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By Mike Ives HONG KONG — A large study in China suggests a link between air pollution and negative effects on people’s language and math skills. The link between pollution and respiratory diseases is well known, and most experts now believe that small particulates may also raise the risk for strokes and heart attacks. Whether this form of air pollution impairs cognition is not yet certain, but several studies have hinted at a connection. The latest study, by researchers based in China and the United States, analyzed how long-term exposure to air pollution affected performance on nationwide math and word-recognition tests by more than 25,000 people across 162 Chinese counties. It was published on Monday in Proceedings of the National Academy of Sciences. The authors based their findings on models they built that combined weather and pollution data from specific locations in China where people had taken nationwide tests in 2010 and 2014, as well as the test scores themselves. Their analysis tried to document how short- and long-term pollution exposure might have affected the scores — and, by extension, the test-takers’ brains. The authors found that the cognitive impact of cumulative exposure among the test takers was especially pronounced among older men, and that the results were troubling in part because cognitive decline and impairment are risk factors for Alzheimer’s disease and other forms of dementia. The study “further amplifies the need to tackle air pollution now to protect the health of particularly the young and elderly populations,” Heather Adair-Rohani, a technical officer for public health and environment at the World Health Organization in Geneva, which was not involved in the study, said in an email. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 25393 - Posted: 08.29.2018

By Melissa Healy At some point in their treatment for cancer, somewhere between 17% and 75% of patients with malignancies that don’t affect the central nervous system report the sensation that a mental fog has set in. For months or years after their hair has grown back, the exhaustion has lifted and the medical appointments taper off, the “new normal” for these patients includes problems with concentration, word-finding, short-term memory and multitasking. Their doctors nod their heads knowingly: It’s “chemobrain,” they report. Among the nation’s roughly 15.5 million cancer survivors, the ranks of those who’ve experienced mental fog after cancer treatment are probably increasing as detection and therapies improve, survival rates rise and lives are extended. But when it comes to cancer’s cognitive aftermath, the medical profession’s expertise ends. Why chemobrain happens, how long it will linger, and what deficits it actually causes — and especially whether it could be treated, or even prevented — are questions for which oncologists have no answers. But they want them. And three specialists from the National Cancer Institute have issued an appeal to neuroscientists for help. “We need an infusion of new ideas," said Todd S. Horowitz, a cognitive psychologist and program director in the institute’s Division of Cancer Control and Population Sciences. “Cognitive neuroscience would help us characterize the deficits people have and allow us to connect them to particular brain systems." Writing this week in the journal Trends in Neurosciences, Horowitz and two fellow researchers at the institute drafted a road map toward a better understanding of the condition officially known as cancer-related cognitive impairment, which was first described by breast cancer survivors.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 25089 - Posted: 06.14.2018

Geoff Brumfiel Sergei Skripal and his daughter, Yulia, were found slumped on a bench in the city of Salisbury on March 4. Experts quickly assessed that Skripal — a former Russian intelligence official accused of spying for the British — had been poisoned with a nerve agent. On Monday, British Prime Minister Theresa May named the agent in a speech before Parliament. "It is now clear that Mr. Skripal and his daughter were poisoned with a military-grade nerve agent of a type developed by Russia," she said. "This is part of a group of nerve agents known as Novichok." Novichok agents are extremely rare. "As far as I know, I don't know anybody who knows how to make it except these guys in Russia," says Dan Kaszeta, a chemical weapons expert with Strongpoint Security in London. "They've been a deep, dark secret." Novichok means "newcomer" in Russian. Kaszeta says that Novichok agents were developed in the 1980s as a new weapon in the waning days of the Cold War. Novichok chemicals were designed to evade equipment carried by NATO troops. "They wanted to develop nerve agents that the West couldn't detect," he says. According to a defector's report published by the Stimson Center in 1995, they were developed at the State Scientific Research Institute of Organic Chemistry and Technology in Moscow. As the U.S. and Russia were laying the groundwork to dismantle their chemical weapons stockpiles, researchers at the institute were working in secret to develop the new Novichok chemicals. © 2018 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24747 - Posted: 03.13.2018

By Richard Stone Even 3 decades later, Seyed Naser Emadi's first encounter with nerve agents haunts him. In 1987, as a soldier fighting for Iran in its war with Iraq, he came across a hillside strewn with comrades killed by an Iraqi nerve agent, perhaps tabun or sarin. Unable to breathe, the victims had clawed at their necks to try to open a hole in their throats, recalls Emadi, now a dermatologist in Tehran. In fact, their windpipes were clear; the nerve agent had shut down control of breathing in the central nervous system. They "had no choice except death," he says. The long-term effects of nerve agents remain uncertain, but with the right antidotes, these poisons need not be an immediate death sentence. A few years after Emadi's experience, U.S. soldiers in 1991's Gulf War carried autoinjectors filled with drugs that—in principle—would keep them breathing and protect them from seizures if Iraqi forces again unleashed nerve agents. They never did, most historians agree, but the threat remains real today, as chemical attacks in Syria's ongoing civil war make clear. It is spurring urgent efforts to find better countermeasures, with several promising compounds in the pipeline. First synthesized by German chemists on the eve of World War II, nerve agents kill by binding to acetylcholinesterase (AChE), an enzyme that dismantles the neurotransmitter acetylcholine when it is released into synapses. One of the most efficient enzymes known, a single AChE molecule can hydrolyze 600,000 acetylcholine molecules per minute, says Palmer Taylor, a pharmacologist at the University of California, San Diego. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24492 - Posted: 01.05.2018

By Nicholas Kristof The colored parts of the image above, prepared by Columbia University scientists, indicate where a child’s brain is physically altered after exposure to this pesticide. This chemical, chlorpyrifos, is hard to pronounce, so let’s just call it Dow Chemical Company’s Nerve Gas Pesticide. Even if you haven’t heard of it, it may be inside you: One 2012 study found that it was in the umbilical cord blood of 87 percent of newborn babies tested. And now the Trump administration is embracing it, overturning a planned ban that had been in the works for many years. The Environmental Protection Agency actually banned Dow’s Nerve Gas Pesticide for most indoor residential use 17 years ago — so it’s no longer found in the Raid you spray at cockroaches (it’s very effective, which is why it’s so widely used; then again, don’t suggest this to Dow, but sarin nerve gas might be even more effective!). The E.P.A. was preparing to ban it for agricultural and outdoor use this spring, but then the Trump administration rejected the ban. That was a triumph for Dow, but the decision stirred outrage among public health experts. They noted that Dow had donated $1 million for President Trump’s inauguration. So Dow’s Nerve Gas Pesticide will still be used on golf courses, road medians and crops that end up on our plate. Kids are told to eat fruits and vegetables, but E.P.A. scientists found levels of this pesticide on such foods at up to 140 times the limits deemed safe. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24264 - Posted: 10.30.2017

Christie Wilcox Many tadpoles ward off predators with potent poisons — but those toxins also seem to help win battles with their own kind, a new study finds. Tadpoles of common toads (Bufo bufo) are more poisonous when raised in crowded conditions, which may give them a competitive edge, according to the work published on 23 September in Functional Ecology1. Many noxious plant species are known to modulate their defences to fend off different threats2, but it is less clear whether animals possess similar toxin-tuning abilities. Although predation pressure is known to induce tadpole chemical defences3, the new findings are the first unequivocal evidence of toxin synthesis spurred by competition in vertebrate animals. Being poisonous can make a species essentially inedible to predators, but making potent toxins comes at a metabolic cost — so it’s best to make that investment count. “It would be very profitable for such animals to kill two birds with one stone by using their anti-predatory toxins as chemical weapons against their competitors, too,” says the study’s lead author, Veronika Bókony, an ecologist with the Hungarian Academy of Sciences in Budapest. Common toads are equipped with bufadienolides, potent toxins that cause harm by accelerating and disrupting the heart’s rhythms4. Field studies have found that common toad toxicity varies geographically, with the intensity of competition being the most reliable predictor5. But it has been unclear whether such patterns occur because populations are genetically isolated from one another in different ponds, or whether they reflect defences induced by environmental factors. © 2017 Macmillan Publishers Limited,

Related chapters from BN8e: Chapter 6: Evolution of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 24124 - Posted: 09.30.2017

By BENEDICT CAREY Dr. Herbert Needleman, whose studies of children exposed to low levels of lead prompted regulations that limited or banned the metal in a range of common products, like gasoline and paint, and set a standard for the modern study of environmental toxins, died on July 18 in Pittsburgh. He was 89. His son, Dr. Joshua Needleman, said the cause was lung failure resulting from edema, an excess of fluid. Dr. Needleman was working at a community psychiatric clinic in North Philadelphia after medical school when he met a young man who would become a touchstone for a crusading career. The boy approached Dr. Needleman and explained his ambitions, which were large, even as the boy struggled with words. He was bright and open; nonetheless he had deficits that struck Dr. Needleman as similar to those found in children with lead poisoning. “I thought, how many of these kids who are coming to the clinic are in fact a missed case of lead poisoning?” he said in a later interview. His clinic office overlooked a school playground; the view gave him an idea. Doctors had long known that exposure to high doses of lead caused mental lapses, even permanent brain damage and death. But what about the low-level exposure that many children, like the ones playing in the yard, absorbed every day — merely by living in older urban neighborhoods thick with lead paint and industrial contamination? No one knew. No one could study the effects carefully, because the available tests for lead exposure were of hair, blood, or fingernails — each flawed in its own way. Bone is the most accurate long-term repository: Once absorbed into the body, lead circulates in the blood and accumulates in the skeleton. But taking bone samples — biopsies — is painful and hardly justifiable for the sake of a hypothesis, especially in young children. Yet Dr. Needleman had seen an earlier study of lead poisoning, a small one, which measured accumulated lead exposure in teeth. Teeth are a part of the human skeleton. And young children shed them. “That was the insight that changed everything,” said Dr. Bernard Goldstein, former dean of the University of Pittsburgh’s graduate school of public health. “Herb became the Tooth Fairy.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23887 - Posted: 07.28.2017

Geoff Brumfiel When the half-brother of North Korean leader Kim Jong Un collapsed at a Malaysian airport last week, poisoning was instantly suspected. But on Friday, Malaysian authorities revealed that an autopsy had turned up not just any poison, but a rare nerve agent known as VX. VX is among the deadliest chemical weapons ever devised. A colorless, odorless liquid, similar in consistency to motor oil, it kills in tiny quantities that can be absorbed through the skin. A relative of the nerve agent Sarin, VX disrupts communications between nerves and muscles. Victims of VX initially experience nausea and dizziness. Without an antidote, the chemical eventually paralyzes the diaphragm, causing suffocation. That may have been the fate of Kim Jong Nam, the estranged half-brother of North Korea's leader. Security footage showed that Kim was approached by two women who appeared to cover his face with a cloth. Moments later, he fell ill and sought help. He died before reaching a hospital. If the Malaysian analysis is correct and VX was the culprit, that would seem to suggest that the North Korean state itself is behind the killing. "Hardly anybody has it," says Dan Kaszeta, a chemical weapons expert and consultant based in London. The U.S. has destroyed nearly all of its stocks of VX in recent years. North Korea is among the few states in the world that have an active chemical weapons program. It is not a signatory to the Chemical Weapons Convention, which bans the use of such weapons. © 2017 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23282 - Posted: 02.25.2017

By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 23190 - Posted: 02.06.2017

By Clare Wilson Traffic fumes go to your head. Tiny specks of metal in exhaust gases seem to fly up our noses and travel into our brains, where they may contribute to Alzheimer’s disease. Iron nanoparticles were already known to be present in the brain – but they were thought to come from the iron naturally found in our bodies, derived from food. Now a closer look at their structure suggests the particles mostly come from air pollution sources, like traffic fumes and coal burning. The findings are a smoking gun, says Barbara Maher of Lancaster University in the UK. Iron is present harmlessly in our bodies in different forms, as it is part of many biological molecules. But the form known as magnetite, or iron oxide, which is highly reactive and magnetic, has been implicated in Alzheimer’s disease. Maher’s team looked at the brains of 37 people who had lived either in Manchester in the UK or Mexico City. All contained millions of magnetite particles per gram of brain tissue, detected by measuring how magnetic the brain tissue was. The surprise came when the team used electron microscopes to take a close look at particles in the front part of the brains of six people. Round particles of magnetite outnumbered angular magnetite crystals by about one hundred to one. Crystal forms are more likely to have a natural source – such as iron that has come out of the body’s cells. But round particles normally come from melting iron at high temperatures, which happens when fuel is burned. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22632 - Posted: 09.06.2016

Merrit Kennedy More than 1,000 residents of a public housing complex in East Chicago, Ind., are now forced to relocate because of dangerously high lead levels in the area's soil. The West Calumet Housing Complex, which houses primarily low-income families, lies on the site of a former lead smelting company, as member station WBEZ reported. In July, the Environmental Protection Agency reported high lead levels in the soil in parts of the complex and notified the residents. The EPA advised parents to stop their kids from playing in the dirt, "to wash their children's toys regularly and to wash children's hands after they play outside." As WBEZ reported, the samples showed lead levels "three times higher than the federal safety standards and in some places even higher, much higher." After that, East Chicago Mayor Anthony Copeland "ordered the removal of 1,200 residents from the West Calumet housing project for safety concerns," according to the member station. The residents have now been informed that the 346-unit complex is set to be demolished. "Residents have been provided vouchers for temporary hotel living until their homes are done being cleaned. The residents will return to their homes for a few more months until vouchers for permanent housing are made available by the U.S. Department of Housing and Urban Development." © 2016 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22619 - Posted: 09.01.2016

by Graham McDougall, Jr., behavioral scientist at U. of Alabama Chemo brain is a mental cloudiness reported by about 30 percent of cancer patients who receive chemotherapy. Symptoms typically include impairments in attention, concentration, executive function, memory and visuospatial skills. Since the 1990s researchers have tried to understand this phenomenon, particularly in breast cancer patients. But the exact cause of chemo brain remains unclear. Some studies indicate that chemotherapy may trigger a variety of related neurological symptoms. One study, which examined the effects of chemotherapy in 42 breast cancer patients who underwent a neuropsychological evaluation before and after treatment, found that almost three times more patients displayed signs of cognitive dysfunction after treatment as compared with before (21 versus 61 percent). A 2012 review of 17 studies considering 807 breast cancer patients found that cognitive changes after chemotherapy were pervasive. Other research indicates that the degree of mental fogginess that a patient experiences may be directly related to how much chemotherapy that person receives: higher doses lead to greater dysfunction. There are several possible mechanisms to explain the cognitive changes associated with chemotherapy treatments. The drugs may have direct neurotoxic effects on the brain or may indirectly trigger immunological responses that may cause an inflammatory reaction in the brain. Chemotherapy, however, is not the only possible culprit. Research also shows that cancer itself may cause changes to the brain. In addition, it is possible that the observed cognitive decline may simply be part of the natural aging process, especially considering that many cancer patients are older than 50 years. © 2016 Scientific American,

Related chapters from BN8e: Chapter 17: Learning and Memory; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21820 - Posted: 01.26.2016

By SINDYA N. BHANOO Climate change may affect wood rats in the Mojave Desert in a most unusual way. A new study finds that warmer weather reduces their ability to tolerate toxins in the creosote bush, which they rely on for sustenance. The consequences may be dire for the wood rats. “There’s not much more they can eat out there,” said Patrice Kurnath, a biologist at the University of Utah and one of the study’s authors. She and her colleagues reported their findings in Proceedings of the Royal Society B: Biological Sciences. The leaves of the creosote bush contain a resin full of toxic compounds. They are known to cause kidney cysts and liver failure in laboratory rats. Wild wood rats, however, generally tolerate the poisons. Ms. Kurnath and her colleagues monitored the wood rats as they ate the leaves in warmer temperatures — around 83 degrees Fahrenheit. Although highs in the Mojave can reach the 80s and 90s during the summer, much of the year is cooler. The rats became less tolerant of the toxins and began to lose weight. The reason may have to do with how the liver functions in warmer weather, Ms. Kurnath said. The liver is the body’s primary detoxifying organ. When a mammalian liver is active, it increases internal body temperature. “In warmer weather, maybe you’re not producing huge amounts of heat and you’re not breaking down the toxins,” Ms. Kurnath said. © 2016 The New York Times Company

Related chapters from BN8e: Chapter 6: Evolution of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 21817 - Posted: 01.25.2016

By Megan Cartwright Don’t pet the platypus. I know it’s tempting: Given the chance, I’d want to stroke their thick brown fur, tickle those big webbed feet, and pat that funny duck bill. And why not? What harm could come from this cute, egg-laying mammal from eastern Australia? Plenty. As someone who doesn’t enjoy “long lasting excruciating pain that cannot be relieved with conventional painkillers,” I’d really regret petting a platypus. Especially a male platypus, in late winter, when there’s only one thing on his mind and, even worse, something nasty on his feet. When British biologist Sir Everard Home got ahold of some platypus specimens in 1801, he told his fellow nerds at the Royal Society how the male specimen had a half-inch long “strong crooked spur” on the heel of each rear foot. The female, however, was spur-free. Home suggested that it “is probably by means of these spurs or hooks, that the female is kept from withdrawing herself in the act of copulation.” A very reasonable suggestion. But a wrong one. To be fair to Home, he could only study dead platypuses. If Home could have spent a year hanging out with living platypuses in their river homes, he would’ve seen that this “shy, semi-aquatic, mainly nocturnal” mammal is mostly interested in hunting on the river bottom for delicious insect larvae, crayfish, and shrimp. In other words, the platypus is usually an eater, not a lover. © 2014 The Slate Group

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21090 - Posted: 06.25.2015

By Nicholas Bakalar Exposure to air pollution may hasten brain aging, a new study has found. Researchers studied 1,403 women without dementia who were initially enrolled in a large health study from 1996 to 1998. They measured their brain volume with M.R.I. scans in 2005 and 2006, when the women were 71 to 89 years old. Using residential histories and air pollution data, they estimated their exposure to air pollution from 1999 to 2006. They used data recorded at monitoring sites on exposure to PM 2.5 — tiny particulate matter that easily penetrates the lungs. Each increase of 3.49 micrograms per cubic centimeter cumulative exposure to pollutants was associated with a 6.23 cubic centimeter decrease in white matter, the equivalent of one to two years of brain aging. The association remained after adjusting for many variables, including age, smoking, physical activity, blood pressure, body mass index, education and income. Previous studies have shown that air pollution can cause inflammation and damage to the vascular system, but this study, in The Annals of Neurology, showed damage to the brain itself. “This tells us that the damage air pollution can impart goes beyond the circulatory system,” said the lead author, Dr. Jiu-Chiuan Chen, an associate professor of preventive medicine at the Keck School of Medicine at the University of Southern California. “Particles in the ambient air are an environmental neurotoxin to the aging brain.” © 2015 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 21082 - Posted: 06.23.2015

By David Shultz The most venomous animal on the planet isn’t a snake, a spider, or a scorpion; it’s a snail—a cone snail, to be precise. The Conus genus boasts a large variety of marine snails that have adopted an equally diverse assortment of venoms. Online today in the Proceedings of the National Academy of Sciences, researchers report an especially interesting addition to the animals’ arsenal: insulin. According to the paper, this marks the first time insulin has been discovered as a component of venom. Not all cone snails incorporate insulin into their venom cocktail, wonderfully known as nirvana cabal; the hormone was found only in a subset of the animals that hunt with a netting strategy that relies on snaring fish in their large, gaping mouthparts. Unlike the feeding tactics of some cone snails that hunt using speedy venom-tipped “harpoons,” the mouth-netting strategy is a rather slow process. For it to work, the fish either needs to be very unaware of its surroundings or chemically sedated. Scientists speculate that it’s the insulin that provides such sedation. Snails like Conus geographus (seen above) actually produce multiple variants of the hormone, some of which, like one called Con-Ins G1, are more similar to fish insulin than snail varieties. Con-Ins G1 isn’t an exact match of fish insulin though; it’s a stripped-down version that the team suspects may be missing bits that would let fish detect the overdose and respond. If they’re correct, the snail’s venom may yield insight into the nuances of how insulin is regulated that may extend to humans. © 2015 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 20501 - Posted: 01.21.2015

By Bethany Brookshire WASHINGTON – Moldy houses are hard on the lungs, and new results in mice suggest that they could also be bad for the brain. Inhaling mold spores made mice anxious and forgetful, researchers reported November 15 at the annual meeting of the Society for Neuroscience. Cheryl Harding, a psychologist at the City University of New York, and colleagues dripped low doses of spores from the toxic mold Stachybotrys into mouse noses three times per week. After three weeks, the mice didn’t look sick. But they had trouble remembering a fearful place. The mice were also more anxious than normal counterparts. The anxiety and memory deficits went along with decreases in new brain cells in the hippocampus — a part of the brain that plays a role in memory — compared with control mice. Harding and colleagues also found that the behaviors linked to increased inflammatory proteins in the hippocampus. Exposure to mold’s toxins and structural proteins may trigger an immune response in the brain. The findings, Harding says, may help explain some of the conditions that people living in moldy buildings complain about, such as anxiety and cognitive problems. C. Harding et al. Mold inhalation, brain inflammation, and behavioral dysfunction. Society for Neuroscience Meeting, Washington, DC, November 15, 2014. © Society for Science & the Public 2000 - 2014.

Related chapters from BN8e: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 20323 - Posted: 11.18.2014

By Elizabeth Pennisi It’s not such a stretch to think that humans can catch the Ebola virus from monkeys and the flu virus from pigs. After all, they are all mammals with fundamentally similar physiologies. But now researchers have discovered that even a virus found in the lowly algae can make mammals its home. The invader doesn’t make people or mice sick, but it does seem to slow specific brain activities. The virus, called ATCV-1, showed up in human brain tissue several years ago, but at the time researchers could not be sure whether it had entered the tissue before or after the people died. Then, it showed up again in a survey of microbes and viruses in the throats of people with psychiatric disease. Pediatric infectious disease expert Robert Yolken from Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues were trying to see if pathogens play a role in these conditions. At first, they didn't know what ATCV-1 was, but a database search revealed its identity as a virus that typically infects a species of green algae found in lakes and rivers. The researchers wanted to find out if the virus was in healthy people as well as sick people. They checked for it in 92 healthy people participating in a study of cognitive function and found it in 43% of them. What’s more, those infected with the virus performed 10% worse than uninfected people on tests requiring visual processing. They were slower in drawing a line connecting a sequence of numbers randomly placed on a page, for example. And they seemed to have shorter attention spans, the researchers report online today in the Proceedings of the National Academy of Sciences. The effects were modest, but significant. © 2014 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20258 - Posted: 10.29.2014

By Jules Wellinghoff A simple change in electric charge may make the difference between someone getting the medicine they need and a trip to the emergency room—at least if a new study bears out. Researchers investigating the toxicity of particles designed to ferry drugs inside the body have found that carriers with a positive charge on their surface appear to cause damage if they reach the brain. These particles, called micelles, are one type of a class of materials known as nanoparticles. By varying properties such as charge, composition, and attached surface molecules, researchers can design nanoparticles to deliver medicine to specific body regions and cell types—and even to carry medicine into cells. This ability allows drugs to directly target locations they would otherwise be unable to, such as the heart of tumors. Researchers are also looking at nanoparticles as a way to transport drugs across the blood-brain barrier, a wall of tightly connected cells that keeps most medication out of the brain. Just how safe nanoparticles in the brain are, however, remains unclear. So Kristina Bram Knudsen, a toxicologist at the National Research Centre for the Working Environment in Copenhagen, and colleagues tested two types of micelles, which were made from different polymers that gave the micelles either a positive or negative surface charge. They injected both versions, empty of drugs, into the brains of rats, and 1 week later they checked for damage. Three out of the five rats injected with the positively charged micelles developed brain lesions. The rats injected with the negatively charged micelles or a saline control solution did not suffer any observable harm from the injections, the team will report in an upcoming issue of Nanotoxicology. © 2014 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19819 - Posted: 07.12.2014

A toxic caffeine level was found in the system of a high school student who died unexpectedly, says a U.S. coroner who warns young people need to be educated about the dangers of taking the potent powder that is sold online. Logan Stiner, 18, was found dead at his family’s home in May. Steiner was an excellent student and a healthy young man who didn’t do drugs, Dr. Stephen Evans, a coroner in Lorain County, Ohio, said Monday. "We sent his blood out for levels, and [when] it came back it was a toxic level. Caffeine toxicity will do exactly what happened to him. It'll lead to things like cardiac arrhytmias and seizures," Evans said in an interview. Use of caffeine from coffee, tea and other beverages is so widespread that it is considered innocuous, but that’s not the case when it’s taken in an overdose amount. Powdered caffeine is sold in bulk over the internet. Problems can arise because adding a teaspoon of the caffeine powder to water is the equivalent of 30 cups of coffee. About one-sixteenth of a teaspoon of the powder is equal to about two cups of coffee. Evans said he recognizes that weightlifters will say Stiner should’ve taken the correct amount. "One-sixteenth of a teaspoon. You expect a kid to figure that out?" He suggested that regulators re-consider internet sales of a pound of powdered caffeine to young people. When Evans and his staff reviewed the pathology literature, they found 18 other cases of deaths in the U.S. from caffeine overdoses. Some were suicides and others were accidental, but he suspects the deaths are underreported since few pathologists investigating deaths from seizure and cardiac arrhytmia check caffeine levels. © CBC 2014

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19774 - Posted: 07.01.2014