ScienceDaily (Feb. 15, 2012) — Brain scans of two strains of mice imbibing significant quantities of alcohol reveal serious shrinkage in some brain regions — but only in mice lacking a particular type of receptor for dopamine, the brain’s “reward” chemical. The study, conducted at the U.S. Department of Energy’s Brookhaven National Laboratory and published in the May 2012 issue of Alcoholism: Clinical and Experimental Research, now online, provides new evidence that these dopamine receptors, known as DRD2, may play a protective role against alcohol-induced brain damage.
"This study clearly demonstrates the interplay of genetic and environmental factors in determining the damaging effects of alcohol on the brain, and builds upon our previous findings suggesting a protective role of dopamine D2 receptors against alcohol’s addictive effects," said study author Foteini Delis, a neuroanatomist with the Behavioral Neuropharmacology and Neuroimaging Lab at Brookhaven, which is funded through the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Coauthor and Brookhaven/NIAA neuroscientist Peter Thanos stated that, "These studies should help us better understand the role of genetic variability in alcoholism and alcohol-induced brain damage in people, and point the way to more effective prevention and treatment strategies."
The current study specifically explored how alcohol consumption affects brain volume — overall and region-by-region — in normal mice and a strain of mice that lack the gene for dopamine D2 receptors. Half of each group drank plain water while the other half drank a 20 percent ethanol solution for six months. Then scientists performed magnetic resonance imaging (MRI) scans on all the mice and compared the scans of those drinking alcohol with those from the water drinkers in each group.
The scans showed that chronic alcohol drinking induced significant overall brain atrophy and specific shrinkage of the cerebral cortex and thalamus in the mice that lacked dopamine D2 receptors, but not in mice with normal receptor levels. Mice in both groups drank the same amount of alcohol.
"This pattern of brain damage mimics a unique aspect of brain pathology observed in human alcoholics, so this research extends the validity of using these mice as a model for studying human alcoholism," Thanos said.
In humans, these brain regions are critically important for processing speech, sensory information, and motor signals, and for forming long-term memories. So this research helps explain why alcohol damage can be so widespread and detrimental.
"The fact that only mice that lacked dopamine D2 receptors experienced brain damage in this study suggests that DRD2 may be protective against brain atrophy from chronic alcohol exposure," Thanos said. "Conversely, the findings imply that lower-than-normal levels of DRD2 may make individuals more vulnerable to the damaging effects of alcohol."
That would in effect deal people with low DRD2 levels a double whammy of alcohol vulnerability: Previous studies conducted by Thanos and collaborators suggest that individuals with low DRD2 levels may be more susceptible to alcohol’s addictive effects.
"The increased addictive liability and the potentially devastating increased susceptibility to alcohol toxicity resulting from low DRD2 levels make it clear that the dopamine system is an important target for further research in the search for better understanding and treatment of alcoholism," Thanos said.
Source: Science Daily
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Alcohol abuse and dependence are common problems in the United States due to a number of factors, two of which may be social drinking by college students and young adults, and risk taking that may lead to heavier drinking later in life. A study of the neural underpinnings of risk-taking in young, non-dependent social drinkers has found that the caudate nucleus and frontal cortex regions of the brain show less activation in people who drink more heavily.
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Segmented synapses Synaptic structures in mice engineered to lack the protein biglycan (bottom row) appear discontinuous compared to the synaptic structures in normal mice (top).
(Credit: Fallon Lab/Brown University)
More: When Nerve Meets Muscle, Biglycan Seals the Deal
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ScienceDaily (Feb. 14, 2012) — Curcumin, a substance extracted from turmeric, prolongs life and enhances activity of fruit flies with a nervous disorder similar to Alzheimers, according to new research. The study conducted at Linköping University, indicates that it is the initial stages of fibril formation and fragments of the amyloid fibrils that are most toxic to neurons.
Above left are the survival curves for “Alzheimer flies” treated (dashed line) and those not treated with curcumin. The flies that were administered curcumin lived longer and were more active. The scientists identified an accelerated formation of amyloid plaque in the treated flies, which seemed to protect the nerve cells. On the right we see microscopic images of neurons (blue) and plaque (green) in the fruit fly’s brain. The study strengthens the hypothesis that a curcumin-based drug can contribute to toxic fibrils being encapsulated (bottom left of the figure). (Credit: Per Hammarström, Ina Caesar)
Ina Caesar, as the lead author, has published the results of the study in the journal PLoS ONE.
For several years curcumin has been studied as a possible drug candidate to combat Alzheimer’s disease, which is characterized by the accumulation of sticky amyloid-beta and Tau protein fibres. Linköping researchers wanted to investigate how the substance affected transgenic fruit flies (Drosophila melanogaster), which developed evident Alzheimer’s symptoms. The fruit fly is increasingly used as a model for neurodegenerative diseases.
Five groups of diseased flies with different genetic manipulations were administered curcumin. They lived up to 75 % longer and maintained their mobility longer than the sick flies that did not receive the substance.
However, the scientists saw no decrease of amyloid in the brain or eyes. Curcumin did not dissolve the amyloid plaque; on the contrary it accelerated the formation of fibres by reducing the amount of their precursor forms, known as oligomers.
"The results confirm our belief that it is the oligomers that are most harmful to the nerve cells," says Professor Per Hammarstrom, who led the study.
"We now see that small molecules in an animal model can influence the amyloid form. To our knowledge the encapsulation of oligomers is a new and exciting treatment strategy," he said.
Several theories have been established about how oligomers can instigate the disease process. According to one hypothesis, they become trapped at synapses, inhibiting nerve impulse signals. Others claim that they cause cell death by puncturing the cell membrane.
Curcumin is extracted from the root of herbaceous plant turmeric and has been used as medicine for thousands of years. More recently, it has been tested against pain, thrombosis and cancer.
Source: Science Daily
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February 14th, 2012
Humans move between ‘patches’ in their memory using the same strategy as bees flitting between flowers for pollen or birds searching among bushes for berries.
Researchers at the University of Warwick and Indiana University have identified parallels between animals looking for food in the wild and humans searching for items within their memory – suggesting that people with the best ‘memory foraging’ strategies are better at recalling items.
Scientists asked people to name as many animals as they could in three minutes and then compared the results with a classic model of optimal foraging in the real world, the marginal value theorem, which predicts how long animals will stay in one patch before jumping to another.
Dr Thomas Hills, associate professor in the psychology department at the University of Warwick, said: “A bird’s food tends to be clumped together in a specific patch – for example on a bush laden with berries.
“But when the berries on a bush are depleted to the point where the bird’s energy is best focused on another more fruitful bush, it will move on.
“This kind of behaviour is predicted by the marginal value theorem, for a wide variety of animals.
“Because of the way human attention has evolved, we wondered if humans might use the same strategies to forage in memory. It turns out, they do.
“When faced with a memory task, we focus on specific clusters of information and jump between them like a bird between bushes. For example, when hunting for animals in memory, most people start with a patch of household pets—like dog, cat and hamster.
“But then as this patch becomes depleted, they look elsewhere. They might then alight on another semantically distinct ‘patch’, for example predatory animals such as lion, tiger and jaguar.”
The study shows that people who either stay too long or not long enough in one ‘patch’ did not recall as many animals as those who better judged the best time to switch between patches.
In other words, people who most closely adhered to the marginal value theorem produced more items.
The study Optimal Foraging in Semantic Memory, published in Psychological Review, asked 141 undergraduates (46 men and 95 women) at Indiana University to name as many animals as they could in three minutes.
They then analysed the responses using a categorisation scheme and also a semantic space model, called BEAGLE, which identifies clusters in the memory landscape based on the way words are related to one another in natural language.
Source: Neuroscience News
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February 14, 2012
(Medical Xpress) — A UT Dallas undergraduate’s research is revealing new information about a key protein’s role in the development of epilepsy, autism and other neurological disorders. This work could one day lead to new treatments for the conditions.
Senior neuroscience student Francisco Garcia has worked closely with Dr. Marco Atzori, associate professor in the School of Behavioral and Brain Sciences (BBS), on several papers that outline their findings about interleukin 6 (IL-6) and hyper-excitability. An article on the project is slated for publication in Biological Psychiatry later this year.
Scientists know that stress elevates the levels of pro-inflammatory cytokines (signaling molecules used in intercellular communication) and promotes hyper-excitable conditions within the central nervous system. This hyper-excitability is thought to be a factor in epilepsy, autism and anxiety disorders.
Garcia and Atzori hypothesized that the protein IL-6 acutely and directly induces hyper-excitability by altering the balance between excitation and inhibition within synaptic communication. In other words, IL-6 is not just present when hyper-excitability occurs in the nervous system. It may actually cause it in some circumstances, Garcia said.
The UT Dallas research team administered IL-6 to rat brain tissue and monitored its synaptic excitability. The brain tissue exhibited higher than normal excitability in their synapses, a symptom that may lead to misfiring of signals in epilepsy and other conditions.
The researchers then injected sgp130 -a novel drug that acts as an IL-6 blocker- into the laboratory animals’ brains. The substance limited excitability and appeared to prevent the conditions that lead to related neurological and psychiatric disorders, Garcia said.
“This finding has the potential to lead to eventual new treatments for epilepsy, anxiety disorders or autism,” Garcia said.
The next stage of his research will involve looking at how IL-6 might affect development of other types of neurological problems. Human trials could follow sometime in the future.
Garcia is a native of Mexico, and he plans to pursue his master’s degree in neuroscience at UT Dallas after finishing his undergraduate studies. He credits the BBS faculty with allowing him to participate in laboratory experiments and expand his research skills.
“The UT Dallas faculty members have been great about giving me the opportunity to learn the techniques of a lab researcher,” he said. “It’s been a great experience to work as an undergraduate with such highly respected scientists as Dr. Atzori and Dr. Michael Kilgard.”
Atzori also praised Garcia’s efforts.
“Francisco has been an intelligent, hard-working and experimentally gifted student who contributed way more than the average undergraduate to the projects of the laboratory,” Atzori said. “I am proud that a fine piece of research with great potential for research and clinical applications has been carried out thanks to his enthusiasm and dedication. Francisco’s work in my laboratory is an example of the achievements possible when an institution like UT Dallas invests in and nurtures its research environment.”
Provided by University of Texas at Dallas
Source: medicalxpress.com
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February 14, 2012 in Neuroscience
The amount and quality of sleep you get at night may affect your memory later in life, according to research that was released today and will be presented at the American Academy of Neurology’s 64th Annual Meeting in New Orleans April 21 to April 28, 2012.
"Disrupted sleep appears to be associated with the build-up of amyloid plaques, a hallmark marker of Alzheimer’s disease, in the brains of people without memory problems," said study author Yo-El Ju, MD, with Washington University School of Medicine in St. Louis and a member of the American Academy of Neurology. "Further research is needed to determine why this is happening and whether sleep changes may predict cognitive decline."
Researchers tested the sleep patterns of 100 people between the ages of 45 and 80 who were free of dementia. Half of the group had a family history of Alzheimer’s disease. A device was placed on the participants for two weeks to measure sleep. Sleep diaries and questionnaires were also analyzed by researchers.
After the study, it was discovered that 25 percent of the participants had evidence of amyloid plaques, which can appear years before the symptoms of Alzheimer’s disease begin. The average time a person spent in bed during the study was about eight hours, but the average sleep time was 6.5 hours due to short awakenings in the night.
The study found that people who woke up more than five times per hour were more likely to have amyloid plaque build-up compared to people who didn’t wake up as much. The study also found those people who slept “less efficiently” were more likely to have the markers of early stage Alzheimer’s disease than those who slept more efficiently. In other words, those who spent less than 85 percent of their time in bed actually sleeping were more likely to have the markers than those who spent more than 85 percent of their time in bed actually sleeping.
"The association between disrupted sleep and amyloid plaques is intriguing, but the information from this study can’t determine a cause-effect relationship or the direction of this relationship. We need longer-term studies, following individuals’ sleep over years, to determine whether disrupted sleep leads to amyloid plaques, or whether brain changes in early Alzheimer’s disease lead to changes in sleep," Ju said. "Our study lays the groundwork for investigating whether manipulating sleep is a possible strategy in the prevention or slowing of Alzheimer disease."
Provided by American Academy of Neurology
Source: medicalxpress.com
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February 14, 2012 by Bob Yirka in Neuroscience
(Medical Xpress) — A small team of researchers has found that various forms of child abuse can lead to stunted development in certain regions of the brain. The research carried out by Martin Teicher, Carl Anderson and Ann Polcari, all working in the Boston area, relied on questionnaires and MRI brain scans to determine that certain parts of the hippocampus, all known to be sensitive to stress, were up to six percent smaller in adults who as children had been sexually, verbally or physically abused. The team has published their results in the Proceedings of the National Academy of Sciences.
The three areas affected: the cornu ammonis, the dentate gyrus and the subiculum, all located in the hippocampus, are known to be vulnerable to stress which leads to less cell development than would normally occur in the absence of abuse.
To test the relationship between brain development and childhood abuse, the research team enlisted a group of otherwise healthy adult volunteers: 73 men and 120 women, all between the ages of 18 and 25. All were given questionnaires that delved into their childhood, specifically addressing issues of verbal, mental and physical abuse and other types of stresses such as the death of someone close to them or problems between parents. All were also given brain scans using an MRI machine. The team then compared the answers given on the questionnaires to the possibly impacted areas in the hippocampus of each volunteer. In so doing, they found that the brain regions under study were 5.8 to 6.5 percent smaller than average for those that reported such childhood stresses.
The researchers suggest that smaller brain regions due to childhood stressmay help explain the abnormally high levels of mental illness (depression, bi-polarism, anxiety, etc.) seen in adults who have endured abuse as children and why so many wind up with drug dependency problems. They also noted that one of the regions impacted, the subiculum, serves as a relay, moving information in and out of the hippocampus, which can have a direct impact on dopamine production. Those with reduced volume have been found to have problems with drug addiction and in some cases develop schizophrenia.
The researchers believe that increased stress leads to higher levels of the hormone cortisol, which in turn can slow or even stop the growth of new neurons in the brain which can result in permanently stunting certain brain regions.
The researchers are hoping their results will further highlight the damage that is done when children are subjected to adverse living conditions, leading perhaps to earlier interventions and possibly a means for developing treatments that may aid in preventing the stunting of brain regions, thus helping to pave the way for a better quality of life for those that have been abused as children.
Source: medicalxpress.com
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Is it possible for one person to love more than another? In an attempt to find out, filmmaker Brent Hoff teamed with Stanford University neuroscientists to test lovers’ abilities, using an fMRI to monitor brain activity and measure whose adoration was the strongest.
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Quantum dots control brain cells for the first time
In an unlikely marriage of quantum physics and neuroscience, tiny particles called quantum dots have been used to control brain cells for the first time.
Having such control over the brain could one day provide a non-invasive treatment for conditions such as Alzheimer’s disease, depression and epilepsy. In the nearer term, quantum dots could be used to treat blindness by reactivating damaged retinal cells.
“Many brain disorders are caused by imbalanced neural activity,” says Lih Linat the University of Washington, Seattle. “Manipulation of specific neurons could permit the restoration of normal activity levels.”
Methods to stimulate the brain artificially already exist, though each has its drawbacks. Deep brain stimulation is used in Parkinson’s disease to trigger brain cell activity and prevent the abnormal signalling that causes debilitating tremors, but placing the electrodes required is highly invasive. Transcranial magnetic stimulation can stimulate brain cells from
outside the head, but is not highly targeted and so affects large areas of the brain at once. Researchers in optogenetics can control genetically modified brain cells using light but because of these modifications, the technique is not yet deemed safe to use in humans.
Lin’s team has now come up with an alternative using quantum dots – light-sensitive, semiconducting particles just a few nanometres in diameter.
First, they cultivated prostate cancer cells on a film covered with quantum dots. The cell membranes of the cancer cells were positioned next to the dots. The team then shone light onto the nanoparticles.
Energy from the light excites electrons within the quantum dot which causes the surrounding area to become negatively charged (see diagram). This caused some of the cancer cells’ ion channels, which are mediated by a voltage, to open, allowing ions to rush in or out of the cells.
In nerve cells, opening ion channels is a crucial step in generating action potentials – the signals by which the cells communicate in the brain. If the voltage change is large enough, an action potential is generated.
When Lin’s team repeated their experiment with nerve cells, they found that stimulating the quantum dots caused ion channels to open and the nerve cell to fire.
In humans, quantum dots would need to be delivered to brain tissue. Lin claims this shouldn’t be a problem. “A significant advantage is that their surface can be modified with various molecules,” she says. These molecules could be attached to the quantum dots in order to target specific brain cells and could be administered intravenously.
A key hurdle would be delivering the light source to the brain. For this reason, Lin reckons the first use for the technique would be in reactivating damaged cells in the retina, which naturally absorb light. Co-author Fred Reike, who specialises in retinal disease, says that quantum dots have great potential in this area because they directly affect ion channels, which play a key part in the signalling pathways of vision.
“Quantum dots have a great future for biomedical applications,” agrees Kevin Critchley at the University of Leeds, UK, but adds that there are limitations such as potential toxicity issues.
“Based on what we have observed, we are optimistic about the potential of this technology in helping us [answer] biological questions, and eventually diagnose and treat human diseases,” Lin says.](http://41.media.tumblr.com/tumblr_lzfd8sP4Gs1qcyo2po1_400.jpg)
