There is no better way to attract reports of the paranormal than to write a story casting doubt on it, and attract them I did. Besides the usual ghost sightings, my favorite was from a nice man in Florida who told me about his wonderful typewriter (note: not a word processor): he would type a few letters of a word and the machine would fill in the rest, apparently having read his thoughts.

Make of that what you will. More interesting, to my mind, was a note from Michael Shermer of the Skeptics Society, who pointed me to his column in the December issue of Scientific American. There, he explores what he calls “patternicity,” the tendency of the human brain to “find meaningful patterns in meaningless noise,” as he puts it, as shown in our tendency to “see faces in nature, interpret window stains as human figures, hear voices in random sounds generated by electronic devices or . . . see the Virgin Mary on the side of a building”—or in a potato chip, as I noted in the story.

Evolution favored humans who were “most successful at finding patterns,” Shermer writes, a process called associative learning that “is fundamental to all animal behavior. . . . Unfortunately, we did not evolve a Baloney Detection Network in the brain to distinguish between true and false patterns.” Hence those Mary sightings.

Shermer cites a fascinating paper to be published in January in the journal Proceedings of the Royal Society B. In it, Kevin Foster of Harvard and Hanna Kokko of the University of Helsinki show that when it costs less to believe in a pattern or connection that isn’t real (believing that a noise in the grass is a hungry tiger when it is only the wind) than to fail to make a connection that is real (ascribing the noise to the wind when it is actually a tiger) people tend to err on the side of patternicity. If our ancestors had erred in the other direction—“oh, that’s usually just wind, nothing to worry about”—they would not have been our ancestors because they would have been eliminated from the gene pool.

A certain spouse of our acquaintance has what we can only assume are religious objections to walking over to a wastepaper basket and dropping in his used Kleenex, crumpled envelope or other trash. Instead, he shoots what amount to living-room foul shots—occasionally hitting someone between him and the basket. This spouse has also been known—rarely!—to throw crumpled paper in anger,intentionally hitting someone. Question: why does it hurt more when he tries to hit you than when he hits you unintentionally? Related question: why does it hurt more if someone purposely stomps on your foot than if she accidentally treads on your toes?

Now Kurt Gray and Daniel M. Wegner of Harvard University have shown it’s not your imagination, or a case of hurt feelings being confused with a physical harm. As they write about “the sting of intentional pain” in the December issue of the journal Psychological Science, “the physical parameters of the harm may not differ—your toe is flattened in both cases,” but the intentional infliction of pain is, well, more painful.

Psychologists have known for years that pain has a strong mental component. The placebo effect (being given a sugar pill or other dummy treatment that a respected authority assures will help you) is especially potent at reducing pain, and the nocebo effect (being told you are about to feel something painful, even though nothing physical is actually administered) can cause pain: when told that a (nonexistent) electric current is passing through their heads, people say they get headaches, as a fascinating 1981 paper found.

For their study, the Harvard scientists paired 43 volunteers with partners (actually, one of the research assistants). The partner, they were told, would decide whether the volunteer would receive an electric shock or not. Sometimes, however, the experimental set-up would deliver a shock even when the partner had called for something else, the volunteers were told. The volunteer could see what the partner had called for and what was actually going to happen. That is, they could tell if the partnermeant to cause the volunteer to feel an electric shock (intentional) or if the shock occurred because of a mix-up (unintentional).

On a scale from 1 to 7, intended pain hurt 3.62 worth. An identical shock, which the volunteers thought was unintentional, hurt 3.00 worth.

Why? One clue comes from the finding that, in the brain, feelings of physical pain and social harm (such as being rejected) are processed by similar regions, as a 2003 study found. Social harms are, typically, intentional, and are more painful to relive than physical harms. If you combine physical pain (electric shock—or getting hit with a wadded-up Kleenex) with social pain (he meant to hit me!), the combination is that much more hurtful.

So if she tries to tell you that that little intentional stomp she gave your foot can't have hurt, or if he insists that a little bop on the head from the paper he hurled at you cannot have been painful, tell them science says otherwise.

Yet another good friend told me over the weekend how she had narrowly (in her estimation) escaped death: she had had a mammogram a few months ago, a lump had been detected and deemed suspicious, surgery was scheduled, the lump was removed and found to be malignant. She is now starting the standard course of radiation, and thanks to the mammogram, she was telling me, her life has been saved.

Maybe. But maybe not. Since she can't re-run her life and not have the mammogram, seeing what would have happened if the lump had not been found and her cancer treated, we'll never know.

The trouble with mammograms is that they not only have a very high rate of false positives (detecting a mass that turns out to be benign, not breast cancer)—according to the American Cancer Society, by the time a woman has 10 mammograms she will also have a 50 percent chance of being told, wrongly, that one is suspicious—but also an unknown rate of true positives (the radiologist finds a mass, and it’s found to be malignant) that, if left alone, would not have posed any threat to a woman’s health or life. In today’s issue of the Archives of Internal Medicine, scientists are reporting a study (the journal has made it available for no charge, so read it yourself and print it out for your doctor) that strongly suggests that some of the cancers detected by mammography would have vanished on their own had they not been detected and treated.

For the study, scientists led by statistician Per-Henrik Zahl of the Norwegian Institute of Public Health examined breast cancer rates among 119,472 women age 50 to 64 who had three screening mammograms between 1996 and 2001. They then counted breast cancers among a control group of 109,784 women who were not screened. Not surprisingly, breast cancer rates were higher among screened women than not-screened women. After 6 years, all the women were invited to undergo a mammogram.

Here’s where the surprise came in. Even at the 6-year screening, the incidence of invasive breast cancer was 22 percent higher in the previously-screened group (1,909 vs. 1,564 per 100,000 women) than the control group. Because the incidence of breast cancer among women in the control group (who were no different in terms of their cancer risk than the screened women) was always less than that of the screened group, write the scientists, “it appears that some breast cancers detected by repeated mammographic screening would not persist to be detectable by a single mammogram at the end of six years. This raises the possibility that the natural course of some screen-detected invasive breast cancers is to spontaneously regress. . . . Although many clinicians may be skeptical of the idea, the excess incidence associated with repeated mammography demands that spontaneous regression be considered carefully.”

Cancer that goes away without treatment? The scientists found only 32 reported cases of spontaneous regression of invasive breast cancer, a tiny number for a relatively common disease. But, they point out, “the fact that documented observations are rare does not mean that regression rarely occurs. It may instead reflect the fact that these cancers are rarely allowed to follow their natural course.”

And that is what remains such a mystery: What is the natural course of a cancer, breast or otherwise? With prostate cancer, oncologists have come around to the idea that “watchful waiting” is appropriate for many men: the prostate tumor can sit there safely until the man dies of something else. An oncologist in favor of watchful waiting for breast cancer is as rare as hens’ teeth, and I can’t think of any woman who would agree to that course of (non) treatment.

But it’s a fascinating question, whether some significant fraction of the cancers doctors are finding with more and more screening actually pose any threat or would go away on their own. Clearly, however, mammograms are responsible for “the detection and treatment of cancers that would otherwise regress,” the scientists write.

The value of mammograms—specifically, whether they save lives—has been controversial more ways than you can count. (But see this, this and this.) In an accompanying editorial, Robert M. Kaplan of UCLA and Franz Porzsolt of the University of Ulm, Germany, argue that “despite the appeal of early detection of breast cancer, uncertainty about the value of mammography continues.”

That’s putting it mildly—but only if you include among the "uncertain" scientists who actually evaluate the data rather than women who are convinced that a mammogram saved their life and clinicians who dare not question the value of one of the only tools they have (and can you imagine the lawsuit if a doctor told a woman not to bother with a mammogram, and she developed cancer that was discovered only in a late, incurable stage?). But as Kaplan and Porzsolt point out, “We know from autopsy studies that a significant number of women die without knowing that they had breast cancer. . . . If the spontaneous remission hypothesis is credible, it should cause a major re-evaluation in the approach to breast cancer research and treatment.”

 I'm not holding my breath.

Sir Ghillean (Iain) T. Prance, the eminent botanist who served as director of Britain’s Royal Botanic Gardens, Kew, from 1988 to 1999, was in New York this week to receive the Gold Medal of The New York Botanical Garden for his contributions to plant science. The award is given infrequently; the last recipient was Edward O. Wilson, in 2002.

Sir Ghillean has done research across the world, including the Amazon, where he has witnessed dramatic changes over 40 years. “I went to Suriname in 1963 and Brazil in 1964, and there was very little damage to the rainforest,” he told me. “But by the 70s they had built a highway across the Amazon, then colonization followed, with cattle ranching in the 1980s and now soybean farming. We’ve lost 23% of the Brazilian Amazon rainforest, but there is still a lot to fight for.”

I asked him what we’ve learned about what works to preserve rainforest and what doesn’t. “Sustainable forestry on the whole hasn’t lived up to its promise,” he said. “Sustainable use is possible, but less than 1% of development in the Amazon is truly sustainable.” The only real hope he sees is for wealthy nations to step up and pay nations with significant remaining rainforest to keep it intact, something Guyana has asked the world to do for its rainforest, as I blogged about last May.

Photo: S.C. Schuster

As scientists led by Stephan C. Schuster of Pennsylvania State University describe today in the journal Nature, they extracted DNA from the hair of several mammoths preserved in permafrost. The scientists estimate that entire mammoth genome is 4.7 billion nucleotides long (humans’ is 3 billion nucleotides; a nucleotide is one of the four chemical “letters,” designated A, C, T or G, that constitute the coding part of DNA), and they figure they’ve sequenced around 80% of it. All told, 28 vertebrate species have had their genomes sequenced, including humans, chimps, mice and dogs, but this is the first extinct animal to join the club (though the extinct cave bear and Neanderthals have been partially sequenced).

In their paper, the scientists emphasize the value of the study for understanding the evolution of elephant species (by comparing the mammoth DNA to that of living African pachyderms), but let’s face it: what we want to know is whether the genome sequence can be used to resurrect mammoths.

Nature writer Henry Nicholls lays out what would be required. “If you want to bring a species back to life,” he notes, “the mammoth would be almost as dramatic as a dinosaur. And unlike Tyrannosaurus rex, the mammoth has close living relatives to lend a hand. It is a fair bet that a complete genome and closely related species would make it easier to pull a Crichton on a mammoth than on a dinosaur.”

“Easier” does not mean “easy,” of course. To go from the genome being announced today to a living, breathing mammoth would require synthesizing a full set of chromosomes from the DNA, packaging them in a nucleus, transferring that nucleus into an egg, and implanting that egg into the womb of a surrogate mother (presumably an elephant). Although none of this has been done—Nature says there are “all but-insurmountable obstacles at every stage, and no evidence that anyone is going to work very hard to solve them”—none are scientifically impossible.

For instance, making a complete, error-free mammoth genome is almost surely in the cards. Figuring out how Mother Nature apportioned the 4.7-billion-nucleotide sequence into chromosomes, which is biologically necessary, is a challenge, but presumably studying how she did it in elephants (which have 56 chromosomes, compared to humans’ 23) would provide clues. Then you’d need the actual DNA—that is, take the known sequence and make all of those 4.7 billion chemicals in test tubes, link them up and actually package them in chromosomes. The largest such “synthetic genome” yet synthesized is the measly 582,970 nucleotide one of the bacterium Mycoplasma genitalium. For mammoths, you’d need to string the 4.7 billion onto 56 chromosomes, each averaging 160 million long. Tough? Sure, but as Nature says, “It is worth remembering that genome synthesis is further developed today, in terms of the maximum lengths achieved, than genome sequencing was when Crichton wrote Jurassic Park. And look how sequencing has progressed since then.”

Once you have your mammoth chromosomes, you have to pack them into a nucleus and then an elephant egg. Elephant eggs are not easy to come by, but it may be possible to harvest a steady supply by collecting tissue from the ovary of a recently deceased elephant and grafting it into a lab mouse or rat—something that has been done: frozen samples of ovarian tissue from African elephants have been transplanted into mice, where egg-making follicles developed.

Finally, you’d have to transfer the mammoth nucleus-encased DNA into the egg, fertilize it, and transfer the four-cell embryo into a surrogate mom (never been done). “Most evidence indicates that newborn woolly mammoths were about the same size as newborn elephants,” Nature notes, so size should not be a problem for the surrogate mom.

So, how feasible is all this? “The fact that just 15 years ago cloning mammals was confidently ruled out by many as being impractical should give people pause before saying any such thing is impossible," Nature concludes. "By 2059, who knows what [extinct species] may have returned, rebooted, to walk the Earth?”

Even when they were first discovered, in 2005, the four graves near Eulau, Germany, made scientists sit up and take notice: at 4,600 years old, they were unusually ancient and well preserved. But now, having performed genetic and isotopic tests on the remains, scientists have realized they have something even more momentous: one group of adults and children buried facing each other is the oldest nuclear family identified with molecular genetic evidence, Australian scientists are reporting today in the online edition of Proceedings of the National Academy of Sciences. And analyses of strontium isotopes in tooth enamel, which reveal where people came from, indicate that the males and children came from around the area where they died, while females came from far away: in this Late Stone Age society, it seems, males found mates from outside the clan and brought them home, the first evidence of a practice that was to become widespread during human prehistory.

This region of Germany is already known in archaeological circles as the discovery site of the Nebra sky disk, a Bronze Age (1600 B.C.) disc that suggests that these ancient Europeans knew a little astronomy . Four graves were discovered in 2005: one with a woman (35–50 years old at death), a man (40–60), and two children (4 to 5 and 8 to 9); a second grave with a woman (30–38) and three children (an infant, a 4-to-5 year old, and 7-to-9-year old); a third with a man (25–40) and two children (4 to 5 and 5 to 6), and the final grave with a woman (25 to 35) and a child (4 to 5).

“Intriguingly,” write the scientists, “the arrangement of the dead seems to mirror their relations in life. The latter is reflected by the face-to-face arrangement of several pairs of individuals and the positioning of their arms and hands, which are interlinked,” suggesting that the dead in each grave constituted a family of some kind. In addition, each grave contained funerary offerings: stone axes for the men and boys, flint tools or animal tooth pendants for the women and girls, and butchered animal bones in each of four graves, reportscientists led by Wolfgang Haak of the Australian Centre for Ancient DNA at the University of Adelaide.

And how did they die, and come to be interred together? The radiocarbon dates for the four graves are identical, the scientists note, strongly suggesting that all four occurred at the same time. A strong clue to what happened is the age of the dead: children no older than 10 and adults 30 or older, but no adolescents or young adults. In addition, five of the dead were victims of violence: a stone projectile point is embedded in a vertebra of one, two others have skull fractures, two men have defensive injuries on the forearm—all of which paints a picture of a violent raid by a rival clan that killed all 13 individuals, conclude the scientists, and the survivors--probably young people old enough to go out hunting or gathering—to bury the dead.

Genetic analysis of the ancient DNA shows that the man, woman and two children facing each other were a nuclear family (the woman is the children’s biological mother, the man, their father). The two children in the second grave are siblings or half-siblings (they had the same mother), but the woman buried with them was not she (she was, instead, either a paternal aunt or perhaps a step-mother). What is remarkable is that the survivors recognized the primacy of the nuclear family, choosing to keep it intact in death as in life.

No child should be born into this world with Batten Disease, which—and here I’ll just quote from the National Institutes of Health—causes “mental impairment, worsening seizures, and progressive loss of sight and motor skills. Eventually, children with Batten disease become blind, bedridden, and demented. Batten disease is often fatal by the late teens or twenties.” And if Mark Chandler has his way, no more will be.

Chandler is chairman and CEO of Biophysical Corp., a pioneering company that, as I wrote about two years ago, offers a battery of tests for “biomarkers” that can indicate the presence of early-stage disease before symptoms appear. (The virtue of testing for biomarkers rather than disease genes is that with the former you are testing for the presence of the actual disease, but with DNA tests you are almost always testing for the possibility of developing a disease in the future.) Now Chandler is hoping to offer tests to identify carriers of rare genetic disorders such as Batten Disease: as carriers, they would not have the disease and so would have no idea they carry silent genes for it until, tragically, their child is born with one of these 1-in-a-million disorders. A genetic test could warn them.

The model is what the Ashkenazi Jewish community has done, beginning in 1969, to screen couples for Tay-Sachs disease, which was more common among that population than Americans generally. If both a husband and wife carried the rare mutation, they were counseled to avoid having children, or (if they had not yet married) even to find other partners, since if two carriers mate their children have a 25 percent chance of having the disease. As a result of the widespread screening, Tay-Sachs has been almost eliminated in American Jewry; of the 20 or so children born with Tay-Sachs in the U.S. each year, most are from Louisiana's Cajun community or are French-Canadians, two population groups that also carry the mutation.

It may seem like overkill to test all couples or would-be couples for diseases that are so rare, but Chandler thinks he can develop a test for the 400 or so “orphan,” diseases such as those on the list of the National Association for Rare Disorders. All are autosomal recessive: if you inherit the mutation from one parent, and therefore have one copy of the disease gene, you do not develop the disease but are a carrier; if you inherit one copy from mom and one from dad because both your parents are carriers, you get the disease. Chandler is confident that new DNA technology can offer the test for all 400 for $125. You can spend more on a maternity dress.

But before the DNA test can be offered, it needs to be validated—that is, known carriers must have their DNA tested, and the screening must correctly identify them as carriers, while not identifying non-carriers as carriers. That is, no false negatives and no false positives—or as near to “no” as one can get, which Chandler believes is 99.9 percent accurate. To validate the test for autosomal recessive orphan diseases, he figures he needs 5 to 10 couples for each disease. If you want to be one of them—volunteering to spare other children these fatal diseases—you can contactKristin Thomas Miskovsky at kmiskovsky@biophysicalcorp.com, or call her at 512.623.4923.

Having recently tipped you off to the most effective way to swat a fly, Lab Notes is now proud to share the secret to killing a skittering, running-for-its-life cockroach. Thanks to research on animals’ predator-escape mechanisms (which we’re sure has relevance to deep mysteries about neural circuitry, or evolutionary biology, or something), it can now be revealed that the best way to smoosh a roach is to aim for a 90-degree angle from where the thing is currently headed (that is, figure it’ll make a sharp right or left turn) or a 180-degree angle (that it’ll reverse course).

Yes, you might need assistance to cover all three possibilities. A 3-to-1 ratio of humans to roaches is about the right show of force, given how the things have outsmarted and out-reproduced us for so long.

As scientists led by Paolo Domenici of Italy’s Istituto per l'Ambiente Marino Costiero report in Current Biology, cockroaches fleeing predators seem to choose an escape route at random. “By using one of a number of possible trajectories,” said Domenici, “cockroaches may behave with sufficient unpredictability to avoid the possibility that predators will learn their escape strategy. The predator is made to guess.” But roaches do not run in random directions. Instead, find the scientists, they select an escape route at only a few fixed angles from the threat: a 90 or 180 degree angle from the attack. “This is where squashing could be aimed,” Domenici said, “although we like cockroaches and would recommend no squashing.”

Each to his own.

While all of us who are rooting for the existence of little green men have been cheered by each discovery of a planet orbiting a star other than our sun—an “exoplanet,” of which there were 322 when I checked the catalog a minute ago—there’s always been a tinge of disappointment. Every validated discovery, starting with the first in 1995, has been indirect. In other words, astronomers didn't actually see the planet beyond our solar system, but instead inferred its existence by, for instance, noticing something funny about how a star moves and realizing, gee, that funny movement must be due to a planet tugging gravitationally on the star. But this afternoon, two separate teams of astronomers, using three different telescopes, are announcing the discovery of exoplanets by, well, looking.

One team, led by Paul Kalas of the University of California, Berkeley, used the Hubble Space Telescope to image a planet they call Fomalhaut b, orbiting the star Fomalhaut, 25 light years away in the constellation Piscis Australis (the Southern Fish). The other team, anchored by Christian Marois of the Herzberg Institute of Astrophysics in Victoria, British Columbia, imaged three planets orbiting a star called HR 8799, 128 light years from Earth, using the Keck and Gemini telescopes. Both are being published this afternoon online by the journal Science, at its Science Express website.

I was intrigued, and a bit alarmed, by a study in this month’s Archives of Neurology. The study used an imaging agent called Pittsburgh Compound B (so-named because it was discovered at the University of Pittsburgh; it detects brain deposits that the conventional medical wisdom claims is the cause of Alzheimer’s disease) to examine the brains of 43 people, age 65 to 88, who had neither Alzheimer’s disease nor mild cognitive impairment. Of the 43, 9 showed evidence of these brain deposits, called amyloid plaques, in at least one brain area.

Uh oh, you might think. But think again. Here is what caught my attention in the paper describing the study: “Neurocognitive performance was not significantly worse among amyloid-positive compared with amyloid-negative participants. . . . [A]myloid deposition was not associated with worse cognitive function, suggesting that an elderly person with a significant amyloid burden can remain cognitively normal.”

So here’s the reason for my alarm: since Pittsburgh Compound B has, since its discovery, been treated like the Second Coming, do we really want to screen people with this technique, telling them omigod you have amyloid plaques—when the cause-and-effect link between the plaques and Alzheimer’s is, shall we say, on shaky ground? Or as the scientists, led by Howard Jay Aizenstein and William E. Klunk of the University of Pittsburgh School of Medicine, write, we’ll need more research to figure out whether “amyloid deposition is not sufficient to cause Alzheimer disease.”

The amyloid hypothesis of Alzheimer’s disease has had the field in a stranglehold for decades, as I’ve written about before. In 2006, for instance, Zaven Khachaturian, who oversaw Alzheimer’s funding at the National Institute on Aging from 1977 to 1995, told me that the theory that amyloid plaques cause AD has become a pernicious “orthodoxy,” and that “having one view prevail is harmful; it becomes a belief system, not science.” And Robert Mahley, president of the J. David Gladstone Institutes, San Francisco, told me that “where the field made its mistake was in trying to make everything fit one common [amyloid] pathway. We’ve got to realize there are multiple ways you can wind up with [Alzheimer’s].”

They, and others, are most upset about what the amyloid orthodoxy has meant for basic research--namely, that scientists with other ideas struggled to get funded. As a result, alternatives have hardly been pursued, and we are no closer to treating, let alone preventing or curing, AD than we were 25 years ago. That’s a tragedy, and perhaps a crime.

But what will the amyloid orthodoxy mean for patients? If it is moved into the clinic with the use of Pittsburgh Compound B, and healthy adults are screened for amyloid plaques with this technique, we'll face a problem just as serious as focusing on a single theory of AD. Doctors will identify these brain deposits in millions of people, and scare them out of their wits by telling them that they have what looks like the cause of a terrifying disease—when the whole idea that the plaques cause AD may be wrong?

Klunk put it this way: “The good news is it appears the brain can tolerate these plaques for years before the effects are apparent. The bad news is that by the time the symptoms emerge, the disease has had perhaps a 10-year head start. We suspect that people with amyloid deposits and normal brain functioning have a high risk of developing Alzheimer’s disease in the future, but we do not yet have proof of this.” No kidding.

Explain this: if Alzheimer’s disease  is caused by the accumulation of sticky amyloid plaques and neurofibrillary tangles that kill neurons (as the leading theories of the disease hold), then how can holding a job that poses minimal cognitive demands and watching a lot of TV raise your risk of developing the disease? Nothing in neuroscience suggests that either activity speeds the formation of plaques or tangles—or, conversely, that mentally-demanding jobs and spending your leisure time in more intellectually-engaging pursuits blocks their formation.

New research is leading to an inescapable conclusion. Being extra brainy when you enter old age has no effect on the basic pathological processes that attack the brain. Sorry. But here’s what it does do: when that pathology kicks in (or even when less insidious, normal brain-aging starts to impair memory and neuronal processing speed), a brain that has a “cognitive reserve” can take more hits before showing the effects than a brain with less cognitive reserve.

Think of it this way: if a cyber-thief siphons $100 a week from your bank account, you’ll have enough to pay the bills longer if you start with a large balance than if you start with a small one. Cognitive reserve is your brain’s bank balance.

This is very different from the commonly-held belief that mental activity slows the rate of cognitive decline, as Timothy Salthouse of the University of Virginia, a veteran of studies on aging and cognition, pointed out in a 2006 analysis. This “mental exercise” hypothesis rests on studies finding that higher mental activity, such as reading and doing crossword puzzles, is associated with better cognitive function in old age. That does not mean, however, that older adults who stay more mentally active are slowing their rate of cognitive decline. Instead, it is becoming increasingly clear, they enter old age (i.e. their 30s, which is the decade when cognitive function starts heading south, accelerating in your 50s) with a cognitive reserve, a sort of mental cushion. That starts them off far enough above the threshold where impaired mental function affects the ability to think and remember that a normal decline leaves them pretty much okay for a longer period. That cyber-thief’s $100-per-week leaves the well-endowed with enough to pay the bills for many years.

But here’s the awful part. In the most mentally-engaged elderly, such as professors who enter their 60s or 70s with smarts to spare, the rate of mental decline is typically just as steep as in dullards. True, a brain functioning far above the average will still be pretty good even with the equal rate of decline—but these people notice their diminishing capacities nonetheless. Sadly, therate of mental decline is not affected by cognitive exercise, Salthouse wrote back in 2006, arguing that there is “little scientific evidence that engagement in mentally stimulating activities alters the rate of mental aging.” The belief that it does is “more of an optimistic hope than an empirical reality.”

The latest study, too, supports the cognitive-reserve idea. People with greater thinking, learning and memory abilities are able to delay symptoms of Alzheimer’s disease—but not necessarily the underlying pathology: their brains still suffer neuron-killing plaques and tangles, but they function adequately longer than people with a smaller cognitive cushion. As Catherine M. Roe and colleagues at the Washington University School of Medicine write in Archives of Neurology in a paper being posted this afternoon, “a greater pathological burden is required to show an effect on cognition among persons with more education.”

They studied 37 people with Alzheimer’s and 161 healthy individuals, noting their education history and giving them cognitive tests. They were then tested for the presence of the beta-amyloid plaques considered a marker of Alzheimer’s. Even in people with lots of beta-amyloid plaques, the more years of education they had had the better they did on the test. “The results support the hypothesis that cognitive reserve influences the association between Alzheimer disease pathological burden and cognition,” the authors write. Translation: the smarter you are, the more beta-amyloid plaques your brain can tolerate before showing symptoms of Alzheimer’s.

As I watch this year’s impatiens, vinca and petunias shrivel up and die, this is what I am not thinking: “oh goodie, I get to plant another crop of annuals next spring!” No, I am thinking, “if a stupid tulip can be a perennial, why can’t these come back every year, too, with minimal intervention on my part?”

I am therefore looking forward to plant breeders taking a discovery published online this afternoon in Nature Genetics and later in a print version of the journal and putting it to widespread use. The discovery is that by turning off a mere two genes (out of some 25,000) in the little flowering annual called thale cress (Arabidopsis thaliana), scientists managed to turn it into a perennial.

Annuals, of course, germinate, grow, blossom and die within one growing season. Perennials overwinter and grow again the following year, thanks to buds, bulbs or tubers that contain groups of non-specialized cells (called meristems) that can differentiate into new organs such as stalks and leaves. Annuals lack these overwintering meristems. Instead, they consume all the meristems during the growing season to produce flowers: once the flower appears, the end is nigh for an annual.

Arabidopsis thaliana has become a favorite of geneticists. The complete sequence of its genome was finished in December 2000, so scientists led by Siegbert Melzer and Tom Beeckman of the Flanders Institute for Biotechnology in Ghent, Belgium, exploited that knowledge to the full. They identified two flower-inducing genes (with the less-than-melodious names SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 and FRUITFULL; I am not yelling at you, but names of genes are, by convention, capitalized). Both genes also affect whether the meristems differentiate. Using standard techniques, the scientists turned off the two genes and watched what happened.

The mutant Arabidopsis plants couldn’t flower, which is what you’d expect when their flower-making genes are knocked out of commission. But the more tantalizing finding is that the mutants do not use up their supply of non-specialized cells—the meristem. As a consequence, they are able to grow like perennials. The resulting plants were woodier and more shrub-like than regular Arabidopsis. (A natural mutation such as this may well account for the evolution of herbaceous, i.e. non-woody, annuals to woody perennials, namely shrubs and trees.) As the scientists write, disabling the two genes produced plants with“recurrent growth cycles, longevity and extensive woodiness, . . . reminiscent of plants with a perennial life style.”

I call first dibs when the geniuses at Spring Hill, Burpee or other plant nursery or breeder put this discovery to use by giving us perennial pansies, petunias, marigolds, zinnias and all the rest. Then when I see the autumnal decline of my garden, I’ll console myself with the knowledge that they’ll all be back in the spring with little to no help from me.

The tragedy of autism is compounded by one fact that makes desperate parents wish they could turn back the hands of time: symptoms of the neurodevelopmental disorder typically show up when a child is 2 or 3 or even older, but by then it may be too late to prevent or reverse whatever glitches in brain development (still pretty much a mystery) underlie the disease. It is even on the late side for getting a child the behavioral interventions and special education that might mitigate some of the worst symptoms.

If scientists at the M.I.N.D. Institute of the University of California, Davis, are right, however, there may be a reliable warning sign of autism much earlier: how a child plays with his or her toys at the tender age of 12 months. In particular, scientists led by Sally Ozonoff will report in the journal Autism (it’s the October issue, but not out yet; keep checking the web site), children who were later diagnosed with autism were more likely to spin, repetitively rotate, stare at and look out of the corners of their eyes at toys such as a rattle.

There is a big research effort aimed at picking up the earliest harbingers of autism. One of the most promising discoveries came in 2003, when researchers led by neuroscientist Eric Courchesne of the University of California, San Diego, concluded that an odd pattern of skull growth might be a tip to autism, as they described in a paper in the Journal of the American Medical Association. Children with autism, the scientists found, had a smaller head circumference at birth than healthy babies, and by 6 to 14 months their head circumference was in the 84th percentile, a huge increase and greater than the rate of increase in healthy children. “The clinical onset of autism appears to be preceded by 2 phases of brain growth abnormality: a reduced head size at birth and a sudden and excessive increase in head size between 1 to 2 months and 6 to 14 months,” the scientists wrote. “Abnormally accelerated rate of growth may serve as an early warning signal of risk for autism.” Still, the correlation wasn’t perfect: 6% of healthy infants in the study also showed abnormal head growth from birth to 6 to 14 months, and 41% of babies later diagnosed as autistic didnot show that pattern.

The American Academy of Pediatrics recommends that all infants be screened for autism twice before they are 2. Pediatricians look for language delays and lack of interest in people, such as not responding to their name and failing to make eye contact. But these can be present even when autism is not. The latest findings are not perfect either, but they are something parents can watch for every day rather than relying on—and waiting for—a short visit to the doctor. “There is an urgent need to develop measures that can pick up early signs of autism, signs present before 24 months,” Ozonoff says. “The finding that the unusual use of toys is also present early in life means that this behavior could easily be added to a parent check-list.”

For the study, Ozonoff recruited 66 1-year-olds; 9 were later diagnosed with autism. The children were given a metal lid, a round plastic ring, a rattle and a baby bottle, one at a time for 30 seconds each while being videotaped. Seven of the 9 later diagnosed with autism were more likely to repeatedly spin and rotate the objects. They were also more likely to look at them in unusual ways, like glancing sideways at them or staring intently at them for a long time—behaviors that were rare in babies not later diagnosed with autism. “About a third of parents notice signs [of autism] before a child’s first birthday,” Ozonoff said. “We felt that our field could do a better job at early diagnosis. Our results suggest that these particular behaviors might be useful to include in screening tests. The earlier you treat a child for autism, the more of an impact you can have on that child’s future.”

It’s no secret that oncologists and cancer researchers have made pitifully little progress against lung cancer, even compared to the less-than-stellar progress against other cancers, as I explained in a recent story. But as the Lung Cancer Alliance, a patient-advocacy group, details in its annual report card—filled with F’s—the news is so grim that it is impossible to avoid the conclusion that we need a whole new approach to this tragic disease.

Some of the highlights—or lowlights—include the fact that lung cancer remains the nation’s #1 cause of cancer death: it will claim another 162,000 lives by the time 2008 ends, triple the number of deaths from prostate cancer, nearly twice as many deaths as from breast cancer and more than from breast, prostate, colon, leukemia, ovarian and cervical cancercombined . Nor has there been any progress on five-year survival: only 15% of patients make it to this milestone, compared to 89% for breast cancer, 99% for prostate cancer and 65% for colon cancer. Because there is no good early-screening technique, only 16% of lung cancers are diagnosed at an early, potentially-curable stage. That compares to 61% for breast cancers, 91% of prostate cancers and 39% of colon cancers.

Why is progress essentially nonexistent? Lung cancer is particularly tricky in terms of its genetics, with malignant cells amassing countless mutations that, among other things, allow them to outfox both standard chemotherapies and newer targeted molecular drugs including angiogenesis inhibitors. There’s nothing we can do about that basic biology.

But oncologists tell me there is another reason: there is such stigma attached to lung cancer, because of the view that only people stupid enough to smoke develop it and it is therefore their own dumb fault, that research funding remains criminally tight, especially compared to “celebrity” cancers such as breast and prostate. Lung cancer doesn't have the celebrity spokespeople that these cancers do, so less money is raised from the public. it doesn't have anything like the pink ribbons and "runs for the cure" of breast cancer, for the same reason. In other words, it's not even a fair fight.

Sure, effects of global warming such as more-intense hurricanes and exacerbated drought/flood cycles are no picnic, but now things are getting really dire: as the world, especially the top of the world, warms, the periodic explosion and crash of lemming populations is history.

It's been a decade since the last massive population explosion that lemmings in southern Norway have experienced for at least the last 1,000 years—typically once every three to five years: the explosion and crash of lemming populations has not been observed since the late 1990s, scientists at the University of Oslo led by Nils Stenseth are reporting in the journal Nature today. It's yet another canary-in-the-coal mine for climate change.

What seems to be happening, they say, is that lemmings and other small rodents depend on the insulated region beneath the snow to stay warm, find food (mostly moss) and stay out of sight of predators such as foxes, owls and birds of prey. Without all of the above, their young (of which females often produce 12 per litter, and three litters per year) do not survive. But recent increases in temperature and humidity are, basically, producing the wrong kind of snow.

Lemmings need a space between the ground and the snow. Such a space forms when warmth from the ground melts a thin layer of snow above it, leaving a gap called a “subnivean space” above the ground (which absorbs the snowmelt). But with rising temperatures, the gap is less likely to form: repeated episodes of warmth cause the snow to melt and refreeze over and over, producing a sheet of ice over the ground (rather than just an air-filled space) that keeps lemmings from feeding on the moss. Fewer offspring survive. As a result, populations do not soar and neither do they crash (as a result of too many mouths to feed).

What is going to happen to the simile, “behaving like lemmings”?

The debate over research on embryonic stem cells can seem pretty abstract, so if you want to get a real feel for the effect of President Bush’s ban on the use of federal money for studies of new stem-cell lines see if you can catch a screening of a documentary called The Accidental Advocate. It was produced and directed by Jessica Gerstle, who was an Emmy Award-winning journalist at Dateline NBC for 12 years and who is—more relevantly—the daughter of Dr. Claude Gerstle, an ophthalmologist who was paralyzed from the neck down after a bicycle accident that, as he says wonderingly in the film, left him with nary a broken bone nor a scratch on his helmet. "Merely" a quadriplegic.

The film chronicles Dr. Gerstle’s wheelchair-bound odyssey to learn whether stem cell research offers him any hope of walking again and, more poignantly, his encounters with politicians who believe it is more ethical to flush unwanted embryos (from IVF clinics) down the sink rather than allow scientists to isolate stem cells from these balls of cells and use them to produce lines of cells that hold therapeutic promise. It’s fascinating, in a cringe-inducing sort of way, to see Dr. Gerstle’s Senate-hallway encounter with Sen. Sam Brownback, who believes that embracing “the culture of life” requires unwanted IVF embryos to be discarded rather than used to help people such as Dr. Gerstle, is priceless. (Just to be clear, while there have been several score “snowflake babies” born from frozen embryos “adopted” by couples after the biological parents no longer needed them, an estimated 20,000 frozen embryos are discarded every year.)

In contrast, Sen. Orin Hatch, the Utah Republican who broke with his party and president to support allowing federal dollars to be used for research on frozen IVF embryos that are headed for the waste bin, graciously sits down with Dr. Gerstle to offer his support.

When Dr. Gerstle is not an advocate—and you marvel at his stamina and dedication, and his willingness to travel the country when he can barely raise himself from his wheelchair to get into an airplane seat—he is a quadriplegic. The film shows his agonizing physical therapy, as he tries to take a few steps using a walker, and his painstaking efforts to do something as simple as lift a sandwich to his lips. As his wife reminds us, it’s the little things—like not being able to brush your own teeth—that can be so wearing on paralyzed patients. As for Dr. Gerstle, he says that what he wants more than anything is to be able to once again hug his wife of 38 years.

This Thursday, Nov. 6, those of you in Salt Lake City can see it at Leonardo, 209 East 500 South, at 7 p.m. The University of Utah geneticist Mario Capecchi will speak.. The film was shown at both the Republican and Democratic nominating conventions this summer, and you can Google the film for other screenings.