sarah-tonin:
Neuroscientists successfully control the dreams of rats. Could humans be next?
By George Dvorsky
Researchers working at MIT have successfully manipulated the content of a rat’s dream by replaying an audio cue that was associated with the previous day’s events, namely running through a maze (what else). The breakthrough furthers our understanding of how memory gets consolidated during sleep — but it also holds potential for the prospect of “dream engineering.”
Working at MIT’s Picower Institute for Learning and Memory, neuroscientist Matt Wilson was able to accomplish this feat by exploiting the way the brain’s hippocampus encodes self-experienced events into memory. Scientists know that our hippocampus is busy at work replaying a number of the day’s events while we sleep — a process that’s crucial for memory consolidation. But what they did not know was whether or not these “replays” could be influenced by environmental cues.
Read More.
This is absolutely amazing. As usual, I have to caution against putting so much weight on correlational data. But since so little work has been done in this area that doesn’t rely on EEGs, I’m going to say it again - this is amazing. I can’t wait till we move on to other animals!
Check out the rest of the io9 article for a quick description of their methods, and if you’re lucky enough to have access, here’s the original paper. Even if you don’t have access, you can still check out their images which are actually really helpful.
12:39 pm • 3 September 2012 • 36 notes
“But there is a problem with this: An account of how the brain constrains our ability to perceive has no greater claim to being an account of our ability to perceive art than it has to being an account of how we perceive sports, or how we perceive the man across from us on the subway. In works about neuroaesthetics, art is discussed in the prefaces and touted on the book jackets, but never really manages to show up in the body of the works themselves!
Some of us might wonder whether the relevant question is how weperceive works of art, anyway. What we ought to be asking is: Why do we value some works as art? Why do they move us? Why does art matter? And here again, the closest neural scientists or psychologists come to saying anything about this kind of aesthetic evaluation is to say something about preference. But the class of things we like, or that we prefer as compared to other things, is much wider than the class of things we value as art. And the sorts of reasons we have for valuing one art work over another are not the same kind of reasons we would give for liking one person more than another, or one flavor more than another. And it is no help to appeal to beauty here. Beauty is both too wide and too narrow. Not all art works are beautiful (or pleasing for that matter, even if many are), and not everything we find beautiful (a person, say, or a sunset) is a work of art.”
From Art and the Limits of Neuroscience by Alva Noe
5:21 pm • 20 August 2012 • 6 notes
“A growing body of evidence suggests that learning to play an instrument and continuing to practice and play it may offer mental benefits throughout life. Hearing has also been shown to be positively affected by making music.
The latest study, published in the July issue of Frontiers in Human Neuroscience, shows that musical instrument training may reduce the effects of mental decline associated with aging. The research found that older adults who learned music in childhood and continued to play an instrument for at least 10 years outperformed others in tests of memory and cognitive ability.
It also revealed that sustaining musical activity during advanced age may enhance thinking ability, neutralizing any negative impact of age and even lack of education. It’s unclear, however, whether starting an instrument in adulthood provides any mental advantages.
“Behaviors can change your brain,” said study author Brenda Hanna-Pladdy, an assistant professor of neurology, radiology and imaging sciences at Emory University, in Atlanta.
The study confirms and refines findings from previous research published April 2011 in the journal Neuropsychology.
In childhood, when the brain is still developing, it seems that learning a musical instrument and continuing to play it for at least a decade or more may lay the groundwork for benefits later in life, Hanna-Pladdy said. But it’s also valuable to then pick up the instrument in middle age and start playing again, she noted.
In this study, 70 musicians and non-musicians aged 59 to 80 were evaluated by neuropsychological tests and surveyed about general lifestyle activities. The musicians scored higher on tests of mental acuity, visual-spatial judgment, verbal memory and recall, and motor dexterity.
Hanna-Pladdy, a flutist, became interested in studying the impact of music education on the brain through her study of people with skilled movement disorders, such as those who had suffered a stroke. She realized that music could be a natural way to offer multi-sensory stimulation, an effective way to treat such disorders. She then became interested in learning more about the actual effect of musical training on the brain.”
From Musicians’ Brains Might Have an Edge on Aging
11:50 am • 6 August 2012 • 4 notes
George A. Miller, a Pioneer in Cognitive Psychology, Is Dead at 92
Psychological research was in a kind of rut in 1955 when George A. Miller, a professor at Harvard, delivered a paper titled “The Magical Number Seven, Plus or Minus Two,” which helped set off an explosion of new thinking about thinking and opened a new field of research known as cognitive psychology.
The dominant form of psychological study at the time, behaviorism, had rejected Freud’s theories of ‘the mind’ as too intangible, untestable and vaguely mystical. Its researchers instead studied behavior in laboratories, observing and recording test subjects’ responses to carefully administered stimuli. Mainly, they studied rats.
Dr. Miller, who died on July 22 at his home in Plainsboro, N.J., at the age of 92, revolutionized the world of psychology by showing in his paper that the human mind, though invisible, could also be observed and tested in the lab.
‘George Miller, more than anyone else, deserves credit for the existence of the modern science of mind,’ the Harvard psychologist and author Steven Pinker said in an interview. ‘He was certainly among the most influential experimental psychologists of the 20th century.’
Dr. Miller borrowed a testing model from the emerging science of computer programming in the early 1950s to show that humans’ short-term memory, when encountering the unfamiliar, could absorb roughly seven new things at a time.
When asked to repeat a random list of letters, words or numbers, he wrote, people got stuck ‘somewhere in the neighborhood of seven.’
Some people could recall nine items on the list, some fewer than seven. But regardless of the things being recalled — color-words, food-words, numbers with decimals, numbers without decimals, consonants, vowels — seven was the statistical average for short-term storage. (Long-term memory, which followed another cognitive formula, was virtually unlimited.)
Dr. Miller could not say why it was seven. He speculated that survival might have favored early humans who could retain ‘a little information about a lot of things’ rather than /a lot of information about a small segment of the environment.’”
11:44 am • 6 August 2012 • 12 notes
ucsdhealthsciences:
Alzheimer’s Cognitive Decline Slows in Advanced Age
The greatest risk factor for Alzheimer’s disease (AD) is advancing age. By age 85, the likelihood of developing the dreaded neurological disorder is roughly 50 percent. But researchers at the University of California, San Diego School of Medicine say AD hits hardest among the “younger elderly” – people in their 60s and 70s – who show faster rates of brain tissue loss and cognitive decline than AD patients 80 years and older.
The findings, reported online in the August 2, 2012 issue of the journal PLOS One, have profound implications for both diagnosing AD – which currently afflicts an estimated 5.6 million Americans, a number projected to triple by 2050 – and efforts to find new treatments. There is no cure for AD and existing therapies do not slow or stop disease progression.
“One of the key features for the clinical determination of AD is its relentless progressive course,” said Dominic Holland, PhD, a researcher at the Department of Neurosciences at UC San Diego who led the study and is the paper’s first author. “Patients typically show marked deterioration year after year. If older patients are not showing the same deterioration from one year to the next, doctors may be hesitant to diagnose AD, and thus these patients may not receive appropriate care, which can be very important for their quality of life.”
Holland and colleagues used imaging and biomarker data from participants in the Alzheimer’s Disease Neuroimaging Initiative, a multi-institution effort coordinated at UC San Diego. They examined 723 people, ages 65 to 90 years, who were categorized as either cognitively normal, with mild cognitive impairment (an intermediate stage between normal, age-related cognitive decline and dementia) or suffering from full-blown AD.
“We found that younger elderly show higher rates of cognitive decline and faster rates of tissue loss in brain regions that are vulnerable during the early stages of AD,” said Holland. “Additionally cerebrospinal fluid biomarker levels indicate a greater disease burden in younger than in older individuals.”
Holland said it’s not clear why AD is more aggressive among younger elderly.
“It may be that patients who show onset of dementia at an older age, and are declining slowly, have been declining at that rate for a long time,” said senior author Linda McEvoy, PhD, associate professor of radiology. “But because of cognitive reserve or other still-unknown factors that provide ‘resistance’ against brain damage, clinical symptoms do not manifest till later age.”
Another possibility, according to Holland, is that older patients may be suffering from mixed dementia – a combination of AD pathology and other neurological conditions. These patients might withstand the effects of AD until other adverse factors, such as brain lesions caused by cerebrovascular disease, take hold. At the moment, AD can only be diagnosed definitively by an autopsy. “So we do not yet know the underlying neuropathology of participants in this study,” Holland said.
Clinical trials to find new treatments for AD may be impacted by the differing rates, researchers said. “Our results show that if clinical trials of candidate therapies predominately enroll older elderly, who show slower rates of change over time, the ability of a therapy to successfully slow disease progression may not be recognized, leading to failure of the clinical trial,” said Holland. “Thus, it’s critical to take into account age as a factor when enrolling subjects for AD clinical trials.”
The obvious downside of the findings is that younger patients with AD lose more of their productive years to the disease, Holland noted. “The good news in all of this is that our results indicate those who survive into the later years before showing symptoms of AD will experience a less aggressive form of the disease.”
(via fyeahmedlab)
11:03 pm • 5 August 2012 • 82 notes
![crystilogic:
Colorized scanning electron microscope image, by Tina Carvalho (c. 2011), of a nerve ending whose cell membrane has broken open, revealing the synaptic vesicles (orange & blue) that store neurotransmitters released when the neuron fires [more info]](http://24.media.tumblr.com/tumblr_m1eadxIS4q1qzouqmo1_500.png)
crystilogic:
Colorized scanning electron microscope image, by Tina Carvalho (c. 2011), of a nerve ending whose cell membrane has broken open, revealing the synaptic vesicles (orange & blue) that store neurotransmitters released when the neuron fires [more info]
(via johnnyappleseedday)
10:12 am • 11 July 2012 • 69 notes
sarah-tonin:
medicalschool:
Neuropathologist arranging slices of a human brain for gross pathology. By studying the shape and structure of a brain, most brain disorders can be diagnosed. For instance, Alzheimer’s disease causes shrinkage and the fissures appear to grow. A stroke causes localized brain tissue death, and Creutzfeldt-Jakob disease gives the brain a spongy appearance with evident holes. This type of pathology is carried out not only to try to find causes of death, but also in research into all brain disorders.
I wish more labs were painted BRIGHT YELLOW.
2:44 pm • 5 July 2012 • 274 notes
“My son’s high-speed adventure raised the question long asked by people who have pondered the class of humans we call teenagers: What on Earth was he doing? Parents often phrase this question more colorfully. Scientists put it more coolly. They ask, What can explain this behavior? But even that is just another way of wondering, What is wrong with these kids? Why do they act this way? The question passes judgment even as it inquires.
Through the ages, most answers have cited dark forces that uniquely affect the teen. Aristotle concluded more than 2,300 years ago that “the young are heated by Nature as drunken men by wine.” A shepherd in William Shakespeare’s The Winter’s Tale wishes “there were no age between ten and three-and-twenty, or that youth would sleep out the rest; for there is nothing in the between but getting wenches with child, wronging the ancientry, stealing, fighting.” His lament colors most modern scientific inquiries as well. G. Stanley Hall, who formalized adolescent studies with his 1904 Adolescence: Its Psychology and Its Relations to Physiology, Anthropology, Sociology, Sex, Crime, Religion and Education, believed this period of “storm and stress” replicated earlier, less civilized stages of human development. Freud saw adolescence as an expression of torturous psychosexual conflict; Erik Erikson, as the most tumultuous of life’s several identity crises. Adolescence: always a problem.
Such thinking carried into the late 20th century, when researchers developed brain-imaging technology that enabled them to see the teen brain in enough detail to track both its physical development and its patterns of activity. These imaging tools offered a new way to ask the same question—What’s wrong with these kids?—and revealed an answer that surprised almost everyone. Our brains, it turned out, take much longer to develop than we had thought. This revelation suggested both a simplistic, unflattering explanation for teens’ maddening behavior—and a more complex, affirmative explanation as well.
The first full series of scans of the developing adolescent brain—a National Institutes of Health (NIH) project that studied over a hundred young people as they grew up during the 1990s—showed that our brains undergo a massive reorganization between our 12th and 25th years. The brain doesn’t actually grow very much during this period. It has already reached 90 percent of its full size by the time a person is six, and a thickening skull accounts for most head growth afterward. But as we move through adolescence, the brain undergoes extensive remodeling, resembling a network and wiring upgrade.
For starters, the brain’s axons—the long nerve fibers that neurons use to send signals to other neurons—become gradually more insulated with a fatty substance called myelin (the brain’s white matter), eventually boosting the axons’ transmission speed up to a hundred times. Meanwhile, dendrites, the branchlike extensions that neurons use to receive signals from nearby axons, grow twiggier, and the most heavily used synapses—the little chemical junctures across which axons and dendrites pass notes—grow richer and stronger. At the same time, synapses that see little use begin to wither. This synaptic pruning, as it is called, causes the brain’s cortex—the outer layer of gray matter where we do much of our conscious and complicated thinking—to become thinner but more efficient. Taken together, these changes make the entire brain a much faster and more sophisticated organ.
This process of maturation, once thought to be largely finished by elementary school, continues throughout adolescence. Imaging work done since the 1990s shows that these physical changes move in a slow wave from the brain’s rear to its front, from areas close to the brain stem that look after older and more behaviorally basic functions, such as vision, movement, and fundamental processing, to the evolutionarily newer and more complicated thinking areas up front. The corpus callosum, which connects the brain’s left and right hemispheres and carries traffic essential to many advanced brain functions, steadily thickens. Stronger links also develop between the hippocampus, a sort of memory directory, and frontal areas that set goals and weigh different agendas; as a result, we get better at integrating memory and experience into our decisions. At the same time, the frontal areas develop greater speed and richer connections, allowing us to generate and weigh far more variables and agendas than before.
When this development proceeds normally, we get better at balancing impulse, desire, goals, self-interest, rules, ethics, and even altruism, generating behavior that is more complex and, sometimes at least, more sensible. But at times, and especially at first, the brain does this work clumsily. It’s hard to get all those new cogs to mesh.
Beatriz Luna, a University of Pittsburgh professor of psychiatry who uses neuroimaging to study the teen brain, used a simple test that illustrates this learning curve. Luna scanned the brains of children, teens, and twentysomethings while they performed an antisaccade task, a sort of eyes-only video game where you have to stop yourself from looking at a suddenly appearing light. You view a screen on which the red crosshairs at the center occasionally disappear just as a light flickers elsewhere on the screen. Your instructions are to not look at the light and instead to look in the opposite direction. A sensor detects any eye movement. It’s a tough assignment, since flickering lights naturally draw our attention. To succeed, you must override both a normal impulse to attend to new information and curiosity about something forbidden. Brain geeks call this response inhibition.”
From “Beautiful Brains” by David Dobbs
8:53 pm • 12 June 2012 • 3 notes
Know Your Neurons: How to Classify Different Types of Neurons in the Brain’s Forest
Different Types of Neurons (click to enlarge). A. Purkinje cell B. Granule cell C. Motor neuron D. Tripolar neuron E. Pyramidal Cell F. Chandelier cell G. Spindle neuron H. Stellate cell (Credit: Ferris Jabr; based on reconstructions and drawings by Cajal)
11:14 pm • 16 May 2012 • 12 notes
