https://aeon.co/essays/what-the-metaphor-of-rewiring-gets-wrong-about-neuroplasticity Can you rewire your brain? Peter Lukacs Popular wisdom holds we can ‘rewire’ our brains: after a stroke, after trauma, after learning a new skill, even with 10 minutes a day on the right app. The phrase is everywhere, offering something most of us want to believe: that when the brain suffers an assault, it can be restored with mechanical precision. But ‘rewiring’ is a risky metaphor. It borrows its confidence from engineering, where a faulty system can be repaired by swapping out the right component; it also smuggles that confidence into biology, where change is slower, messier and often incomplete. The phrase has become a cultural mantra that is easier to comprehend than the scientific term, neuroplasticity – the brain’s ability to change and form new neural connections throughout life. But what does it really mean to ‘rewire’ the brain? Is it a helpful shorthand for describing the remarkable plasticity of our nervous system or has it become a misleading oversimplification that distorts our grasp of science? After all, ‘rewiring your brain’ sounds like more than metaphor. It implies an engineering project: a system whose parts can be removed, replaced and optimised. The promise is both alluring and oddly mechanical. The metaphor actually did come from engineering. To an engineer, rewiring means replacing old and faulty circuits with new ones. As the vocabulary of technology crept into everyday life, it brought with it a new way of thinking about the human mind. Medical roots of the phrase trace back to 1912, when the British surgeon W Deane Butcher compared the body’s neural system to a house’s electrical wiring, describing how nerves connect to muscles much like wires connect appliances to a power source. By the 1920s, the Harvard psychologist Leonard Troland was referring to the visual system as ‘an extremely intricate telegraphic system’, reinforcing the comparison between brain function and electrical networks. © Aeon Media Group Ltd. 2012-2026. -------------------- https://www.nature.com/articles/d41586-026-00311-7 Many people have no mental imagery. What’s going on in their brains? Elizabeth Quill Think about your breakfast this morning. Can you imagine the pattern on your coffee mug? The sheen of the jam on your half-eaten toast? Most of us can call up such pictures in our minds. We can visualize the past and summon images of the future. But for an estimated 4% of people, this mental imagery is weak or absent. When researchers ask them to imagine something familiar, they might have a concept of what it is, and words and associations might come to mind, but they describe their mind’s eye as dark or even blank. Systems neuroscientist Mac Shine at the University of Sydney, Australia, first realized that his mental experience differed in this way in 2013. He and his colleagues were trying to understand how certain types of hallucination come about1, and were discussing the vividness of mental imagery. “When I close my eyes, there’s absolutely nothing there,” Shine recalls telling his colleagues. They immediately asked him what he was talking about. “Whoa. What’s going on?” Shine thought. Neither he nor his colleagues had realized how much variation there is in the experiences people have when they close their eyes. This moment of revelation is common to many people who don’t form mental images. They report that they might never have thought about this aspect of their inner life if not for a chance conversation, a high-school psychology class or an article they stumbled across (see ‘How do you imagine?’). Although scientists have known for more than a century that mental imagery varies between people, the topic received a surge of attention when, a decade ago, an influential paper coined the term aphantasia to describe the experience of people with no mental imagery2. © 2026 Springer Nature Limited -------------------- https://www.nytimes.com/2026/02/02/health/pyschosis-young-people-cannabis-canada.html Psychosis Diagnoses Have Risen Among Young Canadians, Data Shows By Ellen Barry A new analysis of birth cohorts in the Canadian province of Ontario has found a striking rise in the incidence of psychotic disorders among young people, a finding that its authors said could reflect teens’ increasing use of substances like cannabis, stimulants and hallucinogens. The study, published on Monday in The Canadian Medical Association Journal, found that the rate of new diagnoses of psychotic disorders among people ages 14 to 20 increased by 60 percent between 1997 and 2023, while new diagnoses at older ages plateaued or declined. Compared with people born in the late 1970s, those born in the early 2000s were about twice as likely to have been diagnosed with a psychotic disorder by age 20. The researchers included 12 million people born in Ontario between 1960 and 2009, of which 0.9 percent were diagnosed with a psychotic disorder during the study period. The study was epidemiological and did not try to identify a cause for the rising prevalence. There are a number of possible explanations, among them older paternal age, the stress of migration, neonatal health problems and early intervention programs that now regularly identify the disorders at younger ages, the authors note. But Dr. Daniel Myran, one of the study’s authors, said he undertook the study, in part, to follow up on concerns that the legalization of cannabis might increase population-level rates of schizophrenia and other psychotic disorders. “I was expecting to see some increases in these younger folks, but I was quite surprised by the scale,” said Dr. Myran, a family physician and research chair at North York General Hospital. He said the results suggested a need for more research into the impact of expanding cannabis use by young people. © 2026 The New York Times Company -------------------- https://www.sciencenews.org/article/poor-sleep-large-share-dementia-cases Poor sleep may account for a large share of dementia cases By Marla Vacek Broadfoot Nearly 1 in 8 dementia cases — about half a million nationwide — may be linked to insomnia. The new findings, reported December 27 in the Journals of Gerontology: Series A, add weight to growing evidence that sleep is a modifiable risk factor for dementia, akin to hearing loss and hypertension. The study does not establish a direct cause-and-effect relationship between insomnia and dementia for individuals, says Yuqian Lin, a data analyst at Massachusetts General Hospital in Boston. Rather, she says, it looks at the overall extent to which insomnia may contribute to dementia across the population. Lin and her colleagues analyzed data from the National Health and Aging Trends Study, or NHATS, a long-running survey of 5,900 U.S. adults ages 65 and older. Participants reported whether they had difficulty falling asleep, staying asleep or both. Dementia was identified using standard research tools that rely on cognitive testing and reports from family members or caregivers. To estimate the impact of insomnia on the population, Lin and her team calculated the proportion of dementia cases that could theoretically be prevented if insomnia-related sleep disturbances were eliminated. The calculation combined the prevalence of insomnia and dementia in the NHATS population with relative risk estimates drawn from recent large meta-analyses linking insomnia to dementia later in life. © Society for Science & the Public 2000–2026. -------------------- https://www.science.org/content/article/loss-hunger-hormone-has-made-snakes-masters-fasting Loss of ‘hunger hormone’ has made snakes masters of fasting By Jake Buehler Though fearsome predators, snakes can go weeks or even months without eating. Now, scientists think they may know how they do it. Snakes have lost the genes to produce ghrelin, a key hormone that regulates appetite, digestion, and fat storage, researchers report today in Royal Society Open Biology. Chameleons and a group of desert lizards called toadhead agamas that also have huge spaces between meals have also lost the same genes, hinting that cutting off ghrelin is a key way to excel at fasting, possibly by suppressing appetite and holding onto fat stores. “I give [the researchers] a lot of credit for looking more deeply into the data that was staring us all in the face—myself included,” says Todd Castoe, a genomicist at the University of Texas at Arlington not involved with the study. The hormone is ubiquitous across vertebrates, from fish to mammals. So finding that reptiles have repeatedly ditched it is “pretty remarkable,” he says. When scientists first discovered ghrelin nearly 30 years ago, they thought this “hunger hormone” could be key to fighting obesity in humans. But it hasn’t been that simple. Since then, researchers have found that ghrelin has a complicated role within a network of hormones constantly tweaking hunger and energy stores. And even though ghrelin is commonly found in vertebrates, it’s been unclear how it has evolved across various groups of vertebrates. So in the new study, Rui Resende Pinto, an evolutionary biologist at the University of Porto, and his colleagues focused on reptiles, many of which can go long periods without food. The researchers scanned the genomes of 112 species. In snakes, chameleons, and toadhead agamas, ghrelin genes were either missing or so warped by mutations they could no longer encode the hormone, the team found. The degree of the genes’ erosion also varied considerably between snake families: Some snakes such as boas and pythons had malformed ghrelin genes, but others, such as vipers, cobras, and their relatives, barely had anything left. --------------------