Posts tagged brain
Articles and news from the latest research reports.
New Dementia Diagnostic Exams and Gene Findings Bode Well for Treatment
The number of people affected by dementias continues to climb as baby boomers age, increasing the urgency to identify ways to prevent, diagnose and treat these neurodegenerative brain disorders.
Today it is possible to diagnose dementias more accurately than ever before, thanks to improvements in behavioral assessment tools, imaging techniques, gene testing and data collection and analysis, according to Bruce L. Miller, MD, a behavioral neurologist and professor of neurology at UCSF.
Miller, who came to UCSF in 1998 and directs the UCSF Memory and Aging Center, described recent advances during the lecture he gave at UCSF Mission Bay on Oct. 15 as part of receiving the Academic Senate’s 12th Annual Faculty Research Lectureship in Clinical Science.
The ability to diagnose different types of dementias accurately and to distinguish among the biological factors that cause them will become increasingly important as treatments become more promising and better targeted, Miller said.
Despite continued improvements in the tools available to physicians for diagnosing dementias, a common neurodegenerative disease known as frontotemporal dementia (FTD) remains understudied and is very often misdiagnosed, Miller said. For reasons that are in part historical, FTD still is thought of as a rare disease, a misconception that greatly contributes to its being underdiagnosed, he said. While Alzheimer’s disease is the most common dementia overall, among the population aged 65 and younger, FTD is just as common, according to Miller.
Clue to Alzheimer’s cause found in brain samples
Researchers at Washington University School of Medicine in St. Louis have found a key difference in the brains of people with Alzheimer’s disease and those who are cognitively normal but still have brain plaques that characterize this type of dementia.
“There is a very interesting group of people whose thinking and memory are normal, even late in life, yet their brains are full of amyloid beta plaques that appear to be identical to what’s seen in Alzheimer’s disease,” says David L. Brody, MD, PhD, associate professor of neurology. “How this can occur is a tantalizing clinical question. It makes it clear that we don’t understand exactly what causes dementia.”
Hard plaques made of a protein called amyloid beta are always present in the brain of a person diagnosed with Alzheimer’s disease, according to Brody. But the simple presence of plaques does not always result in impaired thinking and memory. In other words, the plaques are necessary – but not sufficient – to cause Alzheimer’s dementia.
The new study, available online in Annals of Neurology, still implicates amyloid beta in causing Alzheimer’s dementia, but not necessarily in the form of plaques. Instead, smaller molecules of amyloid beta dissolved in the brain fluid appear more closely correlated with whether a person develops symptoms of dementia. Called amyloid beta “oligomers,” they contain more than a single molecule of amyloid beta but not so many that they form a plaque.
Oligomers floating in brain fluid have long been suspected to have a role in Alzheimer’s disease. But they are difficult to measure. Most methods only detect their presence or absence, or very large quantities. Brody and his colleagues developed a sensitive method to count even small numbers of oligomers in brain fluid and used it to compare amounts in their samples.
The researchers examined samples of brain tissue and fluid from 33 deceased elderly subjects (ages 74 to 107). Ten subjects were normal – no plaques and no dementia. Fourteen had plaques, but no dementia. And nine had a diagnosis of Alzheimer’s disease – both plaques and dementia.
They found that cognitively normal patients with plaques and Alzheimer’s patients both had the same amount of plaque, but the Alzheimer’s patients had much higher oligomer levels.
But even oligomer levels did not completely distinguish the two groups. For example, some people with plaques but without dementia still had oligomers, even in similar quantity to some patients with Alzheimer’s disease. Where the two groups differed completely, according to Brody and his colleagues, was the ratio of oligomers to plaques. They measured more oligomers per plaque in patients with dementia, and fewer oligomers per plaque in the samples from cognitively normal people.
In people with plaques but no dementia, Brody speculates that the plaques could serve as a buffer, binding with free oligomers and keeping them tied down. And in dementia, perhaps the plaques have exceeded their capacity to capture the oligomers, leaving them free to float in the brain’s fluid, where they can damage or interfere with neurons.
Brody cautions that, due to the difficulty in getting samples, oligomer levels have never been measured in living people. Therefore, it’s possible these floating clumps of amyloid beta only form after death. Even so, he says, there is still a clear difference between the two groups.
“The plaques and oligomers appear to be in some kind of equilibrium,” Brody says. “What happens to shift the relationship between the oligomers and plaques? Like much Alzheimer’s research, this study raises more questions than it answers. But it’s an important next piece of the puzzle.”
(Source: news.wustl.edu)
A circuit diagram of the mouse brain
What happens in the brain when we see, hear, think and remember? To be able to answer questions like this, neuroscientists need information about how the millions of neurons in the brain are connected to each other. Scientists at the Max Planck Institute for Medical Research in Heidelberg have taken a crucial step towards obtaining a complete circuit diagram of the brain of the mouse, a key model organism for the neurosciences. The research group working with Winfried Denk has developed a method for preparing the whole mouse brain for a special microscopy process. With this, the resolution at which the brain tissue can be examined is so high that the fine extensions of almost every single neuron are visible.
Raw Food Not Enough to Feed Big Brains
Eating a raw food diet is a recipe for disaster if you’re trying to boost your species’ brainpower. That’s because humans would have to spend more than 9 hours a day eating to get enough energy from unprocessed raw food alone to support our large brains, according to a new study that calculates the energetic costs of growing a bigger brain or body in primates. But our ancestors managed to get enough energy to grow brains that have three times as many neurons as those in apes such as gorillas, chimpanzees, and orangutans. How did they do it? They got cooking, according to a study published online today in the Proceedings of the National Academy of Sciences.
"If you eat only raw food, there are not enough hours in the day to get enough calories to build such a large brain," says Suzana Herculano-Houzel, a neuroscientist at the Federal University of Rio de Janeiro in Brazil who is co-author of the report. "We can afford more neurons, thanks to cooking."
Humans have more brain neurons than any other primate—about 86 billion, on average, compared with about 33 billion neurons in gorillas and 28 billion in chimpanzees. While these extra neurons endow us with many benefits, they come at a price—our brains consume 20% of our body’s energy when resting, compared with 9% in other primates. So a long-standing riddle has been where did our ancestors get that extra energy to expand their minds as they evolved from animals with brains and bodies the size of chimpanzees?
Study identifies natural process activating brain’s immune cells that could point way to repairing damaged brain
The brain’s key “breeder” cells, it turns out, do more than that. They secrete substances that boost the numbers and strength of critical brain-based immune cells believed to play a vital role in brain health. This finding adds a new dimension to our understanding of how resident stem cells and stem cell transplants may improve brain function.
Many researchers believe that these cells may be able to regenerate damaged brain tissue by integrating into circuits that have been eroded by neurodegenerative disease or destroyed by injury. But new findings by scientists at the Stanford University School of Medicine suggest that another process, which has not been fully appreciated, could be a part of the equation as well. The findings appear in a study published online Oct. 21 in Nature Neuroscience.
“Transplanting neural stem cells into experimental animals’ brains shows signs of being able to speed recovery from stroke and possibly neurodegenerative disease as well,” said Tony Wyss-Coray, PhD, professor of neurology and neurological sciences in the medical school and senior research scientist at the Veterans Affairs Palo Alto Health Care System. “Why this technique works is far from clear, though, because actually neural stem cells don’t engraft well.”
Overcoming memories that trigger cocaine relapse
Researchers identify brain mechanisms that regulating cocaine-seeking behavior
Researchers from the University of Wisconsin-Milwaukee (UWM) have identified mechanisms in the brain responsible for regulating cocaine-seeking behavior, providing an avenue for drug development that could greatly reduce the high relapse rate in cocaine addiction.
The research reveals that stimulation of certain brain receptors promotes inhibition of cocaine-associated memories, helping addicts to stop drug use. This inhibition is achieved through enhancing a process called “extinction learning,” in which cocaine-associated memories are replaced with associations that have no drug “reward.” This reduces drug-seeking behavior in rats.
The work was presented at the annual meeting of the Society for Neuroscience in New Orleans by Devin Mueller, UWM assistant professor of psychology, and doctoral student James Otis.
There are currently no FDA-approved medications to treat cocaine abuse, only treatments that address withdrawal symptoms, says Mueller. Abuse is maintained, in part, through exposure to environmental cues that trigger cocaine-related memories which lead to craving and relapse in recovering addicts. Currently, exposure therapy is used to help recovering addicts suppress their drug-seeking behavior, but with limited success. In exposure therapy, a patient is repeatedly exposed to stimuli that provoke craving. With repeated exposure, the patient experiences extinction, leading to reduced craving when presented with those stimuli.
If extinction could be strengthened, it would increase the effectiveness of exposure therapies in preventing relapse.
Isolating the receptor
The team found that a specific variant of the NMDA receptor, those which contain the NR2B subunit, are critical for extinction learning. They also discovered that drugs known to enhance NR2B function strengthened extinction because they act specifically in a region of the brain that regulates learned behaviors. In their investigation, researchers conditioned rats to associate one distinct chamber, but not another, with cocaine. Following conditioning, the rats were tested for a place preference by allowing drug-free access to both chambers. Rats demonstrating cocaine-seeking behavior spent significantly more time in the previously cocaine-associated chamber. Over several cocaine-free test sessions, addicted rats lost their place preference through extinction learning.
To examine the neural mechanisms of extinction, the researchers administered ifenprodil, which blocks NR2B-containing NMDA receptors, immediately after an extinction test. Ifenprodil-treated rats continued to spend more time in the cocaine-associated chamber even in the absence of cocaine, while saline-treated rats did not. These results were also replicated through specific infusion of ifenprodil into the brain’s infralimbic cortex, localizing a key brain structure in arresting cocaine-seeking.
Other avenues
The results indicate that enhancing NR2B function would boost the effectiveness of extinction-based exposure therapies. Although there are currently no NR2B-enhancing drugs, the NR2B containing receptor can be stimulated using other molecular pathways, says Mueller.
An example is the brain derived neurotrophic factor (BDNF) signaling cascade, which is implicated in neuron survival and growth. The authors targeted this cascade by directly administering BDNF into the infralimbic cortex. In extinction tests, administration of BDNF caused rats to lose their preference for the cocaine-associated chamber faster than rats given a placebo.
Mueller and Otis took these findings even further toward possible therapeutic intervention for addicts.
One issue with giving BDNF to humans is that it is unable to reach the brain through the bloodstream. Therefore, researchers next targeted the TrkB receptor, which is where BDNF normally binds. They did so with a newly synthesized drug that is able to reach the brain due to its small molecular size. This TrkB receptor agonist, known as 7,8 dihydroxyflavone, also strengthened extinction when given to rats during extinction training. The authors conclude that combining TrKB receptor stimulation simultaneously with exposure therapy could be an effective treatment for cocaine abuse, reducing craving and the potential for relapse.
(Source: eurekalert.org)
The Power of Music: Mind Control by Rhythmic Sound
You walk into a bar and music is thumping. All heads are bobbing and feet tapping in synchrony. Somehow the rhythmic sound grabs control of the brains of everyone in the room forcing them to operate simultaneously and perform the same behaviors in synchrony. How is this possible? Is this unconscious mind control by rhythmic sound only driving our bodily motions, or could it be affecting deeper mental processes?
The mystery runs deeper than previously thought, according to psychologist Annett Schirmer reporting new findings today at the Society for Neuroscience meeting in New Orleans. Rhythmic sound “not only coordinates the behavior of people in a group, it also coordinates their thinking—the mental processes of individuals in the group become synchronized.”
This finding extends the well-known power of music to tap into brain circuits controlling emotion and movement, to actually control the brain circuitry of sensory perception. This discovery helps explain how drums unite tribes in ceremony, why armies march to bugle and drum into battle, why worship and ceremonies are infused by song, why speech is rhythmic, punctuated by rhythms of emphasis on particular syllables and words, and perhaps why we dance.
The Neuroscience Of Music
Why does music make us feel? On the one hand, music is a purely abstract art form, devoid of language or explicit ideas. The stories it tells are all subtlety and subtext. And yet, even though music says little, it still manages to touch us deep, to tickle some universal nerves. When listening to our favorite songs, our body betrays all the symptoms of emotional arousal. The pupils in our eyes dilate, our pulse and blood pressure rise, the electrical conductance of our skin is lowered, and the cerebellum, a brain region associated with bodily movement, becomes strangely active. Blood is even re-directed to the muscles in our legs. (Some speculate that this is why we begin tapping our feet.) In other words, sound stirs us at our biological roots. As Schopenhauer wrote, “It is we ourselves who are tortured by the strings.”
We can now begin to understand where these feelings come from, why a mass of vibrating air hurtling through space can trigger such intense states of excitement. A paper in Nature Neuroscience by a team of Montreal researchers marks an important step in revealing the precise underpinnings of “the potent pleasurable stimulus” that is music. Although the study involves plenty of fancy technology, including fMRI and ligand-based positron emission tomography (PET) scanning, the experiment itself was rather straightforward. After screening 217 individuals who responded to advertisements requesting people that experience “chills to instrumental music,” the scientists narrowed down the subject pool to ten. (These were the lucky few who most reliably got chills.) The scientists then asked the subjects to bring in their playlist of favorite songs – virtually every genre was represented, from techno to tango – and played them the music while their brain activity was monitored.
Attention, Learning, and the Value of Information
Despite many studies on selective attention, fundamental questions remain about its nature and neural mechanisms. Here I draw from the animal and machine learning fields that describe attention as a mechanism for active learning and uncertainty reduction and explore the implications of this view for understanding visual attention and eye movement control. I propose that a closer integration of these different views has the potential greatly to expand our understanding of oculomotor control and our ability to use this system as a window into high level but poorly understood cognitive functions, including the capacity for curiosity and exploration and for inferring internal models of the external world.
Our eyes adapt to screens
The time most of us spend looking at a screen has rapidly increased over the past decade. If we’re not at work on the computer, we’re likely to stay tuned into the online sphere via a smart phone or tablet. Shelves of books are being replaced by a single e-book reader; and television shows and movies are available anywhere, any time.
So what does all this extra screen time mean for our eyes?
Well, you’ll be pleased to hear that like many good eye myths, there is simply no evidence to support this old wives’ tale.
Once we reach the age of ten years or so, it is practically impossible to injure the eyes by looking at something – the exception, of course, being staring at the Sun or similarly bright objects. Earlier in life, what we look at – or rather, how clearly we see – can affect our vision because the neural pathways between the eye and brain are still developing.
When we read off a piece of paper, light from the ambient environment is reflected off the surface of the paper and into our eyes. The retina at the back of the eye captures the light and begins the process of converting it into a signal that the brain understands.
The process of reading from screens is similar, except that the light is emitted directly by the screen, rather than being reflected.