How Amnesia Works

Those movies where someone gets hit on the head and can’t remember who they are anymore? They’re actually not too far off from the reality of amnesia. Learn everything about this bizarre and life-robbing condition with Josh and Chuck in this Stuff You Should Know podcast.

And there’s still time to cast your vote for the SYSK podcast to win a Webby Award! Vote here.

stufftoblowyourmind:

The Shadow People: Do strange shadow people haunt the corners of our existence, or is there a scientific answer within the human brain? Join Robert and guests Ben and Matt of Stuff They Don’t Want You To Know as they discuss the answers.

(Source: stufftoblowyourmind.com)

neurosciencestuff:

New ideas change your brain cells
A new University of British Columbia study identifies an important molecular change that occurs in the brain when we learn and remember.
Published this month in Nature Neuroscience, the research shows that learning stimulates our brain cells in a manner that causes a small fatty acid to attach to delta-catenin, a protein in the brain. This biochemical modification is essential in producing the changes in brain cell connectivity associated with learning, the study finds.
In animal models, the scientists found almost twice the amount of modified delta-catenin in the brain after learning about new environments. While delta-catenin has previously been linked to learning, this study is the first to describe the protein’s role in the molecular mechanism behind memory formation.
“More work is needed, but this discovery gives us a much better understanding of the tools our brains use to learn and remember, and provides insight into how these processes become disrupted in neurological diseases,” says co-author Shernaz Bamji, an associate professor in UBC’s Life Sciences Institute.
It may also provide an explanation for some mental disabilities, the researchers say. People born without the gene have a severe form of mental retardation called Cri-du-chat syndrome, a rare genetic disorder named for the high-pitched cat-like cry of affected infants. Disruption of the delta-catenin gene has also been observed in some patients with schizophrenia.
“Brain activity can change both the structure of this protein, as well as its function,” says Stefano Brigidi, first author of the article and a PhD candidate Bamji’s laboratory. “When we introduced a mutation that blocked the biochemical modification that occurs in healthy subjects, we abolished the structural changes in brain’s cells that are known to be important for memory formation.”
Background 
According to the researchers, more work is needed to fully establish the importance of delta-catenin in building the brain connectivity behind learning and memory. Disruptions to these nerve cell connections are also believed to cause neurodegenerative diseases such as Alzheimer’s and Huntington disease. Understanding the biochemical processes that are important for maintaining these connections may help address the abnormalities in nerve cells that occur in these disease states.
(Image: Shutterstock)

neurosciencestuff:

New ideas change your brain cells

A new University of British Columbia study identifies an important molecular change that occurs in the brain when we learn and remember.

Published this month in Nature Neuroscience, the research shows that learning stimulates our brain cells in a manner that causes a small fatty acid to attach to delta-catenin, a protein in the brain. This biochemical modification is essential in producing the changes in brain cell connectivity associated with learning, the study finds.

In animal models, the scientists found almost twice the amount of modified delta-catenin in the brain after learning about new environments. While delta-catenin has previously been linked to learning, this study is the first to describe the protein’s role in the molecular mechanism behind memory formation.

“More work is needed, but this discovery gives us a much better understanding of the tools our brains use to learn and remember, and provides insight into how these processes become disrupted in neurological diseases,” says co-author Shernaz Bamji, an associate professor in UBC’s Life Sciences Institute.

It may also provide an explanation for some mental disabilities, the researchers say. People born without the gene have a severe form of mental retardation called Cri-du-chat syndrome, a rare genetic disorder named for the high-pitched cat-like cry of affected infants. Disruption of the delta-catenin gene has also been observed in some patients with schizophrenia.

“Brain activity can change both the structure of this protein, as well as its function,” says Stefano Brigidi, first author of the article and a PhD candidate Bamji’s laboratory. “When we introduced a mutation that blocked the biochemical modification that occurs in healthy subjects, we abolished the structural changes in brain’s cells that are known to be important for memory formation.”

Background

According to the researchers, more work is needed to fully establish the importance of delta-catenin in building the brain connectivity behind learning and memory. Disruptions to these nerve cell connections are also believed to cause neurodegenerative diseases such as Alzheimer’s and Huntington disease. Understanding the biochemical processes that are important for maintaining these connections may help address the abnormalities in nerve cells that occur in these disease states.

(Image: Shutterstock)

stufftoblowyourmind:

The Night Janitors of the Brain: Do you think other species ever look at humans and raise an eyebrow at the amount of sleep we need? Do cockroaches and eyelash mites leave messages on our foreheads in microscopic Sharpies? Perhaps “I just popped on an apex predator’s head.” We may be the most successful species in existence, but that doesn’t mean sleep is just another one of our “choices” as a human being. It is a necessity for survival, even though it requires immobility and vulnerability. Prepare to meet the night janitors of the human brain.

(Source: stufftoblowyourmind.com)

stufftoblowyourmind:

Fig. 131 - Method of removing the brain after it is severed from the body.

(Source: vtomilk)

neuromorphogenesis:

Your brain sees things you don’t

A doctoral candidate in the UA’s Department of Psychology in the College of Science, Sanguinetti showed study participants a series of black silhouettes, some of which contained meaningful, real-world objects hidden in the white spaces on the outsides. Saguinetti worked with his adviser Mary Peterson, a professor of psychology and director of the UA’s Cognitive Science Program, and with John Allen, a UA Distinguished Professor of psychology, cognitive science and neuroscience, to monitor subjects’ brainwaves with an electroencephalogram, or EEG, while they viewed the objects.

"We were asking the question of whether the brain was processing the meaning of the objects that are on the outside of these silhouettes," Sanguinetti said. "The specific question was, ‘Does the brain process those hidden shapes to the level of meaning, even when the subject doesn’t consciously see them?"

The answer, Sanguinetti’s data indicates, is yes.

Study participants’ brainwaves indicated that even if a person never consciously recognized the shapes on the outside of the image, their brains still processed those shapes to the level of understanding their meaning.

"There’s a brain signature for meaningful processing," Sanguinetti said. A peak in the averaged brainwaves called N400 indicates that the brain has recognized an object and associated it with a particular meaning.

"It happens about 400 milliseconds after the image is shown, less than a half a second," said Peterson. "As one looks at brainwaves, they’re undulating above a baseline axis and below that axis. The negative ones below the axis are called N and positive ones above the axis are called P, so N400 means it’s a negative waveform that happens approximately 400 milliseconds after the image is shown."

The presence of the N400 peak indicates that subjects’ brains recognize the meaning of the shapes on the outside of the figure.

"The participants in our experiments don’t see those shapes on the outside; nonetheless, the brain signature tells us that they have processed the meaning of those shapes," said Peterson. "But the brain rejects them as interpretations, and if it rejects the shapes from conscious perception, then you won’t have any awareness of them."

"We also have novel silhouettes as experimental controls," Sanguinetti said. "These are novel black shapes in the middle and nothing meaningful on the outside."

The N400 waveform does not appear on the EEG of subjects when they are seeing truly novel silhouettes, without images of any real-world objects, indicating that the brain does not recognize a meaningful object in the image.

"This is huge," Peterson said. "We have neural evidence that the brain is processing the shape and its meaning of the hidden images in the silhouettes we showed to participants in our study."

The finding leads to the question of why the brain would process the meaning of a shape when a person is ultimately not going to perceive it, Sanguinetti said.

"The traditional opinion in vision research is that this would be wasteful in terms of resources," he explained. "If you’re not going to ultimately see the object on the outside why would the brain waste all these processing resources and process that image up to the level of meaning?"

"Many, many theorists assume that because it takes a lot of energy for brain processing, that the brain is only going to spend time processing what you’re ultimately going to perceive," added Peterson. "But in fact the brain is deciding what you’re going to perceive, and it’s processing all of the information and then it’s determining what’s the best interpretation."

"This is a window into what the brain is doing all the time," Peterson said. "It’s always sifting through a variety of possibilities and finding the best interpretation for what’s out there. And the best interpretation may vary with the situation."

Our brains may have evolved to sift through the barrage of visual input in our eyes and identify those things that are most important for us to consciously perceive, such as a threat or resources such as food, Peterson suggested.

In the future, Peterson and Sanguinetti plan to look for the specific regions in the brain where the processing of meaning occurs.

"We’re trying to look at exactly what brain regions are involved," said Peterson. "The EEG tells us this processing is happening and it tells us when it’s happening, but it doesn’t tell us where it’s occurring in the brain."

"We want to look inside the brain to understand where and how this meaning is processed," said Peterson.

Images were shown to Sanguinetti’s study participants for only 170 milliseconds, yet their brains were able to complete the complex processes necessary to interpret the meaning of the hidden objects.

"There are a lot of processes that happen in the brain to help us interpret all the complexity that hits our eyeballs," Sanguinetti said. "The brain is able to process and interpret this information very quickly."

Sanguinetti’s study indicates that in our everyday life, as we walk down the street, for example, our brains may recognize many meaningful objects in the visual scene, but ultimately we are aware of only a handful of those objects. The brain is working to provide us with the best, most useful possible interpretation of the visual world, Sanguinetti said, an interpretation that does not necessarily include all the information in the visual input.

(Source: uanews.org)

Video Games and Your Brain

It seems that every few years a new moral panic sweeps through society — and, often, video games get blamed for perceived rises in crime and violence. But is there any solid evidence supporting that? How do video games affect the human brain? Tune in to Stuff They Don’t Want You to Know for more.

Listen to a Brain Seizure Turned into Music

ziyadnazem:

image

Yikes, this is all kinds of creepy. Stanford scientists recently took the EEG signals from a person experiencing a convulsive seizure and converted them to tones that fell within the acoustic spectrum of the human voice. The results will send chills up your spine.

Read More

(Source: ziyadnazem)

ucresearch:

Einstein’s Brain   (…and the neuroscientist who studied it)


Marian Diamond began her graduate work in 1948 and was the first female student in the department of anatomy at UC Berkeley.  The first thing she was asked to do when she got there was sew a cover for a large magnifying machine (?!?!?!?!).

"They didn’t know what to do with me because they weren’t used to having a woman. They thought I was there to get a husband. I was there to learn."

Such challenges were not uncommon. Years later she requested tissue samples of Albert Einstein’s brain from a pathologist in Missouri. He didn’t trust her.

"He wasn’t sure that I was a scientist. This is one thing that you have to face being a woman.  He didn’t think that I should be the one to be looking at Einstein’s brain."

Marian persisted for three years, calling him once every six months, and received four blocks of the physicist’s brain tissue (about the size of a sugar cube).  

Her research found that Einstein had twice as many glial cells as normal males — the discovery caused an international sensation as well as scientific criticism.  

What are glial cells?  Previously, scientists believe that neurons were responsible for thinking and glial cells were support cells in the brain.  Now Researchers believe the glial cells play a critical role in brain development, learning, memory, aging and disease.

Watch her popular course on Human Anatomy

Learn: How Albert Einstein’s Brain Worked 

fastcompany:

When your boss asks why you were napping, tell them science told you to.

neuromorphogenesis:

How old memories fade away

If you got beat up by a bully on your walk home from school every day, you would probably become very afraid of the spot where you usually met him. However, if the bully moved out of town, you would gradually cease to fear that area. 

Neuroscientists call this phenomenon “memory extinction”: Conditioned responses fade away as older memories are replaced with new experiences.

new study from MIT reveals a gene that is critical to the process of memory extinction. Enhancing the activity of this gene, known as Tet1, might benefit people with posttraumatic stress disorder (PTSD) by making it easier to replace fearful memories with more positive associations, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory. 

The Tet1 gene appears to control a small group of other genes necessary for memory extinction. “If there is a way to significantly boost the expression of these genes, then extinction learning is going to be much more active,” says Tsai, the Picower Professor of Neuroscience at MIT and senior author of a paper appearing in the Sept. 18 issue of the journal Neuron.

The paper’s lead authors are Andrii Rudenko, a postdoc at the Picower Institute, and Meelad Dawlaty, a postdoc at the Whitehead Institute.

New and old memories

Tsai’s team worked with researchers in MIT biology professor Rudolf Jaenisch’s lab at the Whitehead to study mice with the Tet1 gene knocked out. Tet1 and other Tet proteins help regulate the modifications of DNA that determine whether a particular gene will be expressed or not. Tet proteins are very abundant in the brain, which made scientists suspect they might be involved in learning and memory.

To their surprise, the researchers found that mice without Tet1 were perfectly able to form memories and learn new tasks. However, when the team began to study memory extinction, significant differences emerged. 

To measure the mice’s ability to extinguish memories, the researchers conditioned the mice to fear a particular cage where they received a mild shock. Once the memory was formed, the researchers then put the mice in the cage but did not deliver the shock. After a while, mice with normal Tet1 levels lost their fear of the cage as new memories replaced the old ones. 

“What happens during memory extinction is not erasure of the original memory,” Tsai says. “The old trace of memory is telling the mice that this place is dangerous. But the new memory informs the mice that this place is actually safe. There are two choices of memory that are competing with each other.”

In normal mice, the new memory wins out. However, mice lacking Tet1 remain fearful. “They don’t relearn properly,” Rudenko says. “They’re kind of getting stuck and cannot extinguish the old memory.”

In another set of experiments involving spatial memory, the researchers found that mice lacking the Tet1 gene were able to learn to navigate a water maze, but were unable to extinguish the memory.

Control of memory genes 

The researchers found that Tet1 exerts its effects on memory by altering the levels of DNA methylation, a modification that controls access to genes. High methylation levels block the promoter regions of genes and prevent them from being turned on, while lower levels allow them to be expressed. 

Many proteins that methylate DNA have been identified, but Tet1 and other Tet proteins have the reverse effect, removing DNA methylation. The MIT team found that mice lacking Tet1 had much lower levels of hydroxymethylation — an intermediate step in the removal of methylation — in the hippocampus and the cortex, which are both key to learning and memory. 

These changes in demethylation were most dramatic in a group of about 200 genes, including a small subset of so-called “immediate early genes,” which are critical for memory formation. In mice without Tet1, the immediate early genes were very highly methylated, making it difficult for those genes to be turned on.

In the promoter region of an immediate early gene known as Npas4 — which Yingxi Li, the Frederick A. and Carole J. Middleton Career Development Assistant Professor of Neuroscience at MIT, recently showed regulates other immediate early genes — the researchers found methylation levels close to 60 percent, compared to 8 percent in normal mice.

“It’s a huge increase in methylation, and we think that is most likely to explain why Npas4 is so drastically downregulated in the Tet1 knockout mice,” Tsai says.

“By demonstrating some of the ways that regulatory genes are methylated in response to Tet1 knockout and behavioral experience, the authors have taken an important step in identifying potential pharmacological treatment targets for disorders such as PTSD and addiction,” says Matthew Lattal, an associate professor of behavioral neuroscience at Oregon Health and Science University, who was not part of the research team.

Keeping genes poised

The researchers also discovered why the Tet1-deficient mice are still able to learn new things. During fear conditioning, methylation of the Npas4 gene goes down to around 20 percent, which appears to be low enough for the expression of Npas4 to turn on and help create new memories. The researchers suspect the fear stimulus is so strong that it activates other demethylation proteins — possibly Tet2 or Tet3 — that can compensate for the lack of Tet1.

During the memory-extinction training, however, the mice do not experience such a strong stimulus, so methylation levels remain high (around 40 percent) and Npas4 does not turn on.

The findings suggest that a threshold level of methylation is necessary for gene expression to take place, and that the job of Tet1 is to maintain low methylation, ensuring that the genes necessary for memory formation are poised and ready to turn on at the moment they are needed. 

The researchers are now looking for ways to increase Tet1 levels artificially and studying whether such a boost could enhance memory extinction. They are also studying the effects of eliminating two or all three of the Tet enzymes. 

“This will not only help us further delineate epigenetic regulation of memory formation and extinction, but will also unravel other potential functions of Tets and methylation in the brain beyond memory extinction,” Dawlaty says.

The research was funded by the National Institutes of Health, the Simons Foundation and the Howard Hughes Medical Institute.

(Source: web.mit.edu)