https://www.quantamagazine.org/how-the-bird-eye-was-pushed-to-an-evolutionary-extreme-20260513/ How the Bird Eye Was Pushed to an Evolutionary Extreme By Yasemin Saplakoglu When an optometrist shines a bright light into your eyes, a vast, branching tree sprouts in your field of vision. This is the shadow of blood vessels. Though we normally can’t perceive them, these vessels always occlude a portion of what we see, and for an important reason. They power the retina, a thin layer of nerve tissue in the back of the eye that communicates light signals to the brain. The retina is one of the body’s most energetically expensive tissues. Built from complex networks of sometimes more than 100 different types of neurons, retinal tissue consumes two to three times more energy than the same mass of typical brain tissue. That’s why most vertebrate retinas, including our own, are furrowed with dense, branching networks of blood vessels: to deliver oxygen and other ingredients for producing energy. But there’s a significant exception to this rule. Birds have retinas that mostly lack blood vessels. This may seem especially strange given birds’ exceptional vision. The bird retina is “one of the most metabolically active tissues in the animal kingdom, yet it worked with no apparent blood perfusion,” said Christian Damsgaard (opens a new tab), an evolutionary physiologist at Aarhus University. “It was a complete paradox.” For centuries this has puzzled scientists, who figured that the bird retina must obtain oxygen through a unique, undiscovered process. Damsgaard is the lead author of a study, published in the journal Nature (opens a new tab) in January 2026, that showed for the first time that bird retinas don’t have some unusual adaptation for acquiring oxygen — they survive without it entirely. Instead, to bring energy to the tissue, they use a process called anaerobic glycolysis that is significantly less efficient than oxygen-powered metabolism but gets the job done. © 2026.Simons Foundation -------------------- https://knowablemagazine.org/content/article/mind/2026/genetic-disease-reveals-role-of-brain-amygdala A social compass in the brain By Richard Stone The wind picks up dust from the unpaved road one afternoon in December as Jack van Honk turns into a ramshackle neighborhood in Lambert’s Bay, on the west coast of South Africa. A stocky woman in a red patterned sundress steps out of a small home painted palest sea green, her ochre-dirt yard crowded with potted plants, many medicinal. She smiles broadly, deep wrinkles creasing a face that is cherubic and yet careworn beyond her 47 years. “Doctor! I missed you,” she beams, her husky voice barely more than a hoarse whisper. Maria carries a rare genetic mutation that is almost unknown outside of southern Africa. Its effects have been to calcify a part of the brain called the basolateral amygdala, and to thicken and scar the vocal cords. A friend of Maria with the same condition lives several hours inland, and sometimes they meet when van Honk brings them to Cape Town for brain scans and other tests. “It helps to know I’m not alone,” Maria says. By every measure of daily life — holding down a job, keeping a household running, raising two teenage sons — Maria is competent and engaged. “You talk to her, and you don’t see anything wrong,” says van Honk, a social neuroscientist at the University of Cape Town. She and others he knows with her condition, Urbach-Wiethe disease, “are kind, sweet people by nature.” In an interview in her kitchen, Maria struggles to recollect even a fleeting moment of unhappiness — before mentioning that she kicked out her partner some years ago because of his drinking. Photograph of a woman in a red dress standing in her yard. Maria lives with a rare genetic disorder that damages part of the amygdala — a brain region increasingly linked not just to fear, but to how humans weigh the needs of others. -------------------- https://www.nytimes.com/2026/05/06/well/als-treatment-tofersen-qalsody.html?searchResultPosition=1 In a Milestone for A.L.S., a Treatment Helps Some Patients Improve By Pam Belluck Time was running out for Amanda Sifford, she and her doctors could tell. A.L.S., the paralyzing neurological disorder, was stealing her ability to breathe. On a breathing test, her lung function was only at 48 percent of capacity, a sharp drop from 86 percent five months earlier. “I couldn’t take 10 steps and be able to breathe,” she said. “I could no longer step up on a curb.” Ms. Sifford, 58, a school psychologist in Cape Coral, Fla., has lost 14 family members, including her father and grandfather, to a rare genetic form of A.L.S., also known as amyotrophic lateral sclerosis or Lou Gehrig’s disease. Her symptoms had been developing gradually, but her breathing suddenly nose-dived. “It was very scary,” said Dr. Nathan Carberry, one of her neurologists at the University of Miami Health System. “I worried that we were looking at months of life left.” “Was I thinking about dying?” said Ms. Sifford, pausing to collect herself. “I had my affairs in order.” It was May 2023, and the Food and Drug Administration had just approved the first therapy for a genetic form of A.L.S., even though clinical trial results had not yet proven the drug would be effective. The drug, tofersen, made by Biogen and marketed as Qalsody, targets the form of A.L.S. that Ms. Sifford inherited, so Dr. Carberry and Dr. Michael Benatar, the executive director of University of Miami A.L.S. Center, scrambled to establish a clinic to administer it. She began receiving tofersen monthly, through infusions into her spinal canal. © 2026 The New York Times Company -------------------- https://www.science.org/content/article/most-dementia-patients-have-multiple-brain-diseases-how-should-they-be-treated Most dementia patients have multiple brain diseases. How should they be treated? By Jennie Erin Smith About 20 years ago, neuropathologists began to report an inconvenient finding in the autopsied brains of people with dementia: Most have evidence of more than one disease. Studies since have shown the brains of up to half of people diagnosed with Alzheimer’s disease also have a key feature of Parkinson’s disease—deposits of the protein alpha synuclein. At the same time, up to half of Parkinson’s patients who develop dementia have elevated levels of beta amyloid and tau proteins, hallmarks of Alzheimer’s. Researchers studying neurodegenerative diseases are catching on to the importance of this phenomenon, often called copathology. It complicates current disease classifications, which are tightly linked to their signature proteins. But it also offers clues as to why some dementia patients show faster cognitive decline, and some people on antiamyloid drugs for Alzheimer’s seem to fare worse than others. Copathology “helps explain why symptoms don’t match biomarkers, why trajectories vary so much, and why treatment results are not necessarily what we expect them to be,” neuropathologist Lea Grinberg of the Mayo Clinic told researchers at the Alzheimer’s and Parkinson’s Diseases Conference (AD/PD) in March. Why the diseases overlap so often remains a mystery, but it’s not a coincidence. “It seems that they stimulate each other,” Grinberg says. Tests now being developed to pick up multiple biomarkers should give a clearer picture of these mixed pathologies in living patients. And an upcoming clinical trial will be the first to take aim at a common dementia copathology, testing the amyloid-clearing Alzheimer’s drug donanemab in people who have both amyloid in their brains and dementia with Lewy bodies—abnormal clumps of alpha synuclein. © 2026 American Association for the Advancement of Science. -------------------- https://www.nytimes.com/2026/05/04/well/mind/gut-brain-fog-health.html?searchResultPosition=1 Foggy Brain? Maybe It’s Your Gut. By Christina Caron Dr. Kyle Staller is a gastroenterologist, so it may be surprising that many of his patients come to him complaining not only about stomach trouble but about their brains, too. Irritable bowel syndrome and other digestive dysfunction can be accompanied by a mental haze. People experiencing constipation and bloating, for example, may describe “a sense of heaviness or being weighed down both physically and mentally,” said Dr. Staller, who works at Massachusetts General Hospital in Boston. “So many of my patients talk about problems like fatigue, brain fog and feeling sluggish,” he added. Scientists are making progress in understanding how the pathway between the brain and the digestive system influences our overall health. They call it the gut-brain axis, and it has been shown to play a big role in immune system support, anxiety, depression, metabolism and disease prevention. It can also affect mental clarity. We asked scientists and clinicians what to know about the gut and brain fog. How does the gut-brain axis work? There are thousands of fibers running from the brain to the abdomen that are known as the vagus nerve. It is a primary conduit of the gut-brain axis. And as the main nerve of the parasympathetic nervous system, it helps the body rest, digest and deter inflammation. Signals also travel back and forth between the gut and brain via stress hormones and immune cells. Crucially, gut bacteria produce chemical messengers (called neurotransmitters) like serotonin, dopamine and GABA that affect the nervous system. When they enter the bloodstream or stimulate the vagus nerve, they can help improve mood, drive motivation, and calm the nervous system. © 2026 The New York Times Company -------------------- https://www.sciencenews.org/article/rats-tickling-preference-happiness Female rats like a different kind of tickling than males By Hannah Thomasy For nearly a decade, Vincent Bombail has been tickling rats. It’s been a standard technique used in the study of animal happiness. But not all rats particularly enjoy the experience, data show. Female rats prefer gentler, more playful tickling than males, Bombail and his colleagues report April 15 in Biology Letters. The findings suggest that the same physical experience evokes a different emotional response in different individuals, potentially influencing the results of studies on animal happiness. “This research helps us understand these animals as playful but also rich and complex and having opinions,” says Daniel Weary, an animal welfare scientist at the University of British Columbia who was not involved in the study. “Understanding the affective lives of animals is actually one of the coolest and most difficult questions there is in science,” he says. As early as the 1930s, researchers deliberately exposed rats to standardized negative experiences to study the physical effects of stress. Figuring out how to study positive experiences took longer. It wasn’t until the 1990s that researchers developed the standard tickling protocol, where a researcher flips a rat over, pins it on its back and tickles its belly. The protocol is intended to mimic the rough-and-tumble play of young male rats. © Society for Science & the Public 2000–2026. --------------------