with two additional independent samples, providing strong assurance that the results are reliable. Both studies confirmed associations with CD2AP, CD33, EPHA1, and MS4A4/MS4A6E, and one of the studies also identified ABCA7. Nature Genetics, Vol 43, 429-435 and 436-441.
Alzheimer's Brain Deficient in β-Amyloid Clearance
It has long been believed that the accumulation of β-Amyloid in the Alzheimer's brain was due to overproduction, but there has been no direct evidence for this process. Using metabolic labeling, researchers at Washington University in Saint Louis found no differences between patients and controls in β-Amyloid production, but clearance was impaired in the patients. This information should be useful in devising treatments for the disease and, possibly, for earlier detection. Science, Vol 330, 1774.
Half of Alzheimer's Cases Misdiagnosed
Researchers at the University of Hawaii have now completed 800 autopsies of elderly men and found that about half of those diagnosed with Alzheimer's were misdiagnosed. Their dementia stemmed from other causes, such as stroke-related tissue damage, accumulation of abnormal proteins known as Lewy bodies, and cell damage. The results are not yet published. CNN Health, February 23, 2011.
Cell Energy Deficit May Precede Alzheimer's
A team of researchers from several Arizona institutions had previously found evidence of reduced expression in energy-making genes in Alzheimer's patients and PET imaging indications of reduced brain activity in young men at genetic risk for Alzheimer's; so for a recent study they proposed that men at risk might have abnormalities in energy utilization or in the mitochondria (organelles in cells that produce energy). In 15 deceased young men carrying the APOE4 allele the researchers found a slight reduction in cytochrome oxidase, an energy-making enzyme in the mitochondria. If this relationship holds up in further research, it could lead to earlier diagnosis and preventive treatment. Journal of Alzheimer's Disease, Vol 22, 307-313.
Heavy Smoking Associated With Later Dementia
Now you can add dementia to the risks of smoking. In a sample of over 5,000 people, those who smoked more than two packs of cigarettes a day were twice as likely to be diagnosed with dementia or Alzheimer's disease at follow-up 23 years later. Results wer adjusted for age, sex, education, race, alcohol use, and a variety of other diseases, making it more likely that tobacco was the real culprit. Archives of Internal Medicine, Vol 171, 333-339.