Older news items (pre-2010) brought over from the old website
August 2009
Overweight and obese elderly have smaller brains
Analysis of brain scans from 94 people in their 70s who were still "cognitively normal" five years after the scan has revealed that people with higher body mass indexes had smaller brains on average, with the frontal and temporal lobes particularly affected (specifically, in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus, in obese people, and in the basal ganglia and corona radiate of the overweight). The brains of the 51 overweight people were, on average, 6% smaller than those of the normal-weight participants, and those of the 14 obese people were 8% smaller. To put it in more comprehensible, and dramatic terms: "The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people." However, overall brain volume did not differ between overweight and obese persons. As yet unpublished research by the same researchers indicates that exercise protects these same brain regions: "The most strenuous kind of exercise can save about the same amount of brain tissue that is lost in the obese."
Raji, C.A. et al. 2009. Brain structure and obesity. Human Brain Mapping, Published Online: Aug 6 2009
https://www.newscientist.com/article/mg20327222-400-expanding-waistlines...
May 2009
Meditation may increase gray matter
Adding to the increasing evidence for the cognitive benefits of meditation, a new imaging study of 22 experienced meditators and 22 controls has revealed that meditators showed significantly larger volumes of the right hippocampus and the right orbitofrontal cortex, and to a lesser extent the right thalamus and the left inferior temporal gyrus. There were no regions where controls had significantly more gray matter than meditators. These areas of the brain are all closely linked to emotion, and may explain meditators' improved ability in regulating their emotions.
Luders, E. et al. 2009. The underlying anatomical correlates of long-term meditation: Larger hippocampal and frontal volumes of gray matter. NeuroImage, 45 (3), 672-678.
http://www.eurekalert.org/pub_releases/2009-05/uoc--htb051209.php
August 2008
One sleepless night increases dopamine
A study has found that sleep deprivation increases the level of the hormone dopamine in two brain structures: the striatum, which is involved in motivation and reward, and the thalamus, which is involved in alertness. The rise in dopamine following sleep deprivation may promote wakefulness to compensate for sleep loss. However, since the amount of dopamine correlated with feelings of fatigue and impaired performance on cognitive tasks, it appears that the adaptation is not sufficient to overcome the cognitive deterioration induced by sleep deprivation and may even contribute to it. Amphetamines increase dopamine levels.
Volkow, N.D. et al. 2008. Sleep Deprivation Decreases Binding of [11C]Raclopride to Dopamine D2/D3 Receptors in the Human Brain. Journal of Neuroscience, 28, 8454-8461.
http://www.eurekalert.org/pub_releases/2008-08/sfn-osn081808.php
April 2008
How chronic exposure to solvents can impair the brain
Chronic occupational exposure to organic solvents, found in materials such as paints, printing and dry cleaning agents, has been linked to long-term cognitive impairment, but chronic solvent-induced encephalopathy (CSE) is still a controversial diagnosis. An imaging study of 10 CSE patients who had been exposed to solvents and had mild to severe cognitive impairment, 10 participants who had been exposed to solvents but had no CSE symptoms, and 11 participants who were not exposed to solvents and had no symptoms, has now found impairment in the frontal-striatal-thalamic (FST) circuitry of CSE patients. The disturbances are predictive of the clinical findings — impaired psychomotor speed and attention — and were also linked to exposure severity.
Visser, I. et al. 2008. Cerebral impairment in chronic solvent-induced encephalopathy (p NA). Annals of Neurology, Published online April 15 2008
http://www.eurekalert.org/pub_releases/2008-04/w-dib041508.php
February 2003
Another step in understanding how sleep affects memory
The value of sleep for memory takes a further step in being understood in new rodent research, which found that, as the rodents slept, the thalamus at the base of their brains originated bursts of electrical activity (“sleep spindles”), which were then detected in the somatosensory neocortex. Some 50 msec later, the hippocampus responded with a pulse of electricity (a “ripple”). "This neocortical-hippocampal dialogue may provide a selection mechanism for the time-compressed replay of information learned during the day." It’s suggested that the ripple is the hippocampus sending back neat, compact waves of memory to the neocortex where they are filed away for future reference. Most of this activity took place during slow wave sleep, the stage which makes up the majority of the sleep cycle.
Sirota, A., Csicsvari, J., Buhl, D. & Buzsáki, G. 2003. Communication between neocortex and hippocampus during sleep in rodents. Proc. Natl. Acad. Sci. USA, 100 (4), 2065-2069.
May 2002
Memories may be hard to find when thalamus fails to synchronize rhythms
Memory codes - the representation of an object or experience in memory - are patterns of connected neurons. The neurons that are linked are not necessarily in the same region of the brain. Exciting new research has measured the electrical rhythms that parts of the brain use to communicate with each other and found that the thalamus regulates these rhythms. "Memory appears to be a constructive process in combining the features of the items to be remembered rather than simply remembering each object as a whole form. The thalamus seems to direct or modulate the brain's activity so that the regions needed for memory are connected." The authors suggest that tips of the tongue experiences (when only part of a memory is recalled) may occur when the rhythms don't synchronize with the regions properly.
Slotnick, S.D., Moo, L.R., Kraut, M.A., Lesser, R.P. & Hart, J. Jr. 2002. Interactions between thalamic and cortical rhythms during semantic memory recall in human. Proc. Natl. Acad. Sci. U.S.A., 99, 6440-6443.
http://www.eurekalert.org/pub_releases/2002-05/uoaf-mi050902.php