Posts tagged science
Articles and news from the latest research reports.
Brain’s flexible hub network helps humans adapt
Switching stations route processing of novel cognitive tasks
One thing that sets humans apart from other animals is our ability to intelligently and rapidly adapt to a wide variety of new challenges — using skills learned in much different contexts to inform and guide the handling of any new task at hand.
Now, research from Washington University in St. Louis offers new and compelling evidence that a well-connected core brain network based in the lateral prefrontal cortex and the posterior parietal cortex — parts of the brain most changed evolutionarily since our common ancestor with chimpanzees — contains “flexible hubs” that coordinate the brain’s responses to novel cognitive challenges.
Acting as a central switching station for cognitive processing, this fronto-parietal brain network funnels incoming task instructions to those brain regions most adept at handling the cognitive task at hand, coordinating the transfer of information among processing brain regions to facilitate the rapid learning of new skills, the study finds.
“Flexible hubs are brain regions that coordinate activity throughout the brain to implement tasks — like a large Internet traffic router,” suggests Michael Cole, PhD., a postdoctoral research associate in psychology at Washington University and lead author of the study published July 29 in the journal Nature Neuroscience.
“Like an Internet router, flexible hubs shift which networks they communicate with based on instructions for the task at hand and can do so even for tasks never performed before,” he adds.
Decades of brain research has built a consensus understanding of the brain as an interconnected network of as many as 300 distinct regional brain structures, each with its own specialized cognitive functions.
Binding these processing areas together is a web of about a dozen major networks, each serving as the brain’s means for implementing distinct task functions — i.e. auditory, visual, tactile, memory, attention and motor processes.
It was already known that fronto-parietal brain regions form a network that is most active during novel or non-routine tasks, but it was unknown how this network’s activity might help implement tasks.
This study proposes and provides strong evidence for a “flexible hub” theory of brain function in which the fronto-parietal network is composed of flexible hubs that help to organize and coordinate processing among the other specialized networks.
This study provide strong support for the flexible hub theory in two key areas.
First, the study yielded new evidence that when novel tasks are processed flexible hubs within the fronto-parietal network make multiple, rapidly shifting connections with specialized processing areas scattered throughout the brain.
Second, by closely analyzing activity patterns as the flexible hubs connect with various brain regions during the processing of specific tasks, researchers determined that these connection patterns include telltale characteristics that can be decoded and used to identify which specific task is being implemented by the brain.
These unique patterns of connection — like the distinct strand patterns of a spider web — appear to be the brain’s mechanism for the coding and transfer of specific processing skills, the study suggests.
By tracking where and when these unique connection patterns occur in the brain, researchers were able to document flexible hubs’ role in shifting previously learned and practiced problem-solving skills and protocols to novel task performance. Known as compositional coding, the process allows skills learned in one context to be re-packaged and re-used in other applications, thus shortening the learning curve for novel tasks.
What’s more, by tracking the testing performance of individual study participants, the team demonstrated that the transfer of these processing skills helped participants speed their mastery of novel tasks, essentially using previously practiced processing tricks to get up to speed much more quickly for similar challenges in a novel setting.
“The flexible hub theory suggests this is possible because flexible hubs build up a repertoire of task component connectivity patterns that are highly practiced and can be reused in novel combinations in situations requiring high adaptivity,” Cole explains.
“It’s as if a conductor practiced short sound sequences with each section of an orchestra separately, then on the day of the performance began gesturing to some sections to play back what they learned, creating a new song that has never been played or heard before.”
By improving our understanding of cognitive processes behind the brain’s handling of novel situations, the flexible hub theory may one day help us improve the way we respond to the challenges of everyday life, such as when learning to use new technology, Cole suggests.
“Additionally, there is evidence building that flexible hubs in the fronto-parietal network are compromised for individuals suffering from a variety of mental disorders, reducing the ability to effectively self-regulate and therefore exacerbating symptoms,” he says.
Future research may provide the means to enhance flexible hubs in ways that would allow people to increase self-regulation and reduce symptoms in a variety of mental disorders, such as depression, schizophrenia and obsessive-compulsive disorder.
Neuroscientists identify protein linked to Alzheimer’s-like afflictions
A team of neuroscientists has identified a modification to a protein in laboratory mice linked to conditions associated with Alzheimer’s Disease. Their findings, which appear in the journal Nature Neuroscience, also point to a potential therapeutic intervention for alleviating memory-related disorders.
The research centered on eukaryotic initiation factor 2 alpha (eIF2alpha) and two enzymes that modify it with a phosphate group; this type of modification is termed phosphorylation. The phosphorylation of eIF2alpha, which decreases protein synthesis, was previously found at elevated levels in both humans diagnosed with Alzheimer’s and in Alzheimer’s Disease (AD) model mice.
"These results implicate the improper regulation of this protein in Alzheimer’s-like afflictions and offer new guidance in developing remedies to address the disease," said Eric Klann, a professor in New York University’s Center for Neural Science and the study’s senior author.
The study’s co-authors also included: Douglas Cavener, a professor of biology at Pennsylvania State University; Clarisse Bourbon, Evelina Gatti, and Philippe Pierre of Université de la Méditerranée in Marseille, France; and NYU researchers Tao Ma, Mimi A. Trinh, and Alyse J. Wexler.
It has been known for decades that triggering new protein synthesis is vital to the formation of long-term memories as well as for long-lasting synaptic plasticity — the ability of the neurons to change the collective strength of their connections with other neurons. Learning and memory are widely believed to result from changes in synaptic strength.
In recent years, researchers have found that both humans with Alzheimer’s Disease and AD model mice have relatively high levels of eIF2alpha phosphorylation. But the relationship between this characteristic and AD-related afflictions was unknown.
Klann and his colleagues hypothesized that abnormally high levels of eIF2alpha phosphorylation could become detrimental because, ultimately, protein synthesis would diminish, thereby undermining the ability to form long-term memories.
To explore this question, the researchers examined the neurological impact of two enzymes that phosphorylate eIF2alpha, kinases termed PERK and GCN2, in different populations of AD model mice — all of which expressed genetic mutations akin to those carried by humans with AD. These were: AD model mice; AD model mice that lacked PERK; and AD model mice that lacked GCN2.
Specifically, they looked at eIF2alpha phosphorylation and the regulation of protein synthesis in the mice’s hippocampus region — the part of the brain responsible for the retrieval of old memories and the encoding of new ones. They then compared these levels with those of postmortem human AD patients.
Here, they found both increased levels of phosphorylated eIF2alpha in the hippocampus of both AD patients and the AD model mice. Moreover, in conjunction with these results, they found decreased protein synthesis, known to be required for long-term potentiation — a form of long-lasting synaptic plasticity—and for long-term memory.
To test potential remedies, the researchers examined phosphorylation of eIF2alpha in mice lacking PERK, hypothesizing that removal of this kinase would return protein synthesis to normal levels. As predicted, mice lacking PERK had levels of phosphorylated eIF2alpha and protein synthesis similar to those of normal mice.
They then conducted spatial memory tests in which the mice needed to navigate a series of mazes. Here, the AD model mice lacking PERK were able to successfully maneuver through the mazes at rates achieved by normal mice. By contrast, the other AD model mice lagged significantly in performing these tasks.
The researchers replicated these procedures on AD model mice lacking GCN2. The results here were consistent with those of the AD model mice lacking PERK, demonstrating that removal of both kinases diminished memory deficits associated with Alzheimer’s Disease.
(Source: eurekalert.org)
5 Disorders Share Genetic Risk Factors, Study Finds
The psychiatric illnesses seem very different — schizophrenia, bipolar disorder, autism, major depression and attention deficit hyperactivity disorder. Yet they share several genetic glitches that can nudge the brain along a path to mental illness, researchers report. Which disease, if any, develops is thought to depend on other genetic or environmental factors.
Their study, published online Wednesday in the Lancet, was based on an examination of genetic data from more than 60,000 people worldwide. Its authors say it is the largest genetic study yet of psychiatric disorders. The findings strengthen an emerging view of mental illness that aims to make diagnoses based on the genetic aberrations underlying diseases instead of on the disease symptoms.
Two of the aberrations discovered in the new study were in genes used in a major signaling system in the brain, giving clues to processes that might go awry and suggestions of how to treat the diseases.
“What we identified here is probably just the tip of an iceberg,” said Dr. Jordan Smoller, lead author of the paper and a professor of psychiatry at Harvard Medical School and Massachusetts General Hospital. “As these studies grow we expect to find additional genes that might overlap.”
The new study does not mean that the of psychiatric disorders are simple. Researchers say there seem to be hundreds of genes involved and the gene variations discovered in the new study confer only a small risk of psychiatric disease.
Steven McCarroll, director of genetics for the Stanley Center for Psychiatric Research at the Broad Institute of Harvard and M.I.T., said it was significant that the researchers had found common genetic factors that pointed to a specific signaling system.
“It is very important that these were not just random hits on the dartboard of the genome,” said Dr. McCarroll, who was not involved in the new study.
The work began in 2007 when a large group of researchers began investigating genetic data generated by studies in 19 countries and including 33,332 people with psychiatric illnesses and 27,888 people free of the illnesses for comparison. The researchers studied scans of people’s DNA, looking for variations in any of several million places along the long stretch of genetic material containing three billion DNA letters. The question: Did people with psychiatric illnesses tend to have a distinctive DNA pattern in any of those locations?
Researchers had already seen some clues of overlapping genetic effects in identical . One twin might have schizophrenia while the other had bipolar disorder. About six years ago, around the time the new study began, researchers had examined the genes of a few rare families in which psychiatric disorders seemed especially prevalent. They found a few unusual disruptions of chromosomes that were linked to psychiatric illnesses. But what surprised them was that while one person with the aberration might get one disorder, a relative with the same mutation got a different one.
Jonathan Sebat, chief of the Beyster Center for Molecular Genomics of Neuropsychiatric Diseases at the University of California, San Diego, and one of the discoverers of this effect, said that work on these rare genetic aberrations had opened his eyes. “Two different diagnoses can have the same genetic risk factor,” he said.
In fact, the new paper reports, distinguishing psychiatric diseases by their symptoms has long been difficult. Autism, for example, was once called childhood schizophrenia. It was not until the 1970s that autism was distinguished as a separate disorder.
But Dr. Sebat, who did not work on the new study, said that until now it was not clear whether the rare families he and others had studied were an exception or whether they were pointing to a rule about multiple disorders arising from a single genetic glitch.
“No one had systematically looked at the common variations,” in DNA, he said. “We didn’t know if this was particularly true for rare mutations or if it would be true for all genetic risk.” The new study, he said, “shows all genetic risk is of this nature.”
The new study found four DNA regions that conferred a small risk of psychiatric disorders. For two of them, it is not clear what genes are involved or what they do, Dr. Smoller said. The other two, though, involve genes that are part of channels, which are used when neurons send signals in the brain.
“The calcium channel findings suggest that perhaps — and this is a big if — treatments to affect calcium channel functioning might have effects across a range of disorders,” Dr. Smoller said.
There are drugs on the market that block calcium channels — they are used to treat — and researchers had already postulated that they might be useful for bipolar disorder even before the current findings.
One investigator, Dr. Roy Perlis of Massachusetts General Hospital, just completed a small study of a calcium channel blocker in 10 people with bipolar disorder and is about to expand it to a large randomized clinical trial. He also wants to study the drug in people with schizophrenia, in light of the new findings. He cautions, though, that people should not rush out to take a calcium channel blocker on their own.
“We need to be sure it is safe and we need to be sure it works,” Dr. Perlis said.
Why the #$%! Do We Swear? For Pain Relief
Bad language could be good for you, a new study shows. For the first time, psychologists have found that swearing may serve an important function in relieving pain.
The study, published in the journal NeuroReport, measured how long college students could keep their hands immersed in cold water. During the chilly exercise, they could repeat an expletive of their choice or chant a neutral word. When swearing, the 67 student volunteers reported less pain and on average endured about 40 seconds longer.
Although cursing is notoriously decried in the public debate, researchers are now beginning to question the idea that the phenomenon is all bad. “Swearing is such a common response to pain that there has to be an underlying reason why we do it,” says psychologist Richard Stephens of Keele University in England, who led the study. And indeed, the findings point to one possible benefit: “I would advise people, if they hurt themselves, to swear,” he adds.
How swearing achieves its physical effects is unclear, but the researchers speculate that brain circuitry linked to emotion is involved. Earlier studies have shown that unlike normal language, which relies on the outer few millimeters in the left hemisphere of the brain, expletives hinge on evolutionarily ancient structures buried deep inside the right half.
One such structure is the amygdala, an almond-shaped group of neurons that can trigger a fight-or-flight response in which our heart rate climbs and we become less sensitive to pain. Indeed, the students’ heart rates rose when they swore, a fact the researchers say suggests that the amygdala was activated.
That explanation is backed by other experts in the field. Psychologist Steven Pinker of Harvard University, whose book The Stuff of Thought (Viking Adult, 2007) includes a detailed analysis of swearing, compared the situation with what happens in the brain of a cat that somebody accidentally sits on. “I suspect that swearing taps into a defensive reflex in which an animal that is suddenly injured or confined erupts in a furious struggle, accompanied by an angry vocalization, to startle and intimidate an attacker,” he says.
But cursing is more than just aggression, explains Timothy Jay, a psychologist at the Massachusetts College of Liberal Arts who has studied our use of profanities for the past 35 years. “It allows us to vent or express anger, joy, surprise, happiness,” he remarks. “It’s like the horn on your car, you can do a lot of things with that, it’s built into you.”
In extreme cases, the hotline to the brain’s emotional system can make swearing harmful, as when road rage escalates into physical violence. But when the hammer slips, some well-chosen swearwords might help dull the pain.
There is a catch, though: The more we swear, the less emotionally potent the words become, Stephens cautions. And without emotion, all that is left of a swearword is the word itself, unlikely to soothe anyone’s pain.
(Source: scientificamerican.com)
Researchers Develop Traffic Light-Inspired Caffeine Detector
While caffeine has become essential for a large portion of the workforce, researchers have developed a new instrument that will be of interest to anyone concerned they might be consuming too much of the popular stimulant on a daily basis.
The instrument in question is known as Caffeine Orange, and according to its creators, it is a fluorescent caffeine sensor that is used in combination with a detection kit. When the stimulant is present in various drinks and/or solutions, the detection kit lights up in much the same way that a traffic light does, they added.
Caffeine Orange was developed by a team of researchers led by Professor Young-Tae Chang from the National University of Singapore and Professor Yoon-Kyoung Cho from Ulsan National Institute of Science and Technology (UNIST) in Korea. A paper detailing their research appears in the July 23 edition of the journal Scientific Reports.
“Caffeine has attracted abundant attention due to its extensive existence in beverages and medicines. However, to detect it sensitively and conveniently remains a challenge, especially in resource-limited regions,” the authors wrote in their study. They explain that their device is a “novel aqueous phase fluorescent caffeine sensor” which exhibits 250-fold fluorescence enhancement upon caffeine activation and high selectivity.”
The caffeine sensor and its companion detection kit are non-toxic and can be used with just the naked eye, the researchers said. It can sense various caffeine concentrations, reporting its findings based on color changes upon irradiation with the detection kit, then emitting a light to the beverage with a green-colored laser pointer.
If a drink or solution has a high concentration of caffeine, it turns red. Beverages with moderate caffeine concentrations turn yellow, and those with low amounts of the stimulant turn green, they said.
While there are health benefits linked to caffeine, overdosing on the substance could lead to caffeine intoxication, the authors said. Symptoms of caffeine intoxication include anxiety, irregular heartbeat, insomnia, and in severe cases, hallucinations, depression, or even death could result.
“Prior to this caffeine ‘traffic-light’ designator, no practically applicable and customer-friendly caffeine detection methods have been reported,” the research team wrote. They added their detection kit had several advantages over other such devices in that it is easy to construct, easy to use, safe, fast and consumer friendly.
“The whole kit requires just one syringe equipped with reverse-phase materials and several washing solutions. Its incorporation into automated system has enhanced the handling even greater,” the authors said. No organic solvent is used in the extraction process, the procedure takes less than one minute, and it can be used to extract caffeine from different beverages that are both chemically and physically complicated, they added.
This Is How Your Brain Becomes Addicted to Caffeine
Within 24 hours of quitting the drug, your withdrawal symptoms begin. Initially, they’re subtle: The first thing you notice is that you feel mentally foggy, and lack alertness. Your muscles are fatigued, even when you haven’t done anything strenuous, and you suspect that you’re more irritable than usual.
Over time, an unmistakable throbbing headache sets in, making it difficult to concentrate on anything. Eventually, as your body protests having the drug taken away, you might even feel dull muscle pains, nausea and other flu-like symptoms.
This isn’t heroin, tobacco or even alcohol withdrawl. We’re talking about quitting caffeine, a substance consumed so widely (the FDA reports thatmore than 80 percent of American adults drink it daily) and in such mundane settings (say, at an office meeting or in your car) that we often forget it’s a drug—and by far the world’s most popular psychoactive one.
Like many drugs, caffeine is chemically addictive, a fact that scientists established back in 1994. This past May, with the publication of the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), caffeine withdrawal was finally included as a mental disorder for the first time—even though its merits for inclusion are symptoms that regular coffee-drinkers have long known well from the times they’ve gone off it for a day or more.
Why, exactly, is caffeine addictive? The reason stems from the way the drug affects the human brain, producing the alert feeling that caffeine drinkers crave.
Soon after you drink (or eat) something containing caffeine, it’s absorbed through the small intestine and dissolved into the bloodstream. Because the chemical is both water- and fat-soluble (meaning that it can dissolve in water-based solutions—think blood—as well as fat-based substances, such as our cell membranes), it’s able to penetrate the blood-brain barrier and enter the brain.
Structurally, caffeine closely resembles a molecule that’s naturally present in our brain, called adenosine (which is a byproduct of many cellular processes, including cellular respiration)—so much so, in fact, that caffeine can fit neatly into our brain cells’ receptors for adenosine, effectively blocking them off. Normally, the adenosine produced over time locks into these receptors and produces a feeling of tiredness.
When caffeine molecules are blocking those receptors, they prevent this from occurring, thereby generating a sense of alertness and energy for a few hours. Additionally, some of the brain’s own natural stimulants (such as dopamine) work more effectively when the adenosine receptors are blocked, and all the surplus adenosine floating around in the brain cues the adrenal glands to secrete adrenaline, another stimulant.
For this reason, caffeine isn’t technically a stimulant on its own, says Stephen R. Braun, the author or Buzzed: the Science and Lore of Caffeine and Alcohol, but a stimulant enabler: a substance that lets our natural stimulants run wild. Ingesting caffeine, he writes, is akin to “putting a block of wood under one of the brain’s primary brake pedals.” This block stays in place for anywhere from four to six hours, depending on the person’s age, size and other factors, until the caffeine is eventually metabolized by the body.
In people who take advantage of this process on a daily basis (i.e. coffee/tea, soda or energy drink addicts), the brain’s chemistry and physical characteristics actually change over time as a result. The most notable change is that brain cells grow more adenosine receptors, which is the brain’s attempt to maintain equilibrium in the face of a constant onslaught of caffeine, with its adenosine receptors so regularly plugged (studies indicate that the brain also responds by decreasing the number of receptors for norepinephrine, a stimulant). This explains why regular coffee drinkers build up a tolerance over time—because you have more adenosine receptors, it takes more caffeine to block a significant proportion of them and achieve the desired effect.
This also explains why suddenly giving up caffeine entirely can trigger a range of withdrawal effects. The underlying chemistry is complex and not fully understood, but the principle is that your brain is used to operating in one set of conditions (with an artificially-inflated number of adenosine receptors, and a decreased number of norepinephrine receptors) that depend upon regular ingestion of caffeine. Suddenly, without the drug, the altered brain chemistry causes all sorts of problems, including the dreaded caffeine withdrawal headache.
The good news is that, compared to many drug addictions, the effects are relatively short-term. To kick the thing, you only need to get through about 7-12 days of symptoms without drinking any caffeine. During that period, your brain will naturally decrease the number of adenosine receptors on each cell, responding to the sudden lack of caffeine ingestion. If you can make it that long without a cup of joe or a spot of tea, the levels of adenosine receptors in your brain reset to their baseline levels, and your addiction will be broken.
Medtronic, Inc. (NYSE: MDT) announced the first implant of a novel deep brain stimulation (DBS) system that, for the first time, enables the sensing and recording of select brain activity while simultaneously providing targeted DBS therapy. This initiates research on how the brain responds to the therapy and could yield insights that one day significantly change the way people with devastating neurological and psychological disorders, such as Parkinson’s disease, essential tremor, dystonia, and treatment-resistant obsessive-compulsive disorder, are treated.
The Activa® PC+S DBS system delivers proven Medtronic DBS Therapy while at the same time sensing and recording electrical activity in key areas of the brain using sensing technology and an adjustable algorithm, which enable the system to gather brain signals at various moments as selected by a physician. Initially, this new technology will be made available to a select group of physicians worldwide for use in clinical studies. These physicians will use the system to map the brain’s responses to Medtronic DBS Therapy and explore applications for the therapy across a range of neurological and psychological conditions.
The Activa PC+S system, which delivers stimulation to targeted areas of the brain like existing Medtronic DBS systems, was implanted for the first time at Ludwig Maximilians University in Munich, Germany in a person with Parkinson’s disease. This patient will be treated by a team that includes neurologist Kai Bötzel, department of neurology, Ludwig Maximilian University and neurosurgeon Jan Mehrkens, M.D., head of functional neurosurgery, Ludwig Maximilian University, who implanted the system.
Dr. Bötzel will be the first to use data gathered by the Activa PC+S system to gain unprecedented insight into how the brain responds to DBS therapy.
“DBS therapy works for people with Parkinson’s disease and other movement disorders, but there is much to learn about how the brain responds to the therapy,” said Dr. Bötzel. “This new system will allow us to treat patients with conventional DBS therapy, while at the same time opening the door for research that was not possible until now. We hope these insights will lead to the development of effective new treatments tailored to the needs of individuals. ”
“Devastating conditions like Parkinson’s disease and obsessive-compulsive disorder take a significant toll on countless people, as well as their loved ones,” said Lothar Krinke, Ph.D., vice president and general manager of the Deep Brain Stimulation business in Medtronic’s Neuromodulation division. “Medtronic is excited to provide this new system to researchers worldwide, and we expect that their respective studies will lead to accelerated understanding of how neurological and psychological conditions develop and progress. This represents a significant milestone for DBS therapy and the long-term journey toward a closed-loop DBS system, which could personalize therapy by using device data to automatically adjust to the needs of individual patients.”
Medtronic’s Activa PC+S system received CE (Conformité Européenne) mark in January 2013. It is not approved by the U.S. Food and Drug Administration for commercial use in the United States, and will be made available to select physicians for investigational use only. Additional implants of the Activa PC+S system, including the first implant in the United States, will take place in the coming months.
Accidentally cut your ear off? Just 3D print a new one
It’s way too late for Vincent van Gogh, but cutting off your ear is a much less impressive gesture now you can get a new one printed.
This week, researchers at Hangzhou Dianzi University in China unveiled their Regenovo 3D printer. Unlike more familiar 3D printers, which work with plastic or metal dust, Regenovo prints living tissue – such as these little ears.
The Hangzhou team aren’t the only ones 3D-printing spare parts for people. Earlier this year, a team at Cornell University in Ithaca, New York, also demonstrated an ear printer, and Organovo in San Diego, California, are on the way to building fresh human livers.
Meanwhile a team at Heriot-Watt University in Edinburgh, UK, has turned human embryonic stem cells into 3D-printer ink. Things are more advanced when it comes to making new bones, as a woman with a 3D-printed titanium jawbone could tell you.
High Blood Sugar Linked to Dementia
People with diabetes face an increased risk of Alzheimer’s disease and other forms of dementia, a connection scientists and physicians have worried about for years. They still can’t explain it.
Now comes a novel observational study of patients at a large health care system in Washington State showing that higher blood glucose levels are associated with a greater risk of dementia — even among people who don’t have diabetes. The results, published Thursday in The New England Journal of Medicine, “may have influence on the way we think about blood sugar and the brain,” said Dr. Paul Crane, the lead author and associate professor of medicine at the University of Washington.
The researchers tracked the blood glucose levels of 2,067 members of Group Health, a nonprofit HMO, for nearly seven years on average. Some patients had Type 2 diabetes when the study began, but most didn’t. None had dementia.
Over the years, as they saw doctors at Group Health, the participants received blood glucose tests. “It’s a common test in routine clinical practice,” Dr. Crane said. “We had an amazing opportunity with all this data. All the lab results since 1988 were available to us.”
The participants (average age at the start: 76) also reported to Group Health every other year for cognitive screening and, if their results were below normal, further testing and evaluation. Over the course of the study, about a quarter developed dementia of some kind, primarily Alzheimer’s disease or vascular dementia.
To measure blood sugar levels, the researchers combined glucose measurements, both fasting and nonfasting, with the HbA1c glycated hemoglobin assay, which provides a more accurate long-term picture. They also adjusted the data for other cardiovascular factors already linked to dementia, like high blood pressure and smoking.
“We found a steadily increasing risk associated with ever-higher blood glucose levels, even in people who didn’t have diabetes,” Dr. Crane said. Of particular interest: “There’s no threshold, no place where the risk doesn’t go up any further or down any further.” The association with dementia kept climbing with higher blood sugar levels and, at the other end of the spectrum, continued to decrease with lower levels.
This held true even at glucose levels considered normal. Among those whose blood sugar averaged 115 milligrams per deciliter, the risk of dementia was 18 percent higher than among those at 100 mg/dL, just slightly lower. The effects were also pronounced among those with diabetes: patients with average glucose levels of 190 mg/dL had a 40 percent higher risk of dementia than those whose levels averaged 160 mg/dL.
Though a longitudinal study like this one provides insight into the differences between people, it can’t explain why higher blood glucose might be connected to dementia, or tell individuals whether lower blood glucose is protective.
“People shouldn’t run for the hills or try crazy diets,” Dr. Crane cautioned. While an epidemiological study like this one can guide further exploration, he said, “This doesn’t show that changes in behavior that lower your individual blood sugar would decrease your individual risk of dementia.”
As for the blood glucose levels the study recorded, “clinically, they’re not big differences,” said Dr. Medha Munshi, a geriatrician and endocrinologist who directs the geriatric diabetes program at the Joslin Diabetes Center in Boston, who was not involved in the study. “I wouldn’t change my goals for diabetes management based on this study.” Nor would she warn someone whose blood glucose hits 115 mg/dL that he or she faces a greater risk of dementia.
But because diabetes itself can pose such a threat to health and quality of life, she still urges patients to adopt healthy practices like exercising regularly and maintaining a normal weight to try to avoid the disease. If by doing so they also lower their dementia risk — and knowing that would require a different study, focused on interventions — that would be a bonus.
This research “offers more evidence that the brain is a target organ for damage by high blood sugar,” said Dr. Munshi. “And everyone is still working on the ‘why’.
Dolphins Have Longest Memories in Animal Kingdom
Marine mammals can remember their friends after 20 years apart, study says.
New experiments show that bottlenose dolphins can remember whistles of other dolphins they’d lived with after 20 years of separation. Each dolphin has a unique whistle that functions like a name, allowing the marine mammals to keep close social bonds.
The new research shows that dolphins have the longest memory yet known in any species other than people. Elephants and chimpanzees are thought to have similar abilities, but they haven’t yet been tested, said study author Jason Bruck, an animal behaviorist at the University of Chicago.
Bruck came up with the idea to study animal memory when his brother’s dog, usually wary of male strangers, remembered and greeted him four years after last seeing him. “That got me thinking: How long do other animals remember each other?”
I Remember You!
Bruck studied dolphins because their social bonds are extremely important and because there are good records for captive dolphins (as opposed to wild ones).
So he collected data from 43 bottlenose dolphins at six facilities in the U.S. and Bermuda, members of a breeding consortium that has swapped dolphins for decades and kept careful records of each animal’s social partners.
He first played recordings of lots of unfamiliar whistles to the dolphins in the study until the subjects got bored and stopped inspecting the underwater speaker making the sounds.
At this point, he played the whistles of the listening dolphins’ old friends.
When the dolphins heard these familiar whistles, they would perk up and approach the speakers, often whistling their own name and listening for a response.
Overall, the dolphins responded more to animals they’d known decades ago than to random animals—suggesting they recognized their former companions, according to the study, published recently in Proceedings of the Royal Society B.
Cheeky Dolphins
Working with animals as intelligent as dolphins was a challenge, Bruck added. The animals loved participating in the experiment so much that they’d often hover over the speaker, blocking the noise.
Others would begin “whistling directly at me as if I could understand them,” he said.
And one set of cheeky young dolphins swam up to Bruck and started whistling the names of the dominant males in their group in order of rank, perhaps suggesting the names they wanted to hear, Bruck said.
Memory Linked to Smarts?
Why dolphins—which live an average of 20 years in the wild—need long-term memory is still unknown. But it may have to do with maintaining relationships, since over time dolphin groups often break up and reorganize into new alliances.
This sort of social system is called “fission-fusion,” and it’s also seen in elephants and chimpanzees—two other highly intelligent and social beings.
Coincidence? Bruck suspects not: “It seems that maybe complex cognition comes from a place of trying to remember who your buddies are,” he said.