Transhumanist Blogs on Religion and Spirituality

Brain Stimulation and Human Cognitive Enhancement

Ron Cole-Turner — Mon, 30 Jan 2012 12:40:00 +0000

Who wouldn't want to be smarter? And what parents don’t want academic success for their children?

Now it appears that simple electrical devices that stimulate the brain are able to enhance human cognitive performance.

An Essay in a recent issue of Current Biology describes recent advances in “non-invasive brain stimulation” (NIBS). One approach in particular—“transcranial direct current stimulation” or TDCS—is described in detail. According to the essay, TDCS is a simple tool that is “portable, painless, inexpensive, apparently safe, and with potential longtermefficacy.” It may be used to help those suffering from impaired cognitive abilities.

More to our point, however, is that TDCS shows remarkable potential for human enhancement. Simply put, this device seems to have the power to make normal children and adults smarter than they would normally be. To quote the essay, TDCS has the potential “to enhance fundamental human capacities, such as motor and sensorimotor skills, vision, decision making and problem solving, mathematical cognition, language, memory, and attention—improvements that seem to persist without apparent cognitive side effects.”

The main point of the essay is to invite broad discussion about the neuroethics of cognitive enhancement. A good deal of attention is focused on whether TDCS or similar techniques should be used on children. The authors argue that having smarter children will benefit everyone. Their conclusion: “If it is handled judiciously, TDCS could prove to be an inexpensive and widely-deployed technology with substantial benefits to individuals and society.”

Anyone following the debate about human enhancement will see this as further evidence that in terms of the technology, “the future is here.”

Sure, there’s a lot to think about here before we rush out and strap TDCS devices on our heads. Anyone worried that mobile phones pose a health risk will probably not think this is such a good idea.

But many of us human beings value our cognitive abilities above everything else. If TDCS is a safe way to become smarter, then why not?

According to the Christian tradition, human beings are created in the image of God. One way we resemble God is through the power of intellect, which we share with the animals but which we alone exhibit to such a lofty degree that we can be compared to God. According to Gregory of Nyssa, one of the great theologians of the fourth century, “The Deity beholds and hears all things, and searches all things out." No surprise there. But then Gregory adds: "You too have the power of apprehension of things by means of sight and hearing, and the understanding that inquires into things and searches them out.”

How expected that by inquiring into all things and searching them out, we now seem to be learning how to enhance the very power of thought and discovery.

If we enhance our intelligence will we become more like God? Not quite. Intelligence may be one way we can and should resemble God, but it's not the only way. In fact, intelligence by itself can be worrisome.

Much to his credit, Julian Savulescu (a co-author in the TDCS essay) is one of very few who has urged us to pay attention to the question of “moral enhancement.” Quite simply, smarter people who are not also morally better people may turn out to be very dangerous people. So after reading the essay on how to enhance cognition, let me suggest you look at a 2008 paper by Ingmar Persson and Julian Savulescu, entitled "THE PERILS OF COGNITIVE ENHANCEMENT AND THE URGENT IMPERATIVE TO ENHANCE THE MORAL CHARACTER OF HUMANITY."

Are We Alone?

Ron Cole-Turner — Wed, 11 Jan 2012 13:01:00 +0000

Our sun is a star, one of hundreds of billions of stars.

In the past 16 years, scientists have founds more than 700 planets orbiting a few of the stars beyond our sun. These distant planets are often called exoplanets, short for extra-solar planet.

Just how many exoplanets are there in our Milky Way galaxy? Were researches just extremely lucky, looking where exoplanets exist? Or do they exist nearly everywhere?

Research published in the January 11, 2012 issue of Nature supports the idea that planets are as common as stars. Each of the 100 billion stars in our galaxy has on average at least one planet.

If life exists out there, it most likely exists on planets that are roughly like our earth. Not too big and neither too far from its sun (perpetual winter) or too close (blazing heat). Of all the planets, how many are roughly on the scale of earth? Half of them at least, maybe more.

Caption: This artist's cartoon view gives an impression of how common planets are around the stars in the Milky Way. The planets, their orbits and their host stars are all vastly magnified compared to their real separations. A six-year search that surveyed millions of stars using the microlensing technique concluded that planets around stars are the rule rather than the exception. The average number of planets per star is greater than one.Credit: ESO/M. Kornmesser

Arnaud Cassan of the Institut dʼAstrophysique de Paris and lead author of the paper explains: “We have searched for evidence for exoplanets in six years of microlensing observations. Remarkably, these data show that planets are more common than stars in our galaxy. We also found that lighter planets, such as super-Earths or cool Neptunes, must be more common than heavier ones,” Cassan said in a press release issued by the European Southern Observatory (ESO).

"We used to think that the Earth might be unique in our galaxy. But now it seems that there are literally billions of planets with masses similar to Earth orbiting stars in the Milky Way," according to Daniel Kubas, co-lead author of the paper.

If there are tens of billions of life-friendly planets just in our own galaxy, how likely is it that life exists out there somewhere? And if life exists, has intelligence evolved?

These are ancient religious and philosophical questions. The latest science certainly tilts the debate in favor of life. Sure, it’s possible that earth beat the odds: of the tens of billions of life-friendly planets, only ours has life.

Right now, there’s no evidence either way. All that science can tell us is that the planets are there, ready for the spark of life to get started.

So we are left to gaze at the night sky and to wonder as never before. For each star, there’s a planet. Is anyone out there looking back?

In Christian theology, one of the earliest statements about the Holy Spirit is that the Spirit is the “giver of life.” Hildegard of Bingen (Symponia) put it this way: “God our life is the life of all.” Or consider John Calvin, who says the Spirit is "everywhere diffused, sustains all things, causes them to grow, and quickens them in heaven and on earth."

To believe in God is to believe in the life-giving presence of God, not just here but everywhere. Thanks to this research, it turns out that the Spirit has many more planets on which to give life.

The article, "One or more bound planets per Milky Way star from microlensing observations", by A. Cassan et al., appears in the 12 January issue of the journal Nature.

Stem Cells and Type I Diabetes

Ron Cole-Turner — Tue, 10 Jan 2012 11:34:00 +0000

Is this just too good to be true? That’s my first reaction when I read the press release with this headline: “Stem cell therapy reverses diabetes.”

The full report was published on January 9 by an open source medical journal, BioMed Central. If the procedure it describes can be replicated, it is promising indeed. Researchers claim to have a device that “educates” the patient’s own stem cells.

The device is called a “Stem Cell Educator.” Apparently when the patient’s blood passes through the device, stem cells naturally occurring in the patient’s blood are “educated” or re-set to a more normal, functional level. The device separates the patients blood, selecting lymphocytes for special treatment by exposing them to stem cells that were originally derived from donor human umbilical cords.

No cells are exchanged or added to the patient’s blood. Instead, the patient’s own cells are reset by exposure to specific factors given off by the donor stem cells that are kept in a living culture inside the device. After two or three hours of “education,” the patient’s lymphocytes seem to perform a lot better.

The result? Researchers claim in their report that “a single treatment produces lasting improvement in metabolic control. In initial results indicate Stem Cell Educator therapy reverses autoimmunity and promotes regeneration of isletβcells.” The need for insulin was reduced and the benefits lasted at least as long as 40 weeks after the treatment.

The study also makes this claim:

Successful immune modulation by CB-SCs and the resulting clinical improvement in patient status may have important implications for other autoimmune and inflammation-related diseases without the safety and ethical concerns associated with conventional stem cell-based approaches.

Whether these findings are replicated is a key question at this point. The claims are pretty extraordinary, but the general strategy of "re-educating" rather than replacing cells seems to be showing a lot of promise. For an example, see my earlier post, "Is Aging a Disease of Stem Cells?"

The study was led Yong Zhao of the University of Illinois at Chicago, who directed an international team and prepared the report, entitled “Reversal of type 1 diabetes via islet beta cell regeneration following immune modulation by cord blood-derived multipotent stem cells.” The full text is published by the online journal BioMed Central and is freely available to the public.

Genes, Hybrids, and Giant Tortoises

Ron Cole-Turner — Mon, 09 Jan 2012 13:11:00 +0000

Charles Darwin visited the Galápagos Islands in 1835. As he moved from island to island, he saw the subtle differences between finches, tortoises, and other animals. These observations led to the discovery of the theory of evolution as an expanding “tree of life,” first sketched by Darwin in his notebook entry dated just two years later in 1837.

The great tortoises of the Galápagos could not fail to impress. The greatest of all, the tortoise Chelonoidis elephantopus, can live to be a hundred years old and grow to six feet and almost 900 pounds.

Until now, it was believed that whalers hunted the great C. elephantopus to extinction shortly after Darwin’s visit. Now, however, new research suggests that a few of the great tortoises may still be alive.

Caption: G. Becky tortoises are native to Isabela Island in the Galapagos chain and have more domed shape shell.Credit: Courtesy Yale University.

Researchers have found what they believe are direct offspring of purebred C. elephantopus tortoises. By testing the genes of living tortoises, researchers concluded that they were studying hybrids. One parent was from a related species, C. becki. But the other parent was clearly C. elephantopus. And since the living tortoises were still quite young, researchers were drawn to the obvious conclusion that the C. elephantopus parent lived until a few decades ago and may still be roaming the slopes of Isabela Island.

So now it’s a race against time to find surviving purebred C. elephantopus tortoises in hopes that enough of them still exist so the species—truly one of the great animal species—can be brought back from what seemed like extinction. According to the report, “purebred tortoises of the recently ‘extinct’ C. elephantopus from Floreana Island are very likely still alive today.”

Caption: This tortoise is a hybrid of G. Becky and C. elephantopus, a species native to Floreana Island some 200 miles away and thought to be extinct. Genetic analysis of tortoise population on Isabela Island suggests purebred individuals of C. elephantopus must still be alive on Isabela.Credit: Courtesy of Yale University

One interesting parallel. Using a similar approach, researchers have recently concluded that human beings are also hybrids. For example, many of us contain genes from our Neandertal ancestors. The big difference, of course, is that our interbreeding occurred tens of thousands of years ago. In either case, hybridization or interbreeding occurs when the twigs at the end of Darwin's tree of life come together. As evolutionary biologists are discovering, speciation (or branching) is critical to evolution, but so is interbreeding or hybridization.

According to the report, “To our knowledge, this is the first rediscovery of a species by way of tracking the genetic footprints left in the genomes of its hybrid offspring.” The report, "Genetic rediscovery of an ‘extinct’ Galápagos giant tortoise species," appears in the January 9, 2012 issue of Current Biology.

Hope for Aging Brains

Ron Cole-Turner — Fri, 06 Jan 2012 12:09:00 +0000

When electrical wires lose their insulation, they have to be replaced. When the nerves and brain cells in our bodies lose theirs, they regenerate it naturally.

Up to a point, that is. As the decades pass, our bodies lose the ability to regenerate themselves. The results are obvious: wrinkled skin, weak muscles, and forgetful brains.

All the more tragic for those among us with diseases that attack the very processes of regeneration. Multiple sclerosis (MS), for example, keeps the body from restoring the insulating layers that protect nerve fibers. The insulation—“myelin”—breaks down naturally. In most human brains, “remyelination” is a constant process, rebuilding the myelin that protects the brain cells and allows them to do their work. For people with MS, remyelination is under attack.

Working with mice, researchers seem to have found a way to reinstate the remyelination process. In a report in the January 6 issue of Cell Stem Cell, researchers at Harvard and Cambridge Universities show that the capacity for remyelination can be restored in aging mice.

The cells that are responsible for remyelination are still present in the aging mouse. It’s just that they have been switched off. By exposing these cells to switching signals present in a much younger mouse, researchers were able to reverse the effects of aging on the cells that do the work of remyelination.

How did they do this? They literally joined the old and the young mouse together surgically. This allows their blood to circulate together. In the young blood, apparently, were various chemical signals that reset the switches in the cells of the brains of the aging mice. The result: spontaneous remyelination.

According to Robin Franklin, one of the researchers, the study shows that “age-associated decline in remyelination is reversible. We found that remyelination in old adult mice can be made to work as efficiently as it does in young adult mice.” Franklin, who is Director of the MS Society's Cambridge Centre for Myelin Repair at the University of Cambridge, made her comments in a press release issued by her university.

What’s perhaps most interesting about this report is that it is a kind of stem cell research that doesn’t implant stem cells. It works on the principle that stem cells already exist in the patient’s body but that they’ve been silenced by age or disease. They need to be switched back on or rejuvenated. According to Franklin, “remyelination therapies do not need to be based on stem cell transplantation since the stem cells already present in the brain and spinal cord can be made to regenerate myelin - regardless of the patient's age."

As interesting as this is, it is important to stress that this is a “proof of concept” study. The techniques here are simply not applicable to human beings. They are encouraging because they suggest that perhaps some day, researchers will discover just what it is in the young body that keeps it young. What are the specific factors that keep the body’s own stem cells switched on? And if it circulates in the blood as this study shows, perhaps these factors could simply be injected.

Of course, if researchers discover how to do this, it’s not just people with diseases like MS who will be interested. One of the interesting social features about this work is that it is funded in part by the UK MS Society and the American MS Society. In other words, the funding is motivated by the search for a cure for a very specific disease. But the mice is the study were aging, not ill. That suggests to me, at least, that the larger portion of the “beneficiaries” of this work will be aging humans, not those with MS. If so, then this study is one more step in the quest of human enhancement, suggesting that it may be possible to reverse aging in the one part of the body where it is most feared—the human brain.

The journal report ends with this comment: “Moreover, this work demonstrates that the CNS maintains its responsiveness to age-regulated circulatory factors, such that age-dependent deficiencies in repair of these tissues can, in part, be reversed by circulating factors.”

The paper, “Rejuvenation of regeneration in the aging central nervous system,”' is published in the January 6 issue of Cell Stem Cell.

Chimeric Monkeys? Where Do We Go From Here?

Ron Cole-Turner — Thu, 05 Jan 2012 15:46:00 +0000

What is a “chimeric monkey”? Why would anyone want to create them? And why should anyone care?

In ancient myth, a chimera was an animal with a human head and, say, the body of a horse or a lion. That’s not what’s going on here.

In biology today, a chimera is an animal that comes from two or more embryos. This happens naturally, when twins are conceived but the two fertilized eggs fuse into one embryo, eventually producing one individual.

In research, scientists create chimeras in order to study how cells function. Mice chimeras are now commonplace in stem cell labs around the world. Researchers add stem cells to an early-stage mouse embryo (a blastocyst). If the experiment goes well, the developing mouse will have cells from two sources: the “host” embryo and the implanted cells. The implanted cells often integrate into the body and brain of the mouse pup. By this test, researchers know that the implanted cells are truly stem cells—or, more precisely, that they are pluripotent, capable of becoming any type of cell in the mouse body.

Caption: Chimero, a chimeric Rhesus monkey produced by aggregating six Rhesus blastocysts. Photo credit: OHSU.

Researchers also implant human stem cells into mice. If they multiply and are fully integrated into the body, it’s pretty clear that they are pluripotent and capable of functioning within a living biological system and not just in a dish in a lab. In that case, the mouse is an “inter-species” chimera. Two embryos, of course, but from two different species, human and mouse.

For all the ways in which mice resemble human beings, there are big differences, some of which are particularly noticeable at the earliest stages of life. So when researchers at the Oregon National Primate Research Center at Oregon Health & Science University tried to put pluripotent monkey stem cells into monkey blastocysts, they failed. At the blastocyst stage, Rhesus monkeys don’t behave like mice.

The Oregon team, led by Shoukhrat Mitalipov, kept trying other approaches, finally discovering a completely different technique. Instead of using embryonic or pluripotent stem cells and adding them to a blastocyst, they backed things up, at least in terms of embryonic development. How far back? All the way to the four-cell stage. When a Rhesus monkey egg is fertilized (in this case, in a lab dish), it divides into two cells, then four. What happens if two cells in one blastocyst were combined with two cells from another blastocyst? Success—but still only partly so.

So they tried another approach, one that seems complex and counterintuitive. Researchers “aggregated” three blastocysts—and “they” began to function as one embryo. Four blastocysts—same result. Five, even six blastocysts. They did this 29 times and produced 29 viable chimeric embryos. Or to quote the original paper: “Remarkably, all 29 aggregates developed to blastocysts…”

Just what will this mean for the field of stem cell research? At the very least, this research points to the complexity of living biological systems. It’s nice to think that researchers can extract pluripotent stem cells, keep them multiplying indefinitely, direct them to develop just the right way, and implant them into the human body to regenerate tissues. If only it were that simple. As the field advances, it is clear that what was once called “pluripotency”—the ability to become any cell type—is anything but clear or simple to define.

All the more reason, I believe, why the field needs to move forward as a whole. It’s morally and scientifically simplistic to say that the field can advance without cells from embryos.

But does the Oregon work suggest a step too far? For many, it may be morally permissible to work with cells derived from blastocysts, perhaps donated from IVF clinics and due to be discarded anyhow. But what the Oregon work seems to signal is that when it comes to primates—including human beings—the cells in the living blastocyst are significantly different from the cells derived from the blastocyst. The cells in the living blastocyst, though dynamic and changing, can be regarded as totipotent, capable of becoming any cell type including the placenta and umbilical cord. Cells derived from the blastocyst—human “embryonic” stem cells or pluripotent cells—have lost part of this potential.

Does this mean that research, in order to go forward, needs access to cells as they exist in living blastocysts? That would be a step clearly beyond federal funding guidelines (the “Dickey-Wicker Amendment”). Even with private funding, it would likely exceed what most Americans can support. In some states and many countries, it would be plainly illegal.

And yet this is exactly what lead Oregon researcher Shoukhrat Mitalipov seems to have in mind. "We need to study not just cultured embryonic stem cells but also stem cells in embryos,” Mitalipov said in a release from the journal Cell. “It's too soon to close the chapter on these cells." Is that OK as long as he sticks to non-human primates?

Mitalipov is clearly right: "We cannot model everything in the mouse." Rodents and primates are different in unexpected ways at the earliest stages. Stem cells inserted in mouse blastocysts form chimeras, but not in primate blastocysts.

Quoting Mitalipov once again: "The possibilities for science are enormous." All the more reason to think this through. As complex as the science might be, the moral and religious implications are even more complex.

I for one need time to think this through. I hope to be back here before long with some more thoughts. For now, let me recommend a statement that I helped prepare a few years ago on the question of chimeras.

The paper, "Generation of Chimeric Rhesus Monkeys," was released on January 5 and will appear in the January 20, 2012 issue of the journal, Cell.

first television appearance

Robert M Geraci — Thu, 05 Jan 2012 06:39:00 +0000

In early December, I went down to a Manhattan studio to tape an appearance on The Agenda with Steve Paikin, a Canadian news journalism show. The show aired last night, and since I haven't watched it I'm still hoping that I didn't say anything too foolish. Follow the link if you want to watch. The show is around 40 minutes long.

The topic of the show was apocalypticism in pop culture, based loosely around the silliness of 2012 doomsday scenarios. You know, the Mayan calandar sorta-kinda ends so the world must be about to. The same way the world blows up each time our Gregorian calendar runs out of days in December. Oh, wait. That doesn't happen. Well, it won't be happening on December 21, 2012 either.

It was a lot of fun doing the taping: all of the others were clever and fun, and I appreciate the invitation from our good neighbors to the north. The is the first step in our all-important quest to end up on The Colbert Report. :)

Is Aging a Disease of Stem Cells?

Ron Cole-Turner — Tue, 03 Jan 2012 11:35:00 +0000

Is aging a disease? And if it is a disease, what “causes” it? Is it simply natural for bodies to age over time, or is something wrong with them, something that could be “fixed”?

In a report in the January 3 issue of Nature Communications, researchers at the University of Pittsburgh School of Medicine report on work with mice that are bred especially to age quickly. The mice have a version of progeria, a disease in humans that causes children to age well before their time.

The research team looked at differences in stem cells or progenitor cells, which healthy bodies naturally keep in reserve as a source for new cells to replace worn-out cells. Not surprisingly, they found that the progeria mice had fewer progenitor cells than their healthy counterparts. What’s more, the few progenitor cells in the progeria mice failed to function normally. For example, they didn’t produce replacement cells as needed.

If that’s the problem, can it be “fixed”? The researchers, led by senior investigators Johnny Huard and Laura Niedernhofer, injected the rapidly-aging progeria mice with progenitor cells from the muscles of healthy mice. The result was pretty amazing.

"We wanted to see if we could rescue these rapidly aging animals, so we injected stem/progenitor cells from young, healthy mice into the abdomens of 17-day-old progeria mice," Dr. Huard said in a press release issued by the University of Pittsburgh. "Typically the progeria mice die at around 21 to 28 days of age, but the treated animals lived far longer—some even lived beyond 66 days. They also were in better general health."

How did this work? Did the injected cells start producing replacement cells? Possibly, but the main effect of the injected cells seems to have been to change the host cells in the body of the progeria mice. In other words, the injected healthy progenitor cells changed the progeria mouse’s own cells into more healthy, more normal cells.

"This leads us to think that healthy cells secrete factors to create an environment that help correct the dysfunction present in the native stem cell population and aged tissue," Dr. Niedernhofer said. "In a culture dish experiment, we put young stem cells close to, but not touching, progeria stem cells, and the unhealthy cells functionally improved." Fascinating!

What about mice that are aging normally? Would the injection of progenitor cells from younger mice, for example, also “rescue” non-progeria but aging mice?

Whether anything like this could be done safely in human beings is a big question that will require a lot more research. It may turn out that injecting progenitor cells into a human patient with premature aging might help stall the aging but might also create other problems, such as cancer. In time, it may be possible to get the benefits while managing the risks.

The Pitt research, although dealing with mice with progeria, opens profound questions about humanity, aging, enhancement, and the possibility of extending the human lifespan.

The biggest question of all is whether something like this would slow the aging process in normal or healthy human beings. In other words, is this yet another possible pathway to human enhancement? Could this be used to “treat aging as a disease”?

Is aging a disease? Dr. Niedernhofer’s comment is revealing: "Our experiments showed that mice that have progeria, a disorder of premature aging, were healthier and lived longer after an injection of stem cells from young, healthy animals," Dr. Niedernhofer said. "That tells us that stem cell dysfunction is a cause of the changes we see with aging." A dysfunction? A disease? A difference?

On the question of religion and the morality of extending the human lifespan, probably the best book on the market is Religion and the Implications of Radical Life Extension, edited by Calvin Mercer and Derek Maher. I have an essay in the book reflecting on the question from the standpoint of Christianity.

My take? Extending the human lifespan is not immoral or obviously wrong, but Christians hope for a transformation, not an extension. More of the same is too little.

The report appeared in the January 3 issue of Nature Communications. It is entitled Muscle-derived stem/progenitor cell dysfunction limits healthspan and lifespan in a murine progeria model and is available free to the public.

Eating, Aging, and the Brain

Ron Cole-Turner — Wed, 28 Dec 2011 22:57:00 +0000

Two recent studies shed new light on the relationship between food and the brain.

The first study involves mice on a calorie-restricted diet. Restricting calories to about 70% of normal intake kept the mice—and their rodent brains—young when compared to control mice who could eat whenever they wanted. And while there’s no proof yet that this works with human beings, there is a lot of interest by researchers in finding out what is going on in the relationship between aging and eating.

The latest research is reported in the December 19 of PNAS. Researchers at the Catholic University of Sacred Heart in Rome report their finding that a naturally-occurring protein, CREB1, plays a key role in mediating between caloric restriction and the delay of aging. Caloric restriction seems to trigger CREB1, which in turn activates many other genes involved in longevity and brain function.

What is new in this research is the relationship between caloric restriction and CREB1 activity. Discovering how these molecules interact opens the possibility that the activity of CREB1 can be increased without having to keep to a fairly austere diet.

According to Giovambattista Pani, one of the lead researchers, “Our hope is to find a way to activate CREB1, for example through new drugs, so to keep the brain young without the need of a strict diet.”

“This discovery has important implications to develop future therapies to keep our brain young and prevent brain degeneration and the aging process. In addition, our study shed light on the correlation among metabolic diseases as diabetes and obesity and the decline in cognitive activities,” according to Dr. Pani.

The second study is published in the December 28 issue of Neurology and does involve human beings. Just in time for New Year’s resolutions, researchers at Oregon State University report on the brains and the diets of 104 seniors with an average age of 87. The result is pretty sobering. Those who ate fast foods and snack loaded with trans-fats scored much worse on cognitive tests than those who ate diets rich in the healthy oils commonly found in fish or consumed high levels of vitamins B, C, D, and E.

How much worse? The fast-food seniors scored 17% lower on thinking and memory tests and had a shocking 37% lower active brain size based on an MRI. And that’s after other factors such as age or education level are removed. Diet alone, it appears, makes a significant difference. Eating the right food seems to help slow down the age-related shrinkage of the brain.

Someday there might be a pill that makes us and our brains resist aging. For now, it’s what we eat that counts. These results need to be confirmed, but obviously it is very exciting to think that people could potentially stop their brains from shrinking and keep them sharp by adjusting their diet," according to Gene Bowman of the Oregon Health & Science University in Portland and author of the study.

This would not have surprised Saint Athanasius, bishop of Alexandria in the mid-4th century. Like many of his age, Athanasius was fascinated by the story of Saint Anthony of Egypt, one of the earliest Christian ascetics. Athanasius wrote a spiritual biography of Anthony, interpreting his life and turning him into the prototype of Christian monks.

Anthony gave away the family fortune and lived in isolation in the Egyptian desert, eating almost nothing. The result? He lived to 105 and was known for his wisdom to the very end.

Todd Daly has written about Athanasius and Anthony, including an essay in my recent book, Transhumanism and Transcendence. Daly makes it clear that Anthony’s purpose was not longevity or a youthful brain. This is no science experiment, and if Anthony is the first monk, he’s not the first transhumanist. But according to Athanasius (and to Daly), Anthony is conducting a spiritual experiment. His question is whether it is possible to regain some small portion of the original human condition…humanity as God intended, in other words, rather than the fallen humanity we experience. By denying his body, he sought to expand his soul. Without realizing it, he kept his brain from shrinking.

The amazing thing is that by asking a seemingly arcane theological question—and by sticking with it for decades—Anthony anticipates today’s research.

The PNAS article was published on December 19. The Oregon study was published online on December 28 by the journal Neurology.

Are You as Empathetic as a Rat?

Ron Cole-Turner — Thu, 08 Dec 2011 14:59:00 +0000

Empathy is the capacity to share the emotional state of another. Politicians claim to have it when they say “I feel your pain.”

Even if they do not always show it, human beings are clearly capable of empathy. Other primates such as chimps have been observed acting in a way that is best explained by empathy. Rather than acting for their own benefit, they sometimes act because they share the feeling or distress of another chimp. Such behavior is said to be “empathy-driven.”

Once it was thought that only human beings could feel empathy. Now researchers are finding that empathy-driven behavior is more widespread than previously imagined. Not just other primates but even rodents, it seems, are biologically capable of empathy. For all the differences between the human and the rat brain, we share fundamental circuits that make it possible to feel the emotions of another, particularly when the other is in pain or distress.

In a simple experiment reported in the December 9 issue of the journal Science, researchers provide solid evidence that the much-maligned rat is capable of acting in a way that is most easily explained by empathy.

"This is the first evidence of helping behavior triggered by empathy in rats," said Jean Decety, a member of the research team at the University of Chicago. "There are a lot of ideas in the literature showing that empathy is not unique to humans, and it has been well demonstrated in apes, but in rodents it was not very clear. We put together in one series of experiments evidence of helping behavior based on empathy in rodents, and that's really the first time it's been seen," Decety said in a release issued by the University.

In order to act in a way that is empathy-driven, an animal must be capable of “emotional contagion.” To test whether rats have this capacity, an experiment was designed Chicago psychology graduate student Inbal Ben-Ami Bartal. Two rats were placed in an enclosure, one of them roaming freely while the other was locked inside a tube. The free rat, in time, could discover how to open the lock, but there was no reward for doing so.

The experiment was designed observe whether rats show they are capable of emotional contagion. Was the free rat biologically capable of emotional concern or what the paper defines as “an other-oriented emotional response elicited by and congruent with the perceived welfare of an individual in distress”?

PHOTO: ©Science/AAAS.

The free rats not only learned to open the container but did so repeatedly when it held another rat, something they did not do if it was empty or if it contained a stuffed animal.

Even more striking was their behavior when chocolate chips were involved. In one variation on the experiment, two enclosures were used, one with an enclosed rat and the other with five pieces of chocolate. The free rat has a choice: free the cagemate or eat the chocolate first. In the absence of empathy, the free rat will make the selfish choice. But at least half the time, the rat freed its cagemate first. According to the report, “these results show that the value of freeing a trapped cagemate is on par with that of accessing chocolate chips.”

"On its face, this is more than empathy, this is pro-social behavior," said Jeffrey Mogil of McGill University, who was not involved in the study. "It's more than has been shown before by a long shot.”

Without claiming to know what rats think, the authors conclude their report with their opinion that “the free rat was not simply empathetically sensitive to another rat’s distress but acted intentionally to liberate a trapped” member of their own species.

If rats are indeed capable of empathetic feelings, then it becomes clear that the biological substrate for shared emotion is deep in our evolutionary past and deep in the earlier parts of our brains. Far from being uniquely human, empathy seems to be widely shared. What is uniquely human, perhaps, is the way we override it with self-interest.

As I prepared this post, I was interrupted several times by others who were speaking of the history of racism in America and particularly the history of slavery. When I saw the pictures of rats in their enclosure, my mind went to chains and slave ships. If empathy is so deep in our mammalian evolution, so deeply rooted in our brains, what extraordinary rationalizations do we conjure up to negate it?

The paper, "Empathy and Pro-Social Behavior in Rats," is published Dec. 9 by the journal Science.http://www.sciencemag.org/content/334/6061/1427.abstract

Enhancing the Brain: A New Approach?

Ron Cole-Turner — Thu, 08 Dec 2011 11:25:00 +0000

A molecule that protects you against viruses may also be slowing down your brain. That’s the startling finding just reported by researchers at the Baylor College of Medicine.

In the December 9 issue of Cell, a research team led by Mauro Costa-Mattioli report on how a key component of the immune system may also play a central role in the brain’s ability to form memories.

The molecule in question is the enzyme “protein kinase RNA-activated” or PKR for short. PKR is well-known to biomedical researchers. It is found in nearly all vertebrates and helps fight viral infections.

What was unknown is how PKR plays a pivotal role in regulating how the brain forms memories. Using mice, Costa-Mattioli’s team found that PKR actually slows down the brain’s ability to form memories. By blocking the production of PKR in mice, Costa-Mattioli’s team was able to produce mice with enhanced memory.

“The molecule PKR (the double-stranded RNA-activated protein kinase) was originally described as a sensor of viral infections, but its function in the brain was totally unknown," said Costa-Mattioli in a press release issued by Baylor Medical College.

The researchers used two methods to block PKR. They produced mice that were genetically modified so they couldn’t produce PKR. But they also used a drug that inhibits the production of PKR. In both cases, memory capacity was enhanced.

How does PKR act in the brain? Apparently by interacting with another key molecule, interferon-γ or IFN-γ, which is also best known for its role in the immune system. Researchers believe that in the brain, PKR and IFN-γ interact, keeping each other in balance. Suppressing PKR seems to increase the role of IFN-γ and the activity of the brain, particularly the neurons that are creating long-term memories.

“These data are totally unexpected, and show that two molecules classically known to play a role in viral infection and the immune response regulate the kind of brain activity that leads to the formation of long-term memory in the adult brain,” said Costa-Mattioli.

What is perhaps most startling about the report is that a drug that inhibits PKR enhances memory in mice. “It is indeed quite amazing that we can also enhance both memory and brain activity with a drug that specifically targets PKR,” according to Costa-Mattioli.

If a drug enhances memory capacity in mice, could it work in humans? That’s a big jump, one that will take much more research before anything is even tested in human beings. But researchers suggest that this is possible and worth exploring. Costa-Mattioli said, "More investigation is undoubtedly necessary to translate these findings to effective therapies but we would be delighted if our scientific studies were to contribute in some way to this ultimate goal."

“Our identity and uniqueness is made up of our memories," Costa-Mattioli said. "This molecule could hold the key to how we can keep our memories longer, but also how we create new ones.”

Will this provide a new strategy in dealing with diseases that rob us of our old memories and of our capacity to create new ones? Given the stakes, research will explore these possibilities.

If the research is applicable to human beings (and why not?) and if it provides a new path to preventing or delaying dementia, it will also open new ways to think about the enhancement of human cognition. The mice in the study were not suffering from any memory loss, but the speed at which they were able to learn a new task was enhanced nearly four-fold.

Given the wide-spread interest in cognitive enhancement, especially on university campuses and among transhumanists, we should expect to hear more about how inhibiting PKR just may make you smarter.

The article, "Suppression of PKR Promotes Network Excitability and Enhanced Cognition by Interferon-γ-Mediated Disinhibition,” appears in the December 9 issue of Cell.

Evolutionary Fast-Track for Human Brains

Ron Cole-Turner — Tue, 06 Dec 2011 17:01:00 +0000

More than 35 years ago, Allan Wilson and Mary-Claire King made an astonishing proposal. Maybe what separates humans and chimps is not just our genes. Maybe it’s also how our genes are expressed or regulated.

Research published in today’s issue of PLoS Biology builds on decades of intervening advances in evolution and genetics and take the question much further. The difference between humans and nonhuman primates in cognitive ability is explained in large part by differences in gene expression, especially during the critical periods when young brains are being formed.

Humans share many of their genes with other species, especially chimps. In fact, we share so many genes that it is hard to explain how we can be so different in terms of cognitive ability. If genes make all the difference, how can they explain the differences between chimp and human brains? And how can a mere six million years of human-chimp divergence give us enough time to accumulate enough genetic change?

The answer seems to lie in the relatively rapid evolution of differences in gene expression. In other words, while the genes themselves evolved slowly, the regulation of their expression evolved more rapidly. It’s not just the genes but their expression that’s important. It’s not just the evolution of genes but the evolution of gene expression that drives the rapid divergence between human and chimp brains.

This is especially true in the genes that control the development of the prefrontal cortex of the brain. In other words, there has been relatively rapid evolution in the genetic mechanisms that regulate genes directly responsible for the early-childhood neural development of the critically-important prefrontal cortex, which is involved in abstract thinking, planning, social intelligence, and working memory.

According to the article, “humans display a 3-5 times faster evolutionary rate in divergence in developmental patterns, compared to chimpanzees.”Most important, however, is the way this research identifies specific regulators that have evolved rapidly since human-chimp divergence. These regulators are “micro-RNAs,” some of which are specifically identified in the article, with the claim that “changes in the expression of a few key regulators may have been a major driving force behind rapid evolution of the human brain.”

According to the study’s senior author, Philipp Khaitovich, this finding suggests that "identifying the exact genetic changes that made us think and act like humans might be easier than we previously imagined." Kkaitovich was quoted in a press release issued by the journal, PLoS Biology.

The article is entitled "Micro-RNA-Driven Developmental Remodeling in the Brain Distinguishes Humans from Other Primates" and appears in the December 6 issue of PLoS Biology, where it is freely available to the public.

Violence and Children's Brains

Ron Cole-Turner — Mon, 05 Dec 2011 15:54:00 +0000

When children are exposed to violence in the family, their brains are visibly changed. That’s the disturbing message of new research published in tomorrow’s issue of Current Biology.

According to the research article, exposure to violence at home can “represent a form of environmental stress that significantly increases [the] risk of later psychopathology, including anxiety.” It’s as if violence tunes the child’s brain to expect more violence.

Earlier studies have shown that physically abused children show “selective hypervigilance to angry cues,” such as pictures of angry faces. Another earlier study used functional magnetic resonance imaging (fMRI) to show increased brain reactivity. When individuals with anxiety disorder where shown angry faces, two brain regions were overly reactive: the anterior insula (AI) and the amygdala. The same response was found in soldiers exposed to combat.

The new research takes this a step further. Children exposed to family violence, including violence between parents, also showed the same increased brain reactivity. The reaction was quite specific in that they responded to pictures of angry faces, not sad faces.

Most important, perhaps, is that this study looked at brain function rather than symptoms of anxiety or depression. In terms of behavior, the children seemed quite normal. Their brains, however, tell a different story, one of being tuned to be anxious.

Some might suggest that given all the violence in the world, the reaction is beneficial. Maybe it’s a good thing that some human beings learn to be especially responsive to potential threats.

But as the researchers note, excessive reactivity “may also constitute a latent neurobiological risk factor increasing vulnerability to psychopathology.” The researchers also found that the degree of the brain reactivity depended on the severity of the violence.

The research “underlines the importance of taking seriously the impact for a child of living in a family characterized by violence. Even if such a child is not showing overt signs of anxiety or depression, these experiences still appear to have a measurable effect at the neural level,” said Eamon McCrory of University College London, lead author, in a press release from the journal.

More than that, this research shows how violence and trauma affect human beings in ways that permanently alter the brain.

The article, “Heightened Neural Reactivity to Threat in Child Victims of Family Violence,” appears in the December 6 issue of Current Biology.

For previous work by some of these same researchers, see “The Impact of Childhood Maltreatment: A Review of Neurobiological and Genetic Factors,” published in July in Frontiers in Psychiatry.

Searching for Life on Other Planets

Ron Cole-Turner — Mon, 05 Dec 2011 09:27:00 +0000

This post is a little bit out of my usual orbit. Literally. It has to do with newly discovered planets that orbit other suns. They’re called “extra-solar planets” or simply “exoplanets.”

Over the past twenty years, scientists have discovered nearly 700 such planets. Most of these are too big and too hot for life. Their powerful gravity and their vaporizing heat make it unlikely that any form of life could arise, much less evolve.

PHOTO CAPTION: Scientists are now starting to identify potential habitable exoplanets after nearly twenty years of the detection of the first planets around other stars. This image shows all known examples using 18 mass and temperature categories similar to a periodic table, including confirmed and unconfirmed exoplanets. Only 16 in the Terrans groups are potential habitable candidates.PHOTO CREDIT: PHL copyright UPR Arecibo

A few exoplanets may have the right conditions for life. So far, at least two exoplanets seem to have roughly “earth-like” conditions, making them what researchers call “habitable exoplanets.”

More will surely be discovered. So many more, in fact, that some sort of catalog is needed. Enter the “Habitable Exoplanets Catalog,” hosted at the University of Puerto Rico. The Catalog is being introduced on December 5, 2011 to astronomers at the Kepler Science Conference in California.

The Catalog is an online database of habitable worlds. There’s no proof yet that life exists on any of them, but many researchers believe that some forms of life will be discovered once our detection technology advances just a bit further, with probes such as NASA’s Kepler.

”New observations with ground and orbital observatories will discover thousands of exoplanets in the coming years. We expect that the analyses contained in our catalog will help to identify, organize, and compare the life potential of these discoveries,” said Abel Méndez, Director of the PHL and principal investigator of the project in a press release issued by the University of Puerto Rico.

One nice feature of the Catalog is its “periodic table of exoplanets.” Everyone remembers the periodic table of elements that hangs in every science classroom. Just as that table organizes elements by their properties, so the table of exoplanets organizes them by habitability. What’s more, because it is an online database, new discoveries are included and organized as they occur.

To achieve this, the Catalog uses data from other databases, such as the Extrasolar Planets Encyclopedia,Exoplanet Data Explorer, the NASA Kepler Mission, and other sources.

The Secret Lives of Cells Revealed

Ron Cole-Turner — Sat, 03 Dec 2011 10:40:00 +0000

Life at the cellular level is chaotic and complex, beautiful and yet deadly.

Even though we are made up of trillions of cells, most of us give our individual cells about as much thought as a piece of sandstone thinks about individual grains of sand.

Enter the new technologies of imaging, which open new worlds. As never before, we can see the very small and the very distant.

On December 3, the American Society for Cell Biology announced the winners of the Celldance 2011 Film and Image Contest Winners.

Take a look. Unless you’re a cell biologist, it will change the way you see the world. It will re-define your relationship to your own body. It will open new vistas on the much quoted “fearfully and wonderfully made.” If only the psalmist could have seen this!

My favorite is the first place winner, “Cancer Dance.” I say “favorite” with a great deal of qualification. It’s hard to look at this film. If you know someone who has faced cancer—and who doesn’t—what you see in this film will shock and anger you. And then you have to think: cancer is happening inside all of us pretty much all the time. Fortunately, it doesn’t get the upper hand…unless it does.

When I teach the introduction to theology, I talk about God, creation, pain in nature, and human suffering at the hands of nature. Cancer is the main example. Describing this disease theologically is a real challenge. Quite simply, cancer uses the mechanisms of life to destroy lives. It turns everything good bad.

I once asked an oncologist friend who is a Christian: “When you look at a cancer cell, theologically, what do you see?” He was so astounded by the question that he couldn’t answer.

Now, thanks to this video, you can ask yourself that question. Theologically, what is going on here? What the bleep is going on here? Why would God design such a system?

So from now on, when I teach theology, I’ll run the video. I won’t have answers. I will hope my students will learn that their standard answers might not be so useful after all.

Finally let me add that I am looking forward to the publication of a book called Chance, Necessity, Love: An Evolutionary Theology of Cancer. It’s the work of Leonard M. Hummel, who teaches Pastoral Theology and Care at the Lutheran Theological Seminary at Gettysburg, and Steve James, Associate Professor of Molecular Biology at Gettysburg College. I’ll update when the book is available.

Here again is the LINK to the videos. Each one is a winner. We nonscientists owe a great debt to the hardworking young researchers who spent hours showing us what we’re made of. For a theologian, it's a revelation.

Cognitive Enhancement: Campus Update

Ron Cole-Turner — Fri, 02 Dec 2011 09:43:00 +0000

Use of drugs to boost academic performance is nothing new, but The Washington Post has just published a news story suggesting that use of these drugs is increasing on college campuses.

The story, written by Post reporter Jenna Johnson, refers to a study at the University of Maryland that suggests that students who take cognitive enhancers study less, party more, and have slightly lower grade point averages than their classmates. That suggests that their main purpose for using the drugs is stay competitive without letting studies get in the way of college.

There is little doubt, however, that the drugs are also being used by highly focused, academically competitive students in demanding programs. Their purpose: to add an edge to their hard work in order to stay in the top one or two percent of the competitive pile. As the Post reports, one name for these drugs is “Ivy League crack.”

The drugs in question are familiar enough—mostly Ritalin and Adderall. Students without prescriptions can easily buy these drugs from other students.

Should use of these drugs be treated as crimes? Or should those who wish to excel academically be allowed to use whatever means helps them achieve that end? For more on that debate, see the now-classic 2008 article in the journal Nature, in which prominent bioethicists such as Stanford’s Henry Greely argue for greater tolerance and openness.

Science and Technology in Theological Perspective

Ron Cole-Turner — Thu, 01 Dec 2011 20:57:00 +0000

Most of the time, my posts address the latest developments in key areas of science and technology.

Occasionally, it’s helpful to stand back and ask whether it is possible to put these developments together into a broader picture. The speed of scientific discovery can make our heads spin. Can we put things together? Is it possible to offer a theologically coherent view of science and technology today?

One of the boldest attempts along this line is the “Pastoral Letter” released by the United Church of Christ early in 2008. The full title of the Letter is "A New Voice Arising: A Pastoral Letter on Faith Engaging Science and Technology."

When the Letter first appeared, one person to recommend it was Alan Leshner, Executive at the American Association for the Advancement of Science. He wrote:

I am delighted to see the United Church of Christ's clear support of science. I believe that science and religion are complementary to each other, and should not be seen as competing ways of looking at the world; they are concerned with different questions. In an era of such rapid science and technology advances – advances that bring benefits as well as, at times, risks -- and when science and technology are becoming ever-more imbedded in every aspect of modern life, it is essential that we maintain an active dialogue among scientists, ethicists, and religious communities. In the same way that UCC states that it cannot ignore the context in which it functions, neither can the scientific community ignore its societal context. For this reason, we see a dialogue between science and religion as vital.

While science and technology have continued to advance rapidly since 2008, the themes expressed in the Letter remain current. Church groups have used it as a study document. Clergy have used it for sermons. My guess is that they will continue to do so.

The Great Migration: Tools Mark the Trail

Ron Cole-Turner — Wed, 30 Nov 2011 16:55:00 +0000

Anatomically modern humans (AMH)—people who looked pretty much like us—migrated out of Africa tens of thousands of years ago and settled across Asia and Europe.

Just who were these people, how long ago did they migrate, and what route did they first take? These are some of the biggest questions in archeology. Now at last researchers seem to be closing in on concrete answers.

In a report published in the November 30 issue of the open-access journal PLoS ONE, an international research team led by Jeffrey Rose presents its analysis of recent work in southern Oman, located on the southeastern corner of the Arabian peninsula.

For years, researchers have debated with each other over the earliest migration route. Was it across the Red Sea to the Arabian boot heel (sea levels being much lower then)? Or was it north from Egypt along the Mediterranean?

Rose and his team found evidence suggesting that AMH residents of the Nile valley migrated—with their distinctive tool technology—to present day Oman. Their analysis of over 100 sites in Oman led researchers to believe that the tool culture was clearly the same in both settings. In other words, one culture spans two continents, clearly supporting the idea of human migration.

Scientists have long known about the Nile valley culture, which they call “Nubian.” The breakthrough reported here is the strong evidence that Nubian toolmakers made their way out of Africa to Arabia, bringing their characteristic stonecutting techniques with them.

The date of migration, according to the report, is at least 106,000 years ago, perhaps earlier.

No human remains were found with the stone tools. This leaves open the possibility that some other humans—“archaic” and not anatomically modern—may be responsible for the stone tools. The researchers dismiss this idea on the grounds that AMH seem to be the only form of humans present in North Africa at the time of the migration.

“After a decade of searching in southern Arabia for some clue that might help us understand early human expansion, at long last we've found the smoking gun of their exit from Africa,” according to Rose, a Research Fellow at the University of Birmingham.

Another surprise contained in the report is that the stone tools were found inland rather than right along the coast. “For a while,” remarks Rose, “South Arabia became a verdant paradise rich in resources – large game, plentiful freshwater, and high-quality flint with which to make stone tools,” according to a press release issued by PLoS One. One possibility is that the “southern route” out of Africa along the southern Arabian peninsula was not so much a coastal expressway to Asia and Europe as it was a settling of the interior of Arabia.

The report, “The Nubian Complex of Dhofar, Oman: An African Middle Stone Age Industry in Southern Arabia,” appears in the November 30, 2011 issue of PLoS ONE

Seminaries and Science

Ron Cole-Turner — Mon, 28 Nov 2011 22:15:00 +0000

How can seminaries do a better job in helping future clergy become more aware of developments in science and technology?

That was the focus of a panel last week at the American Academy of Religion Meeting in San Francisco. Lead-off speakers were Dan Aleshire, Director of the Association of Theological Schools and Jennifer Wiseman, who directs the program of Dialogue on Science, Ethics and Religion at the American Association for the Advancement of Science.

Then it was my turn. I pointed out the obvious. There’s no room in the theological curriculum to add anything. Faculty wouldn’t know what to add if they had the time. Students would be able integrate it into what they are already learning. So why bother?

I suggested that seminaries need to remember that their job is to teach theology. Doing our job well today, I argued, means that we have to take science and technology into account. One reason why this is so is because theological ideas or doctrines come mixed with outdated philosophical notions of nature.

For Christianity, this is a real challenge. Our core idea—redemption—is built on a myth of an original human nature that is lost and then restored. Unless students are minimally aware of how science challenges this thinking, seminaries aren’t doing their job.

I also suggested that for today’s students, my classroom references to current science almost always brought the subject matter to life. Students today are not so familiar with philosophy or other sources of criticism of theology. They have an easier time understanding how science challenges traditional ideas and forces them to think. They welcome the challenge. After all, they like to think that their education is relevant to the world in which they will serve.

Seminaries today need to focus on the basics—like theology—and teach it the right way right from the beginning, starting with introductory courses.

Sure, advanced electives are fine. I teach them myself, everything from “Christianity and Evolution” to “Ethics and the Technologies of Human Enhancement.” But the real key for seminaries, I believe, is to teach the core of the curriculum in a way that is appropriate for the clergy of today.

Here's where you'll find more about the AAAS program on seminary education, including recent news about an earlier program.

Brain Regeneration: Mouse Brains and Human Futures

Ron Cole-Turner — Fri, 25 Nov 2011 15:22:00 +0000

Embryonic stem cells are surprisingly capable of regenerating portions of the brains of mice according to a report published in the November 25 issue of the journal Science. What is unexpected about this report is not the extent of the repairs so much as where they occurred in the brain.

The hypothalamus, which is involved basic metabolism and complex behaviors, has usually been regarded as less open to regeneration, whether naturally or by biomedical intervention. Naturally, a limited number of neurons develop during adulthood, but these are not enough to restore this area of the brain after injury or disease. “The neurons that are added during adulthood in both regions are generally smallish and are thought to act a bit like volume controls over specific signaling,” explained Jeffrey Macklis of Harvard Medical School and one of the lead researchers in the study.

“Here we've rewired a high-level system of brain circuitry that does not naturally experience neurogenesis,” Macklis said, “and this restored substantially normal function.”

The report reached this conclusion: “these experiments demonstrate that synaptic integration… [by] donor neurons can impart an organism-level rescue of metabolic defects, thereby providing a proof of concept for cell-mediated repair of a neuronal circuit controlling a complex phenotype.”

While it is important to underscore that this work is performed on mice, the results suggest that something similar might be possible someday in human beings with brain injuries. “The finding that these embryonic cells are so efficient at integrating with the native neuronal circuitry makes us quite excited about the possibility of applying similar techniques to other neurological and psychiatric diseases of particular interest to our laboratory," according to Matthew Anderson in a press release issued by Harvard Medical School.

For now, research continues using mice as models for human disease or spinal cord injury. “The next step for us is to ask parallel questions of other parts of the brain and spinal cord, those involved in ALS and with spinal cord injuries,” according to Macklis. "In these cases, can we rebuild circuitry in the mammalian brain? I suspect that we can."

This study, coming so quickly on the heels of another report showing the functional integration of human embryonic stem cells into the mouse brain, suggests that embryonic stem cell research may indeed open new ways to treat brain disease or injury. Both studies, however, open the possibility that the use of technologies of brain regeneration will not stop with disease. As always, the growing power of medicine to treat disease is also an expansion of the possibility of human enhancement. All this if far in the future. But already, advocates of human enhancement have noticed its significance. See, for example, the re-posting of the original press release on Ray Kurweil's transhumanist blog.

The report, entitled “Transplanted Hypothalamic Neurons Restore Leptin Signaling and Ameliorate Obesity in db/db Mice,” appears in the November 25, 2011 issue of Science.