You're meeting a friend in a crowded cafeteria. Do your eyes scan the room like a roving spotlight, moving from face to face, or do you take in the whole scene, hoping that your friend's face will pop out at you? And what, for that matter, determines how fast you can scan the room?
Researchers at MIT's Picower Institute for Learning and Memory say you are more likely to scan the room, jumping from face to face as you search for your friend. In addition, the timing of these jumps appears to be determined by waves of activity in the brain that act as a clock. The study, which appears in the Aug. 13 issue of the journal Neuron, sheds new light on a long-standing debate among neuroscientists over how the visual system picks out an object of interest in a complex scene.
In the study, monkeys were given the task of searching for one particular tilted, colored bar among a field of bars on a computer screen. By monitoring the activity of neurons in three of the animals' brain regions, researchers found that the monkeys spontaneously shifted their attention in a sequence, like a moving spotlight that jumped from location to location.
Health & Wellness
Scientists have discovered that even in adults born with extremely impaired sight, the brain can rewire itself to recognize sections of the retina that have been restored by gene therapy.
The discovery of the brain's surprising adaptability comes a year after three blind volunteers received doses of corrective genes to selected areas of their retinas at Shands at the University of Florida medical center.
Now, more than a year later, researchers say tiny portions of the patients' retinas that have received gene therapy have kept their restored function, as much as 1,000-fold increases for day vision and 63,000-fold for night vision.
But in an unexpected finding, scientists writing in Thursday's (Aug. 13) New England Journal of Medicine say the treated parts of the retinas may have acquired enough image-processing strength to rival the retina's normal center for visual perception, called the fovea, for the brain's attention.
The discovery of the brain's surprising adaptability comes a year after three blind volunteers received doses of corrective genes to selected areas of their retinas at Shands at the University of Florida medical center.
Now, more than a year later, researchers say tiny portions of the patients' retinas that have received gene therapy have kept their restored function, as much as 1,000-fold increases for day vision and 63,000-fold for night vision.
But in an unexpected finding, scientists writing in Thursday's (Aug. 13) New England Journal of Medicine say the treated parts of the retinas may have acquired enough image-processing strength to rival the retina's normal center for visual perception, called the fovea, for the brain's attention.
For close to a decade, pharmaceutical researchers have been in hot pursuit of compounds to activate a key nicotine receptor that plays a role in cognitive processes. Triggering it, they hope, might prevent or even reverse the devastation wrought by Alzheimer's disease.
A new study from the Salk Institute for Biological Studies, however, suggests that when the receptor, alpha-7, encounters beta amyloid, the toxic protein found in the disease's hallmark plaques, the two may actually go rogue. In combination, alpha-7 and beta amyloid appear to exacerbate Alzheimer's symptoms, while eliminating alpha-7 seems to nullify beta amyloid's harmful effects.
These findings, reported recently in The Journal of Neuroscience, may shed new light on the processes leading to Alzheimer's and could have important implications for researchers seeking to combat the disease.
A new study from the Salk Institute for Biological Studies, however, suggests that when the receptor, alpha-7, encounters beta amyloid, the toxic protein found in the disease's hallmark plaques, the two may actually go rogue. In combination, alpha-7 and beta amyloid appear to exacerbate Alzheimer's symptoms, while eliminating alpha-7 seems to nullify beta amyloid's harmful effects.
These findings, reported recently in The Journal of Neuroscience, may shed new light on the processes leading to Alzheimer's and could have important implications for researchers seeking to combat the disease.
Life in the fruit bowl is no longer the pits, thanks to a University of Alberta researcher.
Christina Engels has found a way to turn the throwaway kernels in mangos into a natural food preservative that could help prevent Listeriosis outbreaks like the one that killed 21 Canadians last year.
The findings can also apply to other fruit seeds like grapes, said Engels, who conducted the research to earn her master's degree from the Department of Agricultural, Food and Nutritional Science at the U of A. The research is published in the latest Journal of Agricultural and Food Chemistry.
Christina Engels has found a way to turn the throwaway kernels in mangos into a natural food preservative that could help prevent Listeriosis outbreaks like the one that killed 21 Canadians last year.
The findings can also apply to other fruit seeds like grapes, said Engels, who conducted the research to earn her master's degree from the Department of Agricultural, Food and Nutritional Science at the U of A. The research is published in the latest Journal of Agricultural and Food Chemistry.
Our genome is constantly under attack from things like UV light and toxins, which can damage or even break DNA strands and ultimately lead to cancer and other diseases. Scientists have known for a long time that when DNA is damaged, a key enzyme sets off a cellular 'alarm bell' to alert the cell to start the repair process, but until recently little was known about how the cell detects and responds to this alarm. In a study published in Nature Structural and Molecular Biology, researchers at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have identified a whole family of proteins capable of a direct response to the alarm signal.
Our genome is a huge repository of information guiding the construction and function of all the cells in our bodies. Cells sustain many hits to their DNA every day, which can lead tomutations, so they maintain a fleet of DNA repair machinery that can be rapidly mobilized and sent to damaged sites in an emergency.
Because our DNA is so long and unwieldy, it needs to be packaged up with proteins and organized into a complex structure called chromatin. Scientists have known for 50 years that one component of chromatin, an enzyme known as PARP1, is activated by DNA damage and produces a molecular signal, called PAR, which raises the alarm at the site of the damage. In recent weeks, scientists have for the first time worked out how PAR is rapidly detected by the cell; in their Nature Structural and Molecular Biology paper, the group of Andreas Ladurner and their colleagues at EMBL have identified a whole family of proteins that respond to this signal by binding to it directly.
Our genome is a huge repository of information guiding the construction and function of all the cells in our bodies. Cells sustain many hits to their DNA every day, which can lead tomutations, so they maintain a fleet of DNA repair machinery that can be rapidly mobilized and sent to damaged sites in an emergency.
Because our DNA is so long and unwieldy, it needs to be packaged up with proteins and organized into a complex structure called chromatin. Scientists have known for 50 years that one component of chromatin, an enzyme known as PARP1, is activated by DNA damage and produces a molecular signal, called PAR, which raises the alarm at the site of the damage. In recent weeks, scientists have for the first time worked out how PAR is rapidly detected by the cell; in their Nature Structural and Molecular Biology paper, the group of Andreas Ladurner and their colleagues at EMBL have identified a whole family of proteins that respond to this signal by binding to it directly.
New evidence that early modern humans used fire in southern Africa in a controlled way to increase the quality and efficiency of stone tools is changing how researchers understand the evolution of human behavior, and in particular, the evolution of human brain power.
Curtis Marean, a paleoanthropologist with the Institute of Human Origins at Arizona State University, and an international team of researchers with members from South Africa, England, Australia and France found 72,000-year-old, silcrete rocks that had been fired and flaked to make stone tools in a cave along the coast of the southern tip of Africa in Mossel Bay.
The finding indicates that humans' ability to solve complex problems may have occurred at the same time their modern genetic lineage appeared, rather than developing later as has been widely speculated.
Curtis Marean, a paleoanthropologist with the Institute of Human Origins at Arizona State University, and an international team of researchers with members from South Africa, England, Australia and France found 72,000-year-old, silcrete rocks that had been fired and flaked to make stone tools in a cave along the coast of the southern tip of Africa in Mossel Bay.
The finding indicates that humans' ability to solve complex problems may have occurred at the same time their modern genetic lineage appeared, rather than developing later as has been widely speculated.
What do flocks of birds have in common with trust, monogamy, and even breast milk? According to a new report in the journal Science, they are regulated by virtually identical neurochemicals in the brain, known as oxytocin in mammals and mesotocin in birds.
Neurobiologists at Indiana University showed that if the actions of mesotocin are blocked in the brains of zebra finches, a highly social songbird, the birds shift their social preferences. They spend significantly less time with familiar individuals and more time with unfamiliar individuals. The birds also become less social, preferring to spend less time with a large group of same-sex birds and more time with a smaller group. Conversely, if birds are administered mesotocin instead of the blocker, the finches become more social and prefer familiar partners.
Perhaps most striking is the fact that none of the treatments affect males -- only females.
Neurobiologists at Indiana University showed that if the actions of mesotocin are blocked in the brains of zebra finches, a highly social songbird, the birds shift their social preferences. They spend significantly less time with familiar individuals and more time with unfamiliar individuals. The birds also become less social, preferring to spend less time with a large group of same-sex birds and more time with a smaller group. Conversely, if birds are administered mesotocin instead of the blocker, the finches become more social and prefer familiar partners.
Perhaps most striking is the fact that none of the treatments affect males -- only females.
In 1900, only 4.1 percent of U.S. citizens were older than 65; in 2000 that number had jumped to 12.6 percent; and by the year 2030, 20 percent of our population could be in that category.
Cognitive decline was long seen as an inevitable consequence of aging, but recent years have seen a surge of interest in activities and products touted to forestall this outcome. What is the truth? Is decline inevitable, or is there a possibility of retaining our faculties if we exercise them? And which kinds of exercises and products are effective, and which are merely hype?
According to the most rigorous and comprehensive review of the scientific findings ever, there is clear evidence that cognitive-enrichment activities including intellectually stimulating pursuits, social engagement, and especially physical exercise may indeed preserve or enhance various aspects of cognitive functioning as we age.
Cognitive decline was long seen as an inevitable consequence of aging, but recent years have seen a surge of interest in activities and products touted to forestall this outcome. What is the truth? Is decline inevitable, or is there a possibility of retaining our faculties if we exercise them? And which kinds of exercises and products are effective, and which are merely hype?
According to the most rigorous and comprehensive review of the scientific findings ever, there is clear evidence that cognitive-enrichment activities including intellectually stimulating pursuits, social engagement, and especially physical exercise may indeed preserve or enhance various aspects of cognitive functioning as we age.
The genes that play a role in adolescent insomnia are the same as those involved in depression and anxiety, according to a research abstract that will be presented on June 8, at Sleep 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies.
Results of the study indicate that insomnia as a diagnosis has a moderate heritability in 8 to 16 year olds, which is consistent with past studies of insomnia symptoms in adults. Significant genetic effects shared between insomnia, depression and anxiety suggests that overlapping genetic mechanisms exist to link the disorders.
Results of the study indicate that insomnia as a diagnosis has a moderate heritability in 8 to 16 year olds, which is consistent with past studies of insomnia symptoms in adults. Significant genetic effects shared between insomnia, depression and anxiety suggests that overlapping genetic mechanisms exist to link the disorders.
The Centre for Addiction and Mental Health (CAMH) has discovered a new form of intellectual disability involving mental retardation (MR) along with the eye defect retinitis pigmentosa (RP). CAMH also discovered the previously unidentified gene that causes this disorder, CC2D2A. This scientific advance will help understand the developmental and biological processes involved in brain development, and may help identify ways to diagnose and treat intellectual disabilities.
Under the direction of Dr. John Vincent, scientist at CAMH, the team identified a mutation in CC2D2A that causes the production of a shortened protein missing the C2, or calcium-binding, domain. This protein mutation results in faulty cell function, which leads to MR with RP.
Under the direction of Dr. John Vincent, scientist at CAMH, the team identified a mutation in CC2D2A that causes the production of a shortened protein missing the C2, or calcium-binding, domain. This protein mutation results in faulty cell function, which leads to MR with RP.
