By Max Kozlov A sliver of human brain in a small vial starts to melt as lye is added to it. Over the next few days, the caustic chemical will break down the neurons and blood vessels within, leaving behind a grisly slurry containing thousands of tiny plastic particles. Toxicologist Matthew Campen has been using this method to isolate and track the microplastics — and their smaller counterparts, nanoplastics — found in human kidneys, livers and especially brains. Campen, who is at the University of New Mexico in Albuquerque, estimates that he can isolate about 10 grams of plastics from a donated human brain; that’s about the weight of an unused crayon. Microplastics have been found just about everywhere that scientists have looked: on remote islands, in fresh snow in Antarctica, at the bottom of the Mariana Trench in the western Pacific, in food, in water and in the air that we breathe. And scientists such as Campen are finding them spread throughout the human body. Detection is only the first step, however. Determining precisely what these plastics are doing inside people and whether they’re harmful has been much harder. That’s because there’s no one ‘microplastic’. They come in a wide variety of sizes, shapes and chemical compositions, each of which could affect cells and tissues differently. This is where Campen’s beige sludge comes into play. Despite microplastics’ ubiquity, it’s difficult to determine which microplastics people are exposed to, how they’re exposed and which particles make their way into the nooks and crannies of the body. The samples that Campen collects from cadavers can, in turn, be used to test how living tissues respond to the kinds of plastic that people carry around with them. “Morbidly speaking, the best source I can think of to get good, relevant microplastics is to take an entire human brain and digest it,” says Campen. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 15: Language and Lateralization
Link ID: 29669 - Posted: 02.12.2025

Damian Carrington Environment editor The exponential rise in microplastic pollution over the past 50 years may be reflected in increasing contamination in human brains, according to a new study. It found a rising trend in micro- and nanoplastics in brain tissue from dozens of postmortems carried out between 1997 and 2024. The researchers also found the tiny particles in liver and kidney samples. The human body is widely contaminated by microplastics. They have also been found in blood, semen, breast milk, placentas and bone marrow. The impact on human health is largely unknown, but they have been linked to strokes and heart attacks. The scientists also found that the concentration of microplastics was about six times higher in brain samples from people who had dementia. However, the damage dementia causes in the brain would be expected to increase concentrations, the researchers said, meaning no causal link should be assumed. “Given the exponentially rising environmental presence of micro- and nanoplastics, this data compels a much larger effort to understand whether they have a role in neurological disorders or other human health effects,” said the researchers, who were led by Prof Matthew Campen at the University of New Mexico in the US. Microplastics are broken down from plastic waste and have polluted the entire planet, from the summit of Mount Everest to the deepest oceans. People consume the tiny particles via food, water and by breathing them in. A study published on Thursday found tiny plastic pollution to be significantly higher in placentas from premature births. Another recent analysis found that microplastics can block blood vessels in the brains of mice, causing neurological damage, but noted that human capillaries are much larger. © 2025 Guardian News & Media Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 29656 - Posted: 02.05.2025

By Smriti Mallapaty For the first time, scientists have tracked microplastics moving through the bodies of mice in real time1. The tiny plastic particles are gobbled up by immune cells, travel through the bloodstream and eventually become lodged in blood vessels in the brain. It’s not clear whether such obstructions occur in people, say researchers, but they did seem to affect the mice’s movement. Microplastics are specks of plastic, less than 5 millimetres long, that can be found everywhere, from the deep ocean to Antarctic ice. They are in the air we breathe, the water we drink and the food we eat. They can even enter our bloodstreams directly through plastic medical devices. Studies show that microplastics, and smaller nanoplastics, have made their way into humans’ brains, livers and kidneys, but researchers are just beginning to understand what happens to these plastic intruders and their effect on human health. One study last year, for example, found that people with micro- and nano-plastics in fatty deposits in their main artery were more likely to experience a heart attack, stroke or death2. In the latest study, published in Science Advances today, Haipeng Huang, a biomedical researcher at Peking University in Beijing, and his colleagues wanted to better understand how microplastics affect the brain. They used a fluorescence imaging technique called miniature two-photon microscopy to observe what was happening in mouse brains through a transparent window surgically implanted into the animal’s skull. The imaging technique can trace microplastics as they move through the bloodstream, says Eliane El Hayek, an environmental-health researcher at University of New Mexico in Albuquerque. “It’s very interesting, and very helpful.” © 2025 Springer Nature Limited

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Language and Lateralization
Link ID: 29641 - Posted: 01.25.2025

By Apoorva Mandavilli The snake struck 11-year-old Beatrice Ndanu Munyoki as she sat on a small stone, which lay atop a larger one, watching the family’s eight goats. She was idly running her fingers through the dirt when she saw a red head dart from between the stones and felt a sharp sting on her right index finger. Never a crier, she ran to her father, David Mutunga, who was building a fence. He cut the cloth belt on her dress into strips with a machete, tied her arm in three places and rushed her to a hospital 30 minutes away on a motorcycle taxi. As the day stretched on, her finger grew darker, but the hospital in Mwingi, a small town in Kenya, had no antidote for that kind of venom. Finally that evening in November 2023, she was taken by ambulance to another hospital and injected with antivenom. When the finger blistered, swelled and turned black despite a second dose the next day, “I understood that they will now remove that part,” Mr. Mutunga said with tears in his eyes. Beatrice’s finger was amputated. In Kenya, India, Brazil and dozens of other countries, snakes vie for the same land, water and sometimes food as people, with devastating consequences. Deforestation, human sprawl and climate change are exacerbating the problem. According to official estimates, about five million people are bitten by snakes each year. About 120,000 die, and some 400,000 lose limbs to amputation. The real toll is almost certainly much higher. Estimates are generally based on hospital records, but most snakebites occur in rural areas, far from dispensaries that stock antivenom and among people too poor to afford treatment. “We don’t actually know the burden of snakebite for most countries of the world,” said Nicholas Casewell, a snake researcher at the Liverpool School of Tropical Medicine. © 2025 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 29621 - Posted: 01.08.2025

By Kim Tingley There are two opposite paths to achievement in science. The first is straightforward: Identify a problem and set about solving it. The second is rather unscientific-sounding and perhaps more faith-based: Study in obscurity and hope serendipity strikes. In 1980, a young gastroenterologist named Jean-Pierre Raufman wound up taking the latter road through the digestive-diseases branch of the National Institutes of Health. His goal there was to gain research experience. While doing so, he chanced to meet the lead chemist of another laboratory, John Pisano, who had a passion for seeking out new and interesting examples of a specific kind of hormone, called a peptide, in animal venoms. Pisano regularly appealed to local insect and reptile enthusiasts in the classified pages of The Washington Post; in response, they would show up at his office door carrying plastic bags wriggling with possibility. Pisano offered some venom samples to Raufman for his meandering analyses. Over the following month, Raufman experimented with them to see if they stimulated pancreatic cells harvested from guinea pigs. The venom with the biggest effect by far came from a desert reptile that Raufman had never heard of: the Gila monster. Gila monsters — sluggish, thick-tailed ground dwellers — are native to southern Arizona and northern Mexico. They have blunt noses and bumpy black skin with tan, pink or orange squiggles. They spend 95 percent of their lives underground. Like their cousins to the south, Mexican beaded lizards, they are one of the very few lizard species that produces venom, which they excrete from mouth glands into grooves in their serrated teeth. The strength of their jaws is typically enough to subdue their prey (chicks, frogs, worms and the like). But if threatened and unable to escape or hide, they may bite a predator. Whenever they clamp down, piercing the skin, venom enters the victim’s bloodstream. This causes intense pain and can initiate a cascade of other symptoms that, in people, includes vomiting, dizziness, rapid heart rate, low blood pressure and, in rare circumstances, death. © 2024 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: Development of the Brain
Link ID: 29555 - Posted: 11.13.2024

By Kristen French Combat in nature is often a matter of tooth and claw, fang and talon. But some creatures have devised devious and dramatic ways to weaponize their bodily fluids, expelling them in powerful streams for the purposes of attack or self-defense. Researcher Elio Challita became fascinated by fluid ejections in nature when he began studying an insect called the sharpshooter, which pees one droplet at a time using a method called superpropulsion. These insects consume 300 times their own body weight per day in xylem sap, a watery solution of minerals and other nutrients found in the roots, stems, and leaves of plants. To efficiently expel the resulting waste, they use a kind of internal catapult that helps overcome the surface tension in the droplets. Challita and a team of researchers from the Bhamla Lab at Georgia Tech decided to survey the biomechanics and fluid dynamics that govern fluid ejections across the animal kingdom to see what commonalities they could find. Among others, they identified a number of creatures that use bodily fluids as powerful weapons in the fight for survival. These fluid ejections defy gravity and rebel against traditional notions of predator-prey tactics. The team’s review, “Fluid Ejections in Nature,” is forthcoming in the Annual Review of Chemical and Biological Engineering. 1. Ringnecked Spitting Cobra Cobras of the Naja genus defend against threats by spitting venom with extreme precision toward the eyes of an enemy, up to 6.5 feet away. These snakes release the venom through hollow microscopic fangs and can adjust the distribution of their spit with rapid movements. Spitting cobras have a venom discharge orifice that is more circular in shape than non-spitting species, which gives the venom more forward force. Contraction in the venom gland also helps. A 90-degree bend near the lip of the orifice gives the snake more precise control over venom flow. Naja pallida cobras can spit venom at average speeds of 1.27 milliliters per second. © 2024 NautilusNext Inc.,

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 29278 - Posted: 04.30.2024

By Frances Vinall More than two-thirds of young children in Chicago could be exposed to lead-contaminated water, according to an estimate by the Johns Hopkins Bloomberg School of Public Health and the Stanford University School of Medicine. The research, published Monday in the journal JAMA Pediatrics, estimated that 68 percent of children under the age of 6 in Chicago are exposed to lead-contaminated drinking water. Of that group, 19 percent primarily use unfiltered tap water, which was associated with a greater increase in blood lead levels. “The extent of lead contamination of tap water in Chicago is disheartening — it’s not something we should be seeing in 2024,” lead author Benjamin Huynh, assistant professor of environmental health and engineering at the Johns Hopkins Bloomberg School of Public Health, said in a news release. The study suggested that residential blocks with predominantly Black and Hispanic populations were less likely to be tested for lead, but also disproportionately exposed to contaminated water. Gina Ramirez, Midwest regional lead of environmental health for the Natural Resources Defense Council, said she grew up in Chicago drinking bottled water, but now uses filtered water for her own family, because of a generational awareness of “not trusting my tap” to be safe. The study “confirmed my worst fears that children living in vulnerable populations in the city are the most impacted,” she said. “All children deserve to grow up in a healthy city, and to learn that something inside their home is impacting so many kids health and development is a huge wake-up call.”

Related chapters from BN: 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 and Learning; Chapter 4: Development of the Brain
Link ID: 29207 - Posted: 03.23.2024

By Lisa Sanders, M.D. Surrounded by the detritus of a Thanksgiving dinner, the woman was loading the dishwasher when a loud thump thundered through the house. She hurried out of the kitchen to find her husband of 37 years sitting on the second-floor landing. Her son and son-in-law, an emergency-room doctor, crouched at his side. Her husband protested that he was fine, then began to scooch himself on his bottom into the bedroom. The two young men helped him to his feet. The man’s body shook with a wild tremor that nearly knocked him down again. “I was getting into bed and fell,” he explained — though the bed was too far away to make this at all likely. “Get some sleep,” the woman said gently once her husband was settled in the bed. “We’ll go to the hospital in the morning.” Her daughter and son-in-law had arrived that morning and already mentioned the change they noticed in the 70-year-old senior. The normally gregarious man was oddly quiet. And the tremor he had for as long as they could remember was much more prominent. His hands shook so much he had trouble using his fork and ended up eating much of his Thanksgiving dinner with his fingers. And now this fall, this confusion — they were worried. His wife was also worried. Just after Halloween, she traveled for business, and when she came back, her husband was much quieter than usual. Even more concerning: When he spoke, he didn’t always make sense. “Have you had a stroke?” she asked her first day home. He was fine, he insisted. But a few days later she came home from work to find his face covered with cuts. He was shaving, he said, but his hand shook so much that he kept cutting himself. “There is something wrong with me,” he acknowledged. It was Thanksgiving week, but she was able to get him an appointment at his doctor’s office the next day. They were seen by the physician assistant (P.A.). She was kind, careful and thorough. After hearing of his confusion, she asked the man what day it was. “Friday?” he offered uncertainly. It was Wednesday. Could he touch his finger to his nose and then to her finger, held an arm’s length away? He could not. His index finger carved jagged teeth in the air as he sought his own nose then stretched to touch her finger. And when she asked him to stand, his entire body wobbled dangerously. “It’s all happened so quickly,” the man’s wife said. The P.A. reviewed his lab tests. They were all normal. She then ordered an M.R.I. of the brain. That, she explained, should give them a better idea of what direction to take. But, she added, if he falls or seems © 2024 The New York Times Company

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 29182 - Posted: 03.07.2024

By Geoffrey Giller From the brightly colored poison frogs of South America to the prehistoric-looking newts of the Western US, the world is filled with beautiful, deadly amphibians. Just a few milligrams of the newt’s tetrodotoxin can be fatal, and some of those frogs make the most potent poisons found in nature. In recent years, scientists have become increasingly interested in studying poisonous amphibians and are starting to unravel the mysteries they hold. How is it, for example, that the animals don’t poison themselves along with their would-be predators? And how exactly do the ones that ingest toxins in order to make themselves poisonous move those toxins from their stomachs to their skin? Even the source of the poison is sometimes unclear. While some amphibians get their toxins from their diet, and many poisonous organisms get theirs from symbiotic bacteria living on their skin, still others may or may not make the toxins themselves — which has led scientists to rethink some classic hypotheses. Over the long arc of evolution, animals have often turned to poisons as a means of defense. Unlike venoms — which are injected via fang, stinger, barb, or some other specialized structure for offensive or defensive purposes — poisons are generally defensive toxins a creature makes that must be ingested or absorbed before they take effect. Amphibians tend to store their poisons in or on their skin, presumably to increase the likelihood that a potential predator is deterred or incapacitated before it can eat or grievously wound them. Many of their most powerful toxins — like tetrodotoxin, epibatidine and the bufotoxins originally found in toads — are poisons that interfere with proteins in cells, or mimic key signaling molecules, thus disrupting normal function. © 2023 Annual Reviews

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 4: Development of the Brain
Link ID: 28757 - Posted: 04.29.2023

Linda Geddes Science correspondent Lead exposure during childhood may lead to reduced cognitive abilities in later life, meaning people experience symptoms of dementia sooner, data suggest. The study, one of the first to investigate the decades-long consequences of lead poisoning, suggests countries could face an explosion of people seeking support for dementia as individuals who were exposed to high lead levels during early life progress into old age. “In the US, and I would imagine the UK, the prime years when children were exposed to the most lead was in the 1960s and 70s. That’s when the most leaded gasoline was getting used, lead paint was still common, and municipal water systems hadn’t done much to clean up their lead,” said Prof John Robert Warren at the University of Minnesota in Minneapolis, who was involved in the research. “Those children who are now in their 40s, 50s and early 60s, will soon be entering the time of life when cognitive impairment and dementia are really common. So there’s this coming wave, potentially, of problems for the people who were most exposed.” Although scientists have long known that children and adults who are exposed to lead have poorer cognitive and educational outcomes, few studies have investigated the longer-term consequences. Warren and his colleagues combined data from the US-based longitudinal Health and Retirement Study (HRS), which has followed the brain health of thousands of adults over several decades, with census records to pinpoint where 1,089 of these individuals lived as children. They also mapped the locations of towns and cities that used lead pipes and had acidic or alkaline water – a proxy for high lead exposure. The research, published in Science Advances, revealed that people who lived in cities with lead-contaminated water as children had worse baseline cognitive functioning – a measure of their ability to learn, process information, and reason – at age 72, compared with those who did not. The difference was equivalent to being roughly eight years older. © 2022 Guardian News & Media Limited

Related chapters from BN: 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 and Learning; Chapter 4: Development of the Brain
Link ID: 28550 - Posted: 11.13.2022

By Katherine J. Wu For a rodent that resembles the love child of a skunk and a steel wool brush, the African crested rat carries itself with a surprising amount of swagger. The rats “very much have the personality of something that knows it’s poisonous,” says Sara Weinstein, a biologist at the University of Utah and the Smithsonian Conservation Biology Institute who studies them. In sharp contrast to most of their skittish rodent kin, Lophiomys imhausi lumber about with the languidness of porcupines. When cornered, they fluff up the fur along their backs into a tip-frosted mohawk, revealing rows of black-and-white bands that run like racing stripes down their flanks — and, at their center, a thicket of specialized brown hairs with a honeycomb-like texture. Those spongy hairs contain a poison powerful enough to bring an elephant to its knees, and are central to Dr. Weinstein’s recent research, which confirmed ideas about how this rat makes itself so deadly. Give them a chance and African crested rats will take nibbles from the branch of a poison arrow tree. It’s not for nutrition. Instead, they will chew chunks of the plants and spit them back out into their fur, anointing themselves with a form of chemical armor that most likely protects them from predators like hyenas and wild dogs. The ritual transforms the rats into the world’s only known toxic rodents, and ranks them among the few mammals that borrow poisons from plants. Dr. Weinstein’s research, which was published last week in the Journal of Mammalogy, is not the first to document the crested rats’ bizarre behavior. But the new paper adds weight to an idea described nearly a decade ago, and offers an early glimpse into the animals’ social lives. First documented in the scientific literature in 1867, the rarely-glimpsed African crested rat “has captured so much interest for so long,” said Kwasi Wrensford, a behavioral ecologist at the University of California, Berkeley who wasn’t involved in the study. “We’re now just starting to unpack what makes this animal tick.” © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 0: ; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27592 - Posted: 11.27.2020

By Lisa Friedman and Coral Davenport WASHINGTON — The Trump administration on Thursday finalized a decision not to impose any limits on perchlorate, a toxic chemical compound found in rocket fuel that contaminates water and has been linked to fetal and infant brain damage. The move by the Environmental Protection Agency was widely expected, after The New York Times reported last month that Andrew Wheeler, the E.P.A. administrator, had decided to effectively defy a court order that required the agency to establish a safe drinking-water standard for the chemical by the end of June. In addition to not regulating, the E.P.A. overturned the underlying scientific finding that declared perchlorate a serious health risk for five million to 16 million people in the United States. The E.P.A. said California and Massachusetts and other states had already taken regulatory steps to reduce the contamination. “Today’s decision is built on science and local success stories and fulfills President Trump’s promise to pare back burdensome ‘one-size-fits-all’ overregulation for the American people,” Mr. Wheeler said in a statement. “State and local water systems are effectively and efficiently managing levels of perchlorate. Our state partners deserve credit for their leadership on protecting public health in their communities, not unnecessary federal intervention.” Environmentalists said both moves showed a disregard for science, the law and public health, and they criticized the agency for claiming credit for state regulations done in the face of federal inaction. “Today’s decision is illegal, unscientific and unconscionable,” said Erik D. Olson, the senior strategic director for health at the Natural Resources Defense Council, an advocacy group. “The Environmental Protection Agency is threatening the health of pregnant moms and young children with toxic chemicals in their drinking water at levels that literally can cause loss of I.Q. points. Is this what the Environmental Protection Agency has come to?” © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27308 - Posted: 06.19.2020

By Joshua Sokol The city of Minamata, Japan, is dotted with monuments commemorating victims of an industrial mass poisoning decades ago. High in the hills, a small stone memorial honors other deaths—of cats sacrificed in secret to science. Now, after restudying the remains of one of those cats, a team of scientists is arguing, controversially, that the long-standing explanation for the tragedy is wrong. No one questions the root cause of the disaster, which at minimum poisoned more than 2000 people: mercury in a chemical factory’s wastewater that was dumped into Minamata Bay and taken up by seafood eaten by fishermen and their families. At first, the chemical form of the mercury, which ultimately killed many of its victims and left many babies with severe neurological disorders, was unknown. But in 1968, the Japanese government blamed methylmercury, a common byproduct of mercury pollution. Many studies supported that conclusion, finding methylmercury spikes in shellfish, bay sludge, and even hundreds of umbilical cords from babies delivered during the time. But methylmercury is not the culprit, says Ingrid Pickering, an x-ray spectroscopist at the University of Saskatchewan. “Our work is indicating that it’s something else”: an unusual mercury compound that may say little about the broader threat of mercury pollution. Minamata has long been a vivid case study of mercury’s dangers. The metal is toxic on its own, but it becomes far more dangerous when bacteria in natural environments convert it into methylmercury, an organic compound, readily absorbed by living tissues, that can be concentrated and passed up food chains. Since the 1990s, scientists have argued that the Chisso chemical factory in Minamata produced methylmercury and dumped it directly into the bay. © 2020 American Association for the Advancement of Science.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27140 - Posted: 03.25.2020

Davide Castelvecchi The group of nerve agents known as Novichoks are to be added to the Chemical Weapons Convention’s list of controlled substances, in one of the first major changes to the treaty since it was agreed in the 1990s. The compounds, developed by the Soviet Union during the cold war, came to prominence after they were used in a high-profile assassination attempt on a former Russian military officer, Sergei Skripal, in Salisbury, UK, in March last year. The Organisation for the Prohibition of Chemical Weapons (OPCW), which is tasked with enforcing the treaty, announced the decision to explicitly ban Novichoks on 27 November as representatives from the 193 member states met in The Hague this week for a periodic review of the convention. The member states agreed unanimously to classify Novichoks as chemical weapons, the OPCW said. The update to the treaty, which will come into effect in 180 days, was initially proposed by the United States, Canada and the Netherlands. “There is a recognition that we all win with this agreement,” says Alastair Hay, an environmental toxicologist at the University of Leeds, UK, who was at the meeting. “The decision means that OPCW can now keep tabs on these chemicals.” The OPCW has the power to send inspectors to any signatory country to search for evidence of production of banned chemicals. It also can send experts to help countries to investigate crime scenes where chemical agents may have been used. © 2019 Springer Nature Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26863 - Posted: 12.02.2019

By Nicholas Bakalar Long-term exposure to air pollution is associated with lower scores on tests of mental acuity, researchers have found. And one reason may be that air pollution causes changes in brain structure that resemble those of Alzheimer’s disease. The scientists studied 998 women ages 73 to 87 and free of dementia, periodically giving them tests of learning and memory. They used magnetic resonance imaging to detect brain atrophy, or wasting, and then scored the deterioration on its degree of similarity to the brain atrophy characteristic of Alzheimer’s disease. They matched Environmental Protection Agency data on air pollution to the women’s residential addresses. Over 11 years of follow-up, they found that the greater the women’s exposure to PM 2.5, the tiny particulate matter that easily penetrates the lungs and bloodstream, the lower their scores on the cognitive tests. After excluding cases of dementia and stroke, they also found a possible reason for the declining scores: The M.R.I. results showed that increased exposure to PM 2.5 was associated with increased brain atrophy, even before clinical symptoms of dementia had appeared. The study is in the journal Brain. “PM 2.5 alters brain structure, which then accelerates memory decline,” said the lead author, Diana Younan, a postdoctoral researcher at the University of California. “I just want people to be aware that air pollution can affect their health, and possibly their brains.” © 2019 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 26849 - Posted: 11.26.2019

Catherine Offord When Lilian Calderón-Garcidueñas discovered abundant hallmarks of Alzheimer’s disease in a batch of human brain samples a few years ago, she initially wasn’t sure what to make of it. The University of Montana neuropathologist had been studying the brains as part of her research on environmental effects on neural development, and this particular set of samples came from autopsy examinations carried out on people who had died suddenly in Mexico City, where she used to work as a researcher and physician. Although Calderón-Garcidueñas had collected much of the tissue herself while attending the autopsies in Mexico, the light-microscope slides she was analyzing had been prepared by her colleagues, so she was in the dark about what patient each sample came from. By the end of the project, she’d identified accumulations of the Alzheimer’s disease–associated proteins amyloid-ß and hyperphosphorylated tau in almost all of the 203 brains she studied. “When I started opening envelopes to see who [each sample] belonged to . . . I was devastated,” she says. The people whose brains she’d been studying were not only adults, but teens and even children. The youngest was 11 months old. “My first thought was, ‘What am I going to do with this? What am I going to tell people?’” she says. “I was not expecting such a devastating, extreme pathology.” Despite her shock, Calderón-Garcidueñas had a reason to be on the lookout for signs of a disease usually associated with the elderly in these samples. For the last three decades, she’d been studying the health effects of Mexico City’s notoriously polluted air—a blight that earned the capital the dubious distinction of most polluted megacity on the planet from the United Nations in 1992. During that time, she’s discovered many links between exposure to air pollution and signs of neural damage in animals and humans. Although her findings are observational, and the pathology of proteins such as amyloid-ß is not fully understood, Calderón-Garcidueñas argues that air pollution is the most likely culprit behind the development of the abnormalities she saw in her postmortem samples—plus many other detrimental changes to the brains of Mexico City’s residents. © 1986–2019 The Scientist

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 4: Development of the Brain
Link ID: 26665 - Posted: 10.02.2019

The mysterious ailments experienced by some 40 Canadian and U.S. diplomats and their families while stationed in Cuba may have had nothing to do with sonic "attacks" identified in earlier studies. According to a new Canadian study, obtained exclusively by Radio-Canada's investigative TV program Enquête, the cause could instead be neurotoxic agents used in pesticide fumigation. A number of Canadians and Americans living in Havana fell victim to an unexplained illness starting in late 2016, complaining of concussion-like symptoms, including headaches, dizziness, nausea and difficulty concentrating. Some described hearing a buzzing or high-pitched sounds before falling sick. In the wake of the health problems experienced over the past three years, Global Affairs Canada commissioned a clinical study by a team of multidisciplinary researchers in Halifax, affiliated with the Brain Repair Centre, Dalhousie University and the Nova Scotia Health Authority. "The working hypothesis actually came only after we had most of the results," Dr. Alon Friedman, the study's lead author, said in an interview. The researchers identified a damaged region of the brain that is responsible for memory, concentration and sleep-and-wake cycle, among other things, and then looked at how this region could come to be injured. "There are very specific types of toxins that affect these kinds of nervous systems ... and these are insecticides, pesticides, organophosphates — specific neurotoxins," said Friedman. "So that's why we generated the hypothesis that we then went to test in other ways." Twenty-six individuals participated in the study, including a control group of people who never lived in Havana. ©2019 CBC/Radio-Canada

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Higher Cognition
Link ID: 26627 - Posted: 09.20.2019

By Maanvi Singh The world’s most widely used insecticides may delay the migrations of songbirds and hurt their chances of mating. In the first experiment to track the effects of a neonicotinoid on birds in the wild, scientists captured 24 white-crowned sparrows as they migrated north from Mexico and the southern United States to Canada and Alaska. The team fed half of those birds with a low dose of the commonly used agricultural insecticide imidacloprid and the other half with a slightly higher dose. An additional 12 birds were captured and dosed with sunflower oil, but no pesticide. Within hours, the dosed birds began to lose weight and ate less food, researchers report in the Sept. 13 Science. Birds given the higher amount of imidacloprid (3.9 milligrams per kilogram of body mass) lost 6 percent of their body mass within six hours. That’s about 1.6 grams for an average bird weighing 27 grams. Tracking the birds (Zonotrichia leucophrys) revealed that the pesticide-treated sparrows also lagged behind the others when continuing their migration to their summer mating grounds. The findings suggest that neonicotinoid insecticides, already implicated in dropping bee populations, could also have a hand in the decline of songbird populations across North America. From 1966 to 2013, the populations of nearly three-quarters of farmland bird species across the continent have precipitously dropped. The researchers dosed the birds in the lab with carefully measured amounts of pesticide mixed with sunflower oil. In the wild, birds might feed on seeds coated with imidacloprid. The highest dose that “we gave each bird is the equivalent of if they ate one-tenth of [a single] pesticide-coated corn seed,” says Christy Morrissey, a biologist at the University of Saskatchewan in Saskatoon, Canada. “Frankly, these were minuscule doses we gave the birds.” © Society for Science & the Public 2000–2019.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 26608 - Posted: 09.13.2019

Tina Hesman Saey ORLANDO — Being exposed to a chemical early in life can be a bit like a choose-your-own-adventure book: Some things that happen early on may hurt you later, but only if you make certain choices, an unpublished study in mice suggests. Mouse pups were exposed to the chemical bisphenol A (BPA) for only five days after birth, a crucial time during which mice’s livers develop. BPA, once common in plastics, has been linked to a host of health problems in people, from diabetes to heart disease (SN: 10/11/08, p. 14). But depending on diet as adults, the mice either grew up to be healthy or to have enlarged livers and high cholesterol. As long as the BPA-exposed mice ate mouse chow for the rest of their lives, the rodents remained healthy, molecular biologist Cheryl Walker of Baylor College of Medicine in Houston reported April 7 at the 2019 Experimental Biology meeting. But researchers switched some BPA-exposed mice to a high-fat diet as adults. Those mice had larger livers, higher cholesterol and more metabolic problems than mice who ate a high-fat diet but were not exposed to BPA as pups, Walker said. BPA exposure immediately altered epigenetic marks at more than 5,400 genes, including 3,000 involved in aging. Epigenetic marks are chemical tags on DNA or on histones — protein around which DNA winds in a cell — that don’t change information in genes themselves, but affect gene activity. |© Society for Science & the Public 2000 - 2019

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26134 - Posted: 04.13.2019

By Jennifer Couzin-Frankel For the millions of people treated for cancer, “chemo brain” can be an unnerving and disabling side effect. It causes memory lapses, trouble concentrating, and an all-around mental fog, which appear linked to the treatment and not the disease. Although the cognitive effects often fade after chemotherapy ends, for some people the fog persists for years, even decades. And doctors and researchers have long wondered why. Now, a new study suggests an answer in the case of one chemotherapy drug: Brain cells called microglia may orchestrate chemo brain by disrupting other cells that help maintain the brain’s communication system. “I can’t tell you how many patients I see who look at me when I explain [chemo brain] and say, ‘I’ve been living with this for 10 years and thought I was crazy,’” says Michelle Monje, a pediatric neuro-oncologist and neuroscientist at Stanford University in Palo Alto, California. It’s still mostly a mystery how common long-term cognitive impairment is after chemo. In one recent study by clinical neuropsychologist Sanne Schagen at the Netherlands Cancer Institute in Amsterdam, it affected 16% of breast cancer survivors 6 months after treatment. Monje began to probe the cognitive effects of cancer treatment in the early 2000s, starting with radiation, a therapy that can be far more debilitating than chemotherapy. A Science paper she and her colleagues published in 2003 suggested radiation affected a type of brain cell called microglia, which protect the brain against inflammation. Just like immune cells in the blood, microglia—which make up at least 10% of all brain cells—become activated during injury or infection. © 2018 American Association for the Advancement of Science

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25759 - Posted: 12.07.2018