Hit a 95 mph baseball? Scientists pinpoint how we see it coming
How does San Francisco Giants slugger Pablo Sandoval swat a 95 mph fastball, or tennis icon Venus Williams see the oncoming ball, let alone return her sister Serena’s 120 mph serves? For the first time, vision scientists at the University of California, Berkeley, have pinpointed how the brain tracks fast-moving objects.
The discovery advances our understanding of how humans predict the trajectory of moving objects when it can take one-tenth of a second for the brain to process what the eye sees.
That 100-millisecond holdup means that in real time, a tennis ball moving at 120 mph would have already advanced 15 feet before the brain registers the ball’s location. If our brains couldn’t make up for this visual processing delay, we’d be constantly hit by balls, cars and more.
Thankfully, the brain “pushes” forward moving objects so we perceive them as further along in their trajectory than the eye can see, researchers said.
“For the first time, we can see this sophisticated prediction mechanism at work in the human brain,” said Gerrit Maus, a postdoctoral fellow in psychology at UC Berkeley and lead author of the paper published today (May 8) in the journal, Neuron.
A clearer understanding of how the brain processes visual input – in this case life in motion – can eventually help in diagnosing and treating myriad disorders, including those that impair motion perception. People who cannot perceive motion cannot predict locations of objects and therefore cannot perform tasks as simple as pouring a cup of coffee or crossing a road, researchers said.
This study is also likely to have a major impact on other studies of the brain. Its findings come just as the Obama Administration initiates its push to create a Brain Activity Map Initiative, which will further pave the way for scientists to create a roadmap of human brain circuits, as was done for the Human Genome Project.
Using functional Magnetic Resonance Imaging (fMRI) Gerrit and fellow UC Berkeley researchers Jason Fischer and David Whitney located the part of the visual cortex that makes calculations to compensate for our sluggish visual processing abilities. They saw this prediction mechanism in action, and their findings suggest that the middle temporal region of the visual cortex known as V5 is computing where moving objects are most likely to end up.
For the experiment, six volunteers had their brains scanned, via fMRI, as they viewed the “flash-drag effect,”(a, b) a visual illusion in which we see brief flashes shifting in the direction of the motion.
“The brain interprets the flashes as part of the moving background, and therefore engages its prediction mechanism to compensate for processing delays,” Maus said.
The researchers found that the illusion – flashes perceived in their predicted locations against a moving background and flashes actually shown in their predicted location against a still background – created the same neural activity patterns in the V5 region of the brain. This established that V5 is where this prediction mechanism takes place, they said.
In a study published earlier this year, Maus and his fellow researchers pinpointed the V5 region of the brain as the most likely location of this motion prediction process by successfully using transcranial magnetic stimulation, a non-invasive brain stimulation technique, to interfere with neural activity in the V5 region of the brain, and disrupt this visual position-shifting mechanism.
“Now not only can we see the outcome of prediction in area V5,” Maus said. “But we can also show that it is causally involved in enabling us to see objects accurately in predicted positions.”
On a more evolutionary level, the latest findings reinforce that it is actually advantageous not to see everything exactly as it is. In fact, it’s necessary to our survival:
“The image that hits the eye and then is processed by the brain is not in sync with the real world, but the brain is clever enough to compensate for that,” Maus said. “What we perceive doesn’t necessarily have that much to do with the real world, but it is what we need to know to interact with the real world.”
Bursts of Brain Activity May Protect Against Alzheimer's Disease
TAU reveals the missing link between brain patterns and Alzheimer’s
Evidence indicates that the accumulation of amyloid-beta proteins, which form the plaques found in the brains of Alzheimer’s patients, is critical for the development of Alzheimer’s disease, which impacts 5.4 million Americans. And not just the quantity, but also the quality of amyloid-beta peptides is crucial for Alzheimer’s initiation. The disease is triggered by an imbalance in two different amyloid species — in Alzheimer’s patients, there is a reduction in a relative level of healthy amyloid-beta 40 compared to 42.
Now Dr. Inna Slutsky of Tel Aviv University’s Sackler Faculty of Medicine and the Sagol School of Neuroscience, with postdoctoral fellow Dr. Iftach Dolev and PhD student Hilla Fogel, have uncovered two main features of the brain circuits that impact this crucial balance. The researchers have found that patterns of electrical pulses (called “spikes”) in the form of high-frequency bursts and the filtering properties of synapses are crucial to the regulation of the amyloid-beta 40/42 ratio. Synapses that transfer information in spike bursts improve the amyloid-beta 40/42 ratio.
This represents a major advance in understanding that brain circuits regulate composition of amyloid-beta proteins, showing that the disease is not just driven by genetic mutations, but by physiological mechanisms as well. Their findings were recently reported in the journal Nature Neuroscience.
Tipping the balance
High-frequency bursts in the brain are critical for brain plasticity, information processing, and memory encoding. To check the connection between spike patterns and the regulation of amyloid-beta 40/42 ratio, Dr. Dolev applied electrical pulses to the hippocampus, a brain region involved in learning and memory.
When increasing the rate of single pulses at low frequencies in rat hippocampal slices, levels of both amyloid-beta 42 and 40 grew, but the 40/42 ratio remained the same. However, when the same number of pulses was distributed in high-frequency bursts, researchers discovered an increased amyloid-beta 40 production. In addition, the researchers found that only synapses optimized to transfer encoded by bursts contributed towards tipping the balance in favor of amyloid-beta 40. Further investigations conducted by Fogel revealed that the connection between spiking patterns and the type of amyloid-beta produced could revolve around a protein called presenilin. “We hypothesize that changes in the temporal patterns of spikes in the hippocampus may trigger structural changes in the presenilin, leading to early memory impairments in people with sporadic Alzheimer’s,” explains Dr. Slutsky.
Behind the bursts
According to Dr. Slutsky, different kinds of environmental changes and experiences — including sensory and emotional experience — can modify the properties of synapses and change the spiking patterns in the brain. Previous research has suggested that a stimulant-rich environment could be a contributing factor in preventing the development of Alzheimer’s disease, much as crossword and similar puzzles appear to stimulate the brain and delay the onset of Alzheimer’s. In the recent study, the researchers discovered that changes in sensory experiences also regulate synaptic properties — leading to an increase in amyloid-beta 40.
In the next stage, Dr. Slutsky and her team are aiming to manipulate activity patterns in the specific hippocampal pathways of Alzheimer’s models to test if it can prevent the initiation of cognitive impairment. The ability to monitor dynamics of synaptic activity in humans would be a step forward early diagnosis of sporadic Alzheimer’s.
Human Connectome Project releases major data set on brain connectivity
The Human Connectome Project, a five-year endeavor to link brain connectivity to human behavior, has released a set of high-quality imaging and behavioral data to the scientific community. The project has two major goals: to collect vast amounts of data using advanced brain imaging methods on a large population of healthy adults, and to make the data freely available so that scientists worldwide can make further discoveries about brain circuitry.
The initial data release includes brain imaging scans plus behavioral information — individual differences in personality, cognitive capabilities, emotional characteristics and perceptual function — obtained from 68 healthy adult volunteers. Over the next several years, the number of subjects studied will increase steadily to a final target of 1,200. The initial release is an important milestone because the new data have much higher resolution in space and time than data obtained by conventional brain scans.
The Human Connectome Project (HCP) consortium is led by David C. Van Essen, PhD, Alumni Endowed Professor at Washington University School of Medicine in St. Louis, and Kamil Ugurbil, PhD, Director of the Center for Magnetic Resonance Research and the McKnight Presidential Endowed Chair Professor at the University of Minnesota.
“By making this unique data set available now, and continuing with regular data releases every quarter, the Human Connectome Project is enabling the scientific community to immediately begin exploring relationships between brain circuits and individual behavior,” says Van Essen. “The HCP will have a major impact on our understanding of the healthy adult human brain, and it will set the stage for future projects that examine changes in brain circuits underlying the wide variety of brain disorders afflicting humankind.”
The consortium includes more than 100 investigators and technical staff at 10 institutions in the United States and Europe (www.humanconnectome.org). It is funded by 16 components of the National Institutes of Health via the Blueprint for Neuroscience Research (www.neuroscienceblueprint.nih.gov).
“The high quality of the data being made available in this release reflects an intensive, multiyear effort to improve the data acquisition and analysis methods by this dedicated international team of investigators,” says Ugurbil.
The data set includes information about brain connectivity in each individual, using two distinct magnetic resonance imaging (MRI) approaches. One, called resting-state functional connectivity, is based on spontaneous fluctuations in functional MRI signals that occur in a complex pattern in space and time throughout the gray matter of the brain. Another, called diffusion imaging, provides information about the long-distance “wiring” – the anatomical pathways traversing the brain’s white matter. Each method has its own limitations, and analyses of both functional connectivity and structural connectivity in each subject should allow deeper insight than by either method alone.
Each subject is also scanned while performing a variety of tasks within the scanner, thereby providing extensive information about “Task-fMRI” brain activation patterns. Behavioral data using a variety of tests performed outside the scanner are being released along with the scan data for each subject. The subjects are drawn from families that include siblings, some of whom are twins. This will enable studies of the heritability of brain circuits.
The imaging data set released by the HCP takes up about two terabytes (2 trillion bytes) of computer memory — the equivalent of more than 400 DVDs — and is stored in a customized database called “ConnectomeDB.”
“ConnectomeDB is the next-generation neuroinformatics software for data sharing and data mining. It’s a convenient and user-friendly way for scientists to explore the available HCP data and to download data of interest for their research,” says Daniel S. Marcus, PhD, assistant professor of radiology and director of the Neuroinformatics Research Group at Washington University School of Medicine. “The Human Connectome Project represents a major advance in sharing brain imaging data in ways that will accelerate the pace of discovery about the human brain in health and disease.”