Whose Brain Is It? [April 2012 – Leena Prasad]

Whose brain is it?

by Leena Prasad

Presented within the flow of the lives of fictional characters, this is a monthly column with a journalist’s perspective on brain research.


I catch a glimpse of rice and mackerel. She is holding a small piece in-between her thumb and index finger. That’s the authentic way of eating sushi, instead of using chopsticks, I think.

But something else happens in my mind also. My friend and I have just been seated at the Japanese restaurant and have not even looked at the menu. Yet I can almost taste the saba (rice and mackerel) and memories of the sour salty taste make my mouth water. I recall a class lecture from my neuroscience class about mirror neurons.

I am not in the medical profession but studied artificial intelligence as part of my computer science curriculum and later worked in the field. This led to an interest in neuroscience. I use my graduate school training as a journalist to research and explore the brain using what I learned in the introductory neuroscience class as a basic foundation for my journey.

But, this is not a story about me or about sushi.  It’s about specific neurons in my brain and in yours – nerve cells that help us connect to each other’s experiences. These neurons are helping to answer questions ranging from feeling hungry while watching someone else eat to feeling the pain of another person to the excitement felt by sport audiences, to learning by watching someone do something.

When I see the saba, the occipital lobe in the back of the brain, processes the visual information. The hippocampus and other parts of the brain retrieve the memory of my own experiences with saba. When I eat the sushi, neurons in the premotor cortex, in the frontal lobe of the brain, enable me to use my fingers to pick up the sushi, bring it to my mouth, and to eat it. Every single action, from the details of the movement of my arms and fingers to the complexities of biting and chewing are handled by the premotor nerve cells.

But if I am not eating the rice and mackerel myself, how is it that my mouth waters as if I can taste the sushi?

As human beings, most of us (excluding people with autism and other brain related diseases) understand empathy. Now, neuroscientists are exploring the coding of empathy within our brain. They have discovered nerve cells which mirror the actions of other people as if we are experiencing what we see. These neurons reside in the premotor cortex along with the premotor neurons which cause motor reflexes. Mirror neurons are a special subset of the premotor neurons and they fire whether we perform an action ourselves or watch others perform the action.

Mirror neurons were discovered by researchers in Parma, Italy in 1992. The scientists had placed electrodes in the brain of a monkey to record and study nerve cell activity by amplifying the sounds made inside the brain when a neuron fires. By chance, they heard the same set of premotor neurons fire off both when the monkey was picking up a peanut and also when the monkey was just watching someone else pick up a peanut. Similar experiments were repeated in monkeys and humans by several follow-up studies conducted by the scientists at Parma and by other scientists around the world.

“I predict that mirror neurons will do for psychology what DNA did for biology,” says Dr. Vilayanur Subramanian Ramachandran, a Professor in the Department of Psychology and the Neurosciences Graduate Program at the University of California, San Diego. In a recent TED lecture entitled “The neurons that shaped civilization” Dr. Ramachandran theorizes that a lot of human learning, and thus evolution, probably speeded up due to mirror neurons.

There are two types of mirror neurons, according to Dr. Christian Keysers, a Professor at Netherlands’ largest medical faculty, the University Medical Center in Groningen. The two types are: strictly congruent and broadly congruent. The strictly congruent neurons are activated for very specific familiar actions. So, when I watch someone eat saba or eat it myself, I’m using strictly congruent neurons. The broadly congruent neurons are activated for actions that might be unfamiliar to me. For example, if I start taking classes in auto repair, I would be using broadly congruent neurons since I do not know much about this topic.

This is an exciting discovery. I found many articles and books and videos on the topic.  A lot of the current research is speculation and excitement with a smattering of data to backup the assertions.  There are ongoing discussions and experiments to locate mirror neurons in other parts of the brain, in addition to those in the premotor cortex. This trendy subject has been used to explain a range of behavioral phenomena such as language learning, empathy, and lack of emotional intelligence in autism. I look forward to learning more about these neurons as scientists gather more data and develop theories on how the knowledge can be used to understand and fine-tune human behavior. For now, at least I understand why I can taste the sushi by just looking at someone else put it in her mouth.

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Please send feedback and suggestions for future columns to leena@fishridingabike.com. Go to WhoseBrainIsIt.com for links to past columns and to FishRidingABike.com for Leena’s writing portfolio. Leena has a journalism degree from Stanford University.

Dr. Nicola Wolfe is a neuroscience consultant for this column. She earned her Ph.D. in Clinical Psychopharmacology from Harvard University and has taught neuroscience courses for over 20 years at various universities.

References:

Ramachandran. Vilayanur Subramanian. Ph.D. The neurons that shaped civilization: VS Ramachandran. TED Talk, January 4, 2010

Keysers, Christian, Ph.D. The Empathic Brain. Social Brain Press, 2011

 

NCSWA Spring lecture/dinner on Wednesday March 21, 2012, at The Basque Cultural Center in San Francisco, CA

The Topic of Aging

By Suzanne Birrell

 

“And so, from hour to hour, we ripe and ripe,

And then, from hour to hour, we rot and rot.”

Shakespeare’s “As You Like It”; Act II Scene 7

 

Does anyone really know what time is? Or does?

Does the passing of time have to result in a body getting old?

Why is it that a body, which apparently miraculously rapidly grows from a single stem cell to a complex, fully grown, functioning, thinking and reasoning (two different things), self repairing entity with a frequent cellular turnover, can’t seem to keep itself going indefinitely?

But since the fact that the body doesn’t simply replace cells indefinitely, then the big question we really want to know (we who are feeling the aches and pains of age in our bones and muscles) is:

Can we reset the Aging Clock?

These questions and more were the topic of the latest NCSWA Spring lecture/dinner on Wednesday March 21, 2012 at The Basque Cultural Center in San Francisco.  Featured as the quest lecturer for the Northern California Science Writers Associations quarterly dinner was:

Tom Rando, MD, PhD, Director of the Glenn Laboratories at Stanford, (One of four such centers funded by the Paul. F. Glenn Foundation)

Professor Tom Rando - Photograph by Chuck Jones

Professor Rando enthusiastically spoke about his cutting-edge research.  Apparently research is very exciting when you find out things you didn’t expect to find out, and we were told frequently that Professor Rando and his team did not expect results they have so far observed.

Rando’s team started with the goal of defining bio-markers which indicate the age of a cell: or in other words: is it possible to measure aging on the cellular level?  They started by studying aging and longevity, which are two different issues.

The average lifespan 15,000 years ago in Europe was 25 years.  Then in Rome 11,000 years ago it was up to 35 years.  The average life span in the USA in 1900 was 50, but by 1970 it was up to 70 years old, and in 2010 the average was up to 80 years.  Up to the turn of the century, keeping babies alive has been the primary factor in the dramatic increase of the “average life-span.”  However the number of centenarians is increasing all over the world with many who are in the 110-120 year age bracket.

Though the good news is, as photographs show, we are reaching older age while looking better, the question is why?  Rando’s team asked the questions “What happens as we get old?” and “Can aging be slowed?”

Research has demonstrated that 55% fewer calories can contribute to almost a 50% greater lifespan!  And, results can be enjoined at a later age (meaning that you can start your mean and lean diet after you are older and may enjoy the benefits of the 50% increase in life span!)

However, before you start on your starvation diet, you should know that is not only fewer calories BUT fewer calories with adequate nutrition.   A problem with this modicum of knowledge is, as Professor Rando pointed out, we really don’t know what adequate nutrition is, and nutritional deficiencies can result in early death.

Since the results of caloric adjustments have demonstrated that aging can be slowed, Rando’s team moved on to attempt to identify what exactly happens to a single cell as the body ages.  The moot point to boot was that a single stem cell grows to a beautiful smooth skinned child.  The skin cells replace themselves with new skin cells every few days, but a sure sign of age is the appearance of skin.  What causes this epigenetic (resulting from external rather than genetic influences) change?   Committed skin stem cells give rise to new skin cells.  The stem cells are all there, but the tissues do not regenerate as well which means that the older body is slower to heal from an injury.

Dolly the sheep was cloned from a single stem cell of a mature animal.  In that case the age of the cell was started again at zero and then differentiated.  Professor Rando was curious as to why new skin shows epigenetic changes as a body ages when a whole new body can be cloned from a single stem cell of the same aged body.

Rando’s team found that as body gets older, the skin cells show a reduction in the amount of a protein within the cell.  When they parabioticly conjoined a young mouse to its genetically identical older twin, the scientist were astonished to observe that the amount of protein in the older mouse’s skin cells increased while the younger mouse’s protein count decreased.  In effect they were able to reset the aging clock of the older mouse.  When they separated the mice, however, the protein levels returned to their initial state.  The team also simply gave the blood of a younger mouse to that of the older mouse and saw minute changes which did not last long at all.

Though Rando’s investigations suggest we mortals might someday be able to rejuvenate our aging bodies with the proteins abundant in young blood, Rando and his team are hoping this knowledge leads to the ability to help older people heal faster.

It was a fascinating lecture.  The Q & A afterwards was particularly engaging.

I simply listened, but I do, upon retrospect, have a few questions:

1.  Are vampires really all about keeping those youthful protein levels high?

2.  If we gave our blood in abundance when we were young, could we get it back when we are old thereby keeping our regenerating proteins at a high level?

3. Do I really want to live to be as old as Adam (930 years)?  That’s an awful lot of taxes.

Professor Tom Rando (standing left) - Photograph by Chuck Jones

I do invite you again to check out the NCSWA website: http://www.ncswa.org/index.htmlthe

Their next lecture should be in June and I promise it will be interesting with great food and scintillating conversation.  The NSCSWA also has field trips and workshops.

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You can reach Suzanne Birrell at Suzanne@thisoldhippy.com.