Tuesday, June 9, 2015
The WHO says more than 20,000 people could be infected by November, while the CDC estimates the epidemic will strike some 500,000 people by the end of January.
WIKIMEDIA, PLOS BIOLOGYMore than 20,000 people are likely to have been infected with Ebola by November 2, the World Health Organization (WHO) Ebola Response Team predicted in the New England Journal of Medicine today (September 23). Extrapolating data from the beginning of the outbreak and accounting for theincreased pace of infections, the team noted that “transmission has to be a little more than halved to achieve control of the epidemic and eventually to eliminate the virus from the human population.”
Meanwhile, at the current rate of transmission and without any further aid, scientists from the US Centers for Disease Control and Prevention (CDC) estimate that “the Ebola epidemic sweeping West Africa could infect up to 500,000 people by the end of January,” The Washington Post reported (via Bloomberg News). The Post also noted that the CDC prediction, which is still under development and set to be released next week, is subject to change. “One of the scary things about this outbreak is that all the general models of the past have been broken,” microbiologist John Connor of Boston University School of Medicine told the newspaper.
Update (September 23): In a Morbidity and Mortality Weekly Report article issued after this post was published, the CDC presented a worst-case scenario prediction that—assuming transmission “trends continue without additional interventions,”and correcting for under-reporting—as many as 1.4 million people could be infected with Ebola by January 20, 2015. “It is still possible to reverse the epidemic,” CDC Director Thomas Frieden said in a statment. “Once a sufficient number of Ebola patients are isolated, cases will decline very rapidly—almost as rapidly as they rose.”
The United Nations Security Council declares the situation in West Africa a “threat to international peace and security” and calls for even more resources to fight the spread of the Ebola virus.
WIKIMEDIA, PLOS PATHOGENS, THOMAS W. GEISBERTWith more than 2,600 lives now lost to the ongoing Ebola outbreak in West Africa, according to the World Health Organization (WHO), “the gravity and scale of the situation now require a level of international action unprecedented for a health emergency,” United Nations (UN) Secretary General Ban Ki-moon said at an emergency meeting of the UN Security Council last week (September 18).
To curb the spread of the deadly virus, which is now infecting twice as many people every three weeks, the council proposed a resolution that calls for countries to provide even more aid—as much as 20 times the response that has already been put in action, BBC News reported. Specifically, the resolution, which was cosponsored by a record-setting 130 nations, asks countries to send supplies and medical staff to Liberia, Guinea, and Sierra Leone, and to lift travel restrictions in the affected countries to allow aid workers easier access.
“The UN Security Council is charged with the essential duty to maintain international peace and security,” according to a statement from the O’Neill Institute for National & Global Health Law on the resolution. “[A] UNSC resolution could establish a well-coordinated and orderly international response to this unprecedented health crisis.”
In total, the UN estimates that it will cost some $1 billion to contain the virus, Nature news blog reported. “This is likely the greatest peace-time challenge that the United Nations and its agencies have ever faced,” WHO director-general Margaret Chan told the council.
Scientists are using pupil measurements to study a wide range of psychological processes and to get a glimpse into the mind.
What do an orgasm, a multiplication problem and a photo of a dead body have in common? Each induces a slight, irrepressible expansion of the pupils in our eyes, giving careful observers a subtle but meaningful signal that thoughts and feelings are afoot.
|Wikimedia, Steve Jurvetson|
For more than a century, scientists have known that our pupils respond to more than changes in light. They also betray mental and emotional commotion within. In fact, pupil dilation correlates with arousal so consistently that researchers use pupil size, or pupillometry, to investigate a wide range of psychological phenomena. And they do this without knowing exactly why our eyes behave this way. “Nobody really knows for sure what these changes do,” said Stuart Steinhauer, who directs the Biometrics Research Lab at the University of Pittsburgh School of Medicine.
While the visual cortex in the back of the brain assembles the images we see, a different, older part of our nervous system manages the continuous tuning of our pupil size, alongside other functions—like heart rate and perspiration—that operate mostly outside our conscious control. This autonomic nervous system dictates the movement of the iris, like the lens of a camera, to regulate the amount of light that enters the pupil.
The iris is made of two types of muscle: in a brightly lit environment, a ring of sphincter muscles that encircle and constrict the pupil down to as little as a couple of millimeters across; in the dark, a set of dilator muscles laid out like bicycle spokes, which can expand the pupil up to 8 millimeters—approximately the diameter of a chickpea.
Cognitive and emotional events can also dictate pupil constriction and expansion, though such events occur on a smaller scale than the light reflex, causing changes generally less than half a millimeter. But that’s enough. By recording subjects’ eyes with infrared cameras and controlling for other factors that might affect pupil size, like brightness, color, and distance, scientists can use pupil movements as a proxy for other processes, like mental strain.
Princeton psychologist Daniel Kahneman showed several decades ago that pupil size increases in proportion to the difficulty of the task at hand. Calculate 9 times 13, and you pupils will dilate slightly. Try 29 times 13, and they will widen further and remain dilated until you reach the answer or stop trying. As Kahneman says in his recent book, Thinking Fast and Slow, he could divine when someone gave up on a multiplication problem simply by watching for pupil contraction during the experiment.
“The pupils reflect the extent of mental effort in an incredibly precise way,” Kahneman told the German news magazine Der Spiegel, adding, “I have never done any work in which the measurement is so precise.” When he instructed subjects to remember and recite a series of seven digits, their pupils grew steadily as the numbers were presented one-by-one and shrunk steadily as they unloaded the digits from memory.
Subsequent research found that the pupils of intelligent people (as defined by their SAT scores) dilated less in response to cognitive tasks compared to those of less intelligent participants, possibly indicating a more efficient use of brainpower.
Scientists have since used pupillometry to assess everything from sleepiness to introversion, race bias,schizophrenia, sexual interest, moral judgment, autism, and depression. And while they haven’t been reading people’s thoughts per se, they’ve come pretty close.
“Pupil dilation can betray an individual’s decision before it is openly revealed,” concluded a 2010 study led by Wolfgang Einhäuser-Treyer, a neurophysicist at The Philipp University of Marburg in Germany. In the study, participants were told to press a button at any point during a 10 second interval, and their pupil size correlated with the timing of their decision. The dilation began about 1 second before they pressed the button and peaked 1 to 2 seconds after.
But are pupils informative outside the lab? Men’s Health Magazine says you can tell when it’s “time to make your move” by watching your date’s pupils, but some skepticism is warranted. “It is unclear to me to what extent this can be exploited in completely unrestrained settings,” Einhäuser-Treyer wrote in an email, pointing out that light conditions could easily interfere with attempts at interpersonal pupillometry.
Other efforts to exploit pupil dilations for purposes beyond scientific research have failed. During the Cold War, Canadian officials tried to develop a device they called the “fruit machine” to detect homosexuality among government employees by measuring how their pupils responded to racy images of women and men. The machine, which never worked, was to aid the government’s purge of gay men and lesbians from the civil service and thereby purportedly reduce their vulnerability to Soviet blackmail.
A pupil test for sexual orientation remains as unlikely as it was in the 1960s. Researchers at Cornell University recently showed that sexual orientation correlated with pupil dilation to erotic videos of their preferred gender, but the trend was only apparent when averaged across subjects, and only for male subjects. While pupillometry shows promise as a noninvasive measure of sexual response, they concluded, “not every participant’s sexual orientation was correctly classified” and “an observable amount of variability in pupil dilation was unrelated to the participant’s sexual orientation.”
Pupillometry also became popular in the advertising industry during the 1970s as a way to test consumers’ responses to television commercials, said Jagdish Sheth, a marketing professor at Emory University. But the practice was eventually abandoned. “There was no scientific way to establish whether it measured interest or anxiety,” Sheth said.
Indeed, pupillometry is limited in its ability to distinguish between the many types of cognitive and emotional processes that can affect pupil dilation. “All we can do is watch the change at the end,” Steinhauer said. “We can't monitor everything going into it.”
Still, he added, our eyes are easy to observe and provide a sensitive indicator of cognitive, emotional, and sensory response, making pupillometry a valuable tool for psychological research. “It's like having an electrode permanently implanted in the brain.”
This article is provided by Scienceline, a project of New York University's Science, Health and Environmental Reporting Program.
Scientists devise an antibody-based test that can generate a person’s complete “viral history” with just one drop of blood.
|FLICKR, ALDEN CHADWICK|
Last summer, infectious disease specialist Gregory Poland saw a patient at the Mayo Clinic in Rochester, Minnesota, who had a fever, a rash, kidney failure, and—despite seeing several doctors—no diagnosis. Only after talking with the patient for hours and digging into her medical and travel history could Poland generate a potential diagnosis. To test his theory, he had to send a serum sample to researchers at the US Centers for Disease Control and Prevention in Atlanta, who confirmed that his patient had chikungunya.
Situations like this, explained Poland, are not uncommon. “I can’t tell you how many times we don’t know what’s going on,” he said. When tests for all of the usual suspects come back negative, it’s difficult to know what to try next. On top of that, he added, some disease-causing agents are rare. “There are viruses that I know the name of, but I’ve never seen the disease.”
Thanks to a method described today (June 4) in Science, it may be soon be possible to test patients for previous exposures to all human-tropic viruses at once. Virologist Stephen Elledge of Harvard Medical School and the Brigham and Women’s Hospital in Boston and his colleagues have built such a test, called “VirScan,” from a bacteriophage-based display system they developed in 2011. The scientists programmed each phage to expresses a unique viral peptide, collectively producing about 100 peptides from each of the 206 known human-tropic viral species.
The team combined the phage with serum collected from 569 donors in the U.S., Thailand, Peru, and South Africa, allowing antibodies in each sample to bind their target peptides. The researchers then isolated the antibody-peptide-phage complexes, and harvested and sequenced the DNA inside each. The sequences, which can be read millions at a time, represent peptides recognized by the antibodies, revealing which viruses a given donor’s immune system had previously seen.
“This is far beyond anything we’ve had before regarding the human antibody response to viruses,” said Kristine Wylie, a microbiologist at Washington University in St. Louis who was not involved in the work.
Scientists like Wylie have been cataloging viruses living in and on humans for years, typically by searching for viral DNA and RNA sequences in blood and tissues. “Healthy people carry a lot of viruses, asymptomatically,” she said. Knowledge of prior viral exposures can improve health care. For example, it’s good to know whether a patient about to start chemotherapy carries a latent virus that could resurge during treatment.
Detecting a virus by the presence of its genes, however, depends on the virus being present at high enough levels and in easily accessed fluids or tissues. Measuring antibodies produced in response to viruses makes it possible to detect an infection weeks or decades later using only blood serum. But this approach is typically limited to testing for antibodies against one virus at a time. According to Poland, testing for many viruses at once is currently too expensive and requires too much blood to be routinely feasible.
VirScan requires just one drop of blood and, for about $25, screens for antibodies against 206 viruses, covering 1,000 strains. Using the technique, Elledge’s team identified high rates of exposure to common viruses like Epstein–Barr virus (found in 87 percent of adult donors screened) and rhinovirus (found in around 70 percent), many of which Wylie said are consistent with the rates she and others have seen in asymptomatic adults.
Some viruses showed up at lower frequencies than expected. Influenza, for example, appeared to affect only 53 percent of the donors, and chickenpox, just 24 percent. Elledge noted that these apparently low rates may be the result of a potential limitation of the test: the 56 amino acid peptides used for VirScan may have been too short to attract antibodies that only bind longer spans of folded-up peptides called conformational epitopes. Despite this, the team detected antibody responses against 4,406 unique epitopes, most of which had not been recorded in the Immune Epitope Database.
Unexpectedly, each person sampled showed a strong response to just three or fewer peptides per virus, making those peptides immunodominant. Although immunodominant peptides don’t always make the best vaccines, Elledge noted they might still be useful for vaccine design. “You might be able to piggyback on pre-existing immune responses and use that to your advantage,” he said.
Improvements to VirScan—such as the inclusion of conformational epitopes and a reduction in cross-reactivity between viruses with similar proteins—are in the works, said Elledge. Going forward, the team would like to extend its approach to screen for other pathogens, like bacteria, and to use VirScan to look for correlations between viral infections and chronic conditions, such as autoimmune diseases.
Down the line, Poland sees a place for VirScan in the clinic. “They’ve made real progress in what could have been seen as a pipe dream,” he said. “If they can perfect this and move this forward, this changes everything.”
G.J. Xu, et al. “Comprehensive serological profiling of human populations using a synthetic human virome,” Science, 348:1106-1114, 2015.
How motion illusions trick the visual system, and what they can teach us about how our eyes and brains evolved.
Animal vision has not evolved as one might think. In contrast to the invention of photography and film—which began with the first black-and-white daguerreotypes in 1839, then added color in 1861, and finally motion in 1891—motion perception in animals appears to have evolved long before color vision. Indeed, as vision researcher Gordon Walls declared in 1942, perceiving motion is one of the most ancient and primitive forms of vision.
Even the humble housefly, which can only distinguish four to six different colors, is remarkably good at seeing motion. Try to swat a fly with your hand, and it will be gone long before you even get close. (The best way is to clap your hands above it so that it flies up between your hands. Wear gloves.) Oddly, however, while a fly is quick to register these fast movements, it cannot recognize slow movement at all. Move your hand very, very slowly toward a fly, and you can tap its back before it knows that you are there.
As good as animals are at detecting motion, they can also be fooled. Seeing the errors that a system makes can help us to understand how that system works normally.
Much of the early research on motion perception was performed on insects,1 but similar results have been found for a huge range of species, from fishes to birds to mammals. Frogs, which eat insects, respond to small, rapidly moving prey, as well as to overall dimming or darkening that likely signals an approaching predator, but they often ignore stationary objects, perhaps because they cannot see them.2
Mammals are likewise tuned in to motion. Although many people believe that it is the bright red color of the matador’s cape that enrages the bull, the popular TV program Mythbusters found that the color made no difference; it was the motion of the cape’s fabric that mattered. Red, blue, and white capes got equal, half-hearted attacks when they were motionless, but waving the capes elicited an aggressive charge. In fact, most mammals, including domestic and big cats, deer, cattle, and dogs, appear to be color-blind. Apes may have evolved color vision in order to find the ripe fruit among green leaves (see “The Rainbow Connection,” The Scientist, October 2014), but lions eat other mammals, most of which have evolved to match their surroundings, rendering color vision useless in finding prey. When a gazelle runs away, however, it becomes a strong stimulus for the lion’s keen motion vision. It’s no wonder that young deer will often freeze when they sense danger. Correspondingly, prey animals would find color vision of little use, but they are extremely good at seeing the motion of an approaching predator.
But as good as animals are at detecting motion, they can also be fooled. I study visual illusions of motion because seeing the errors that a system makes can help us to understand how that system works normally. Visual perception goes far beyond our retinal images, which provide only partial sensory information. We use our knowledge and expectations of the world to fill in the gaps, for instance, when an object is partly hidden. Ambiguous illusions that can be interpreted in two different ways, but not both ways at the same time, can also shed light on how we perceive the world around us.
Illusions of movement
Visual movement can be thought of as a change in brightness, or luminance, over space and time. A white spot that glides across a black screen shows real movement. If the same spot jumps back and forth between two positions, or makes a series of intermittent forward jumps, the brain can still perceive movement. Small, fast jumps give the smoothest impression of movement, but even large, slow jumps give a strong impression that the spot is, in fact, moving across the screen.
Why does the visual system treat this jumping dot as a single object in motion, instead of seeing one spot disappear while an unrelated spot appears nearby at the same instant? First, the brain usually treats “suspicious coincidences” as being more than coincidences: it is more likely that this is a single spot in motion rather than two separate events. Second, the visual system is tolerant of brief gaps in stimuli, filling in those gaps when necessary. This perception of apparent motion is, of course, the basis of the entire movie and TV industries, as viewers see a smooth motion picture when in reality they are simply watching a series of stationary stills.
We can pose a riddle to the visual system by presenting two apparent motions in opposite directions simultaneously. For example, an image of a white horse and an image of a black horse suddenly exchange positions. But you do not see each horse independently changing in color. Rather, you see the horses jumping from one location to the other. The coincidence is too great, and, instead of two independent events, the visual system economically infers a single event: the jumping horse.
But which horse jumps? The answer depends on the context. On a dark background, the white horse appears to jump back and forth; on a light background, the black horse appears to move. In other words, the horse with the higher contrast wins. This is because the strength of a motion signal in the brain of the observer is equal to the product of the contrast of each horse against the background color, a measure called motion energy.3 Interestingly, if contrast is held constant, the color of the horses makes no difference because color has little or no input into the motion pathways of the brain.4
Contrast can also explain why a black or white object on a background of the opposite color seems to move faster than a gray object on a gray background, and why cars appear to move more slowly in the fog. Indeed, we tend to judge motion not in absolute terms, but relative to the background: the perceived strength and speed of motion depend on the contrast of the moving object against its surroundings.5 In fact, a driver partly judges his own speed by the rate at which landmarks such as trees flash past him. In the fog, the trees appear slowed down, so he underestimates the speed of all cars, including his own, with potentially disastrous consequences.6
Combining movement and changes in contrast results in an even more complex outcome. Suppose that a black spot on a medium-gray background makes a small jump to the right—a total distance much smaller than the diameter of the spot itself—and, at the same time, instantaneously changes to white. Instead of seeing a slight motion to the right, one sees something quite unexpected: the spot appears to move to theleft, toward the starting position and opposite to the physical displacement.
MOTION IN CONTEXT: A yellow bug and a red bug both fly around in perfect clockwise circles of the same size, though the red bug moves much more rapidly. When a background is added that also circles clockwise, the yellow bug’s orbit, which syncs up with the motion of the background, seems to shrink to about half the size of the red bug's orbit.
This effect, known as reverse phi, is particularly strong in peripheral vision: if someone fixes his gaze on a small stationary cross and observes the moving spot out of the corner of his eye, the backwards leap will be even more pronounced.7,8 Once again, this phenomenon is consistent with the idea that perceived motion depends on motion energy, or the product of the contrasts of moving objects.3 If the spot makes a long series of jumps to the right, changing between black and white on each jump, one still sees steady motion to the left, but after a while the observer will recognize that, paradoxically, the spot is now farther to the right, demonstrating that position and motion are signaled independently.
Why we are fooled
The phenomena described above are “low-level” illusions that are probably based on “bottom-up” sensory signals from brain cells in the visual system that are specialized to detect motion. Normally, sensory information agrees. If a cat is partly hidden behind a tree, for example, all the cues of color, shadows, and texture tell the same story—that the hidden part of the cat exists out of view behind the tree. The brain acts like a judge, confirming the same story as told by independent witnesses. The brain also strengthens this verdict with “top-down” information based upon prior learning: if the cat’s whiskers stick out on one side of the tree, and its tail on the other, the brain automatically “fills in” that there is a continuous cat partly hidden by the tree, not two unrelated cat bits. This interpolation process, called visual amodal completion, starts from a representation of the visible features of the stimulus in early visual cortex, probably an area called V1, and ends with a completed representation of the stimulus in the inferior temporal cortex.9 Jay Hegdé of the University of Minnesota and colleagues even found two regions in the object-processing pathways of the brain that actually responded more strongly to partly hidden objects than to complete ones.10
Visual object recognition thus involves two stages: a bottom-up inputting of perceptual information, and a top-down memory stage in which perceptual information is matched with an object’s stored representation. Tomoya Taminato of Tohoku University School of Medicine in Japan and colleagues last year presented volunteers with blurry pictures that gradually became sharper. Observers responded once when they could guess the identity of the object in the image, representing the perception stage, and a second time when they were certain of the identity, the memory stage. Their results attributed the perception stage to the right medial occipitotemporal region of the brain, and the memory stage to the posterior part of the rostral medial frontal cortex.11
If a cat’s whiskers stick out on one side of the tree, and its tail on the other, the brain automatically “fills in” that there is a continuous cat partly hidden by the tree, not two unrelated cat bits.
Visualizing motion is similarly subject to both bottom-up and top-down processes. Reverse phi, in which an object that changes contrast as it travels is viewed as moving in the reverse direction, is a bottom-up illusion that happens early in the brain’s visual processing pathway. Researchers have tracked the origin of this illusion to V1 cells, which in awake monkeys respond to the reverse phi illusion in the same way they respond to backwards-moving objects.12 Meanwhile, top-down processes predict what objects these signals probably represent, based upon memory and previous learning. Object parsing, for example, is a process that guides perception by deciding what objects are likely to be present based upon prior knowledge of the world.13
Consider the closing blades of a pair of scissors. The intersection itself is not an object; only the blades are. This distinction is not lost on the visual system. Observers make 10 times the tracking errors—their eyes deviating from the target—when they attempt to follow a sliding rather than a rigid intersection.14 Although you can sense the movement of a sliding intersection, you do not interpret it as an object.
This phenomenon stems from the fact that smooth eye movements require a smoothly moving target. Move your thumb from side to side in front of you and ask a friend to follow your thumb with his eyes. Watch his eyes and you will see them move smoothly from side to side. Now hold up both your thumbs a yard apart and ask him to move his eyes smoothly from one stationary thumb to the other. He cannot do it! You will see his eyes moving in a series of jerky eye movements called saccades. This shows that a moving object is necessary to drive smooth-pursuit eye movements.
Visual signals flow forward from the visual cortex at the back of the brain, then travel along the ventral stream for the decision about what objects are present, and also up along the dorsal stream to the medial temporal area, which analyzes motion. Finally, the nerve signals travel forward to the frontal eye fields that control eye movements. A sliding intersection is not parsed as a real object, and it cannot support smooth eye movements.
The visual system can also flip between local and global motions, but it cannot see both at once. The brain considers incompatible interpretations—Are there many small groups, or a few large groups?—and adopts them in alternation, but never both at the same time. The shape and spacing of spots on a screen, the duration and position of your fixations, and other factors can all influence which percept you see.
LOCAL OR GLOBAL: At first, viewers see pairs of spots, each pair rotating about their common center. But if you watch for a while, you will suddenly see it reorganize into two larger squares on top, or eight interdigitating octagons on the bottom. The visual system can alternate between either percept, but it cannot see both at once.
Motion can shift an object’s perceived position. If an image of an upright cross flashes briefly on a textured wheel that is rotating clockwise, the cross itself will appear to be tilted clockwise, and it sometimes even looks distorted. Notably, only the motion of the background that occurs after the flash can drag the cross along: motion beforehand has no effect.15
In sum, illusions teach us that perception goes far beyond the information picked up by our senses. Perception is an indirect, interpretive top-down process that is not driven simply by stimulus patterns, but is instead a dynamic, active search for the best interpretation of the available sensory data.
Stuart Anstis is a professor of psychology at the University of California, San Diego, and a visiting fellow at Pembroke College in Oxford, U.K. Working with international collaborators, he has published some 170 articles on visual perception.
The brain contains lymphatic vessels similar to those found elsewhere in the body, a mouse study shows.
uring an infection. The brain is considered “immune privileged,” such that when exposed to foreign material, it takes longer to mount an immune response than does the rest of the body. Furthermore, to date, traditional lymphatic vessels had not been found there.
Several nontraditional routes of fluid circulation in the brain have been described, however. In recent years, neuropathologists Roxana Carare and Roy Weller of the University of Southampton, U.K., reported a system by which CSF—produced in the ventricles—exits the brain via the mucous membranes of the nose and by which interstitial fluid (ISF)—solute-bearing liquid filtered from the blood—leaves by traveling along the basement membranes of capillaries and cerebral arteries. In 2012, Maiken Nedergaard of the University of Rochester Medical Center in New York and her colleagues reported that the circulation of CSF and ISF in the brain was facilitated by water channels in the glial cells that abut the brain vasculature, and coined the term “glymphatic system.”
The Kipnis team’s latest finding represents an additional lymphatic pathway for the brain. Working in mice, Kipnis and his colleagues found that vessels expressing markers of lymphatic vessels elsewhere in the body ran along the dural sinuses, drainage lines in the brain that collect outgoing blood and CSF, emptying these fluids into the jugular vein. They also found that the vessels contained immune cells.
|WIKIMEDIA, DATABASE CENTER FOR LIFE SCIENCE|
The researchers also probed the circulatory pathways of these vessels by injecting mice with two different tracers—one intravenously, to the circulatory system, and one into the subarachnoid space, a fluid-filled space between the inner two meninges. The tracer injected into the brain stained the newly discovered lymphatic vessels, indicating that CSF passes through them, while the intravenous dye stained separate blood vessels.
Further, the researchers injected Evans blue dye into the subarachnoid space and found that it stained the deep, though not the superficial, cervical lymph nodes. Investigating this pathway from the other direction, they sewed together channels of the cervical lymph nodes and found that fluid backed up in the new lymphatic vessels.
Carare, who was not involved in the study, noted that in a previous study led by Weller, tracer injected into the subarachnoid space traveled to the cervical lymph nodes through the nasal route. “The presence of Evans blue in the present study may be a result of a combination of drainage mechanisms and pathways,” she wrote in an e-mail to The Scientist.
CSF drainage through the nasal pathway “may represent a highly specialized system of the dural lymphatics described in this paper,” Carare added.
While much remains to be worked out, Kipnis noted that, at the very least, these latest results add to mounting evidence of immune activity in the healthy brain. “If you go into the literature, 20 years ago, the idea was that if you see immune cells in the brain, something must be going wrong,” he said. “Now we know that we see immune cells in healthy brains. . . . It’s part of normal physiology; it should be there. Immune activity in the brain is not always pathological.”
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