In 1972, Britain bumped up the total school years mandated for its children from 15 to 16 years. That created a “natural experiment”: Would Britons who got that extra year of education fare any better, neurologically, as they aged? Unfortunately, the answer is “no.” “This surprised us,” said study co-author and brain researcher Nicholas Judd, from Radboud University Medical Center (Radboudumc) in Nijmegen, The Netherlands. “We know that education is beneficial, and we had expected education to provide protection against brain aging,” he said in a medical center news release. “Aging shows up in all of our MRI measures, for instance we see a decline in total volume, surface area, cortical thickness and worse water diffusion in the brain. However, the extra year of education appears to have no effect here.” The findings were published Nov. 5 in the journal eLife. Judd and Radboudumc co-researcher Rogier Kievit accessed the MRI brain scans of more than 30,000 adult Britons taken an average of 46 years after they attended school in the early 1970s. Education has long been associated with brain resiliency, so it was assumed that the brains of people who went to school that extra year might differ in subtle ways from those who graduated before the new law was enacted. But Judd and Kievit saw no differences in various aspects of brain structure that they…  read on >  read on >

Poorer folks’ access to blockbuster weight-loss drugs through Medicaid remains limited, a new KFF analysis has found. Only 13 states currently allow Medicaid to cover treatment of obesity using glucagon-like peptide-1 agonist (GLP-1) medications, researchers discovered. Under the Medicaid system, individual states are allowed to decide whether to cover GLP-1 drugs, which include Wegovy (semaglutide), Zepbound (tirzepatide) and Saxenda (liraglutide), the KFF report noted. Among those states that don’t cover the drugs, half reported that they are considering adding coverage in the near future, the researchers added. But GLP-1 drugs are pricey, and nearly two-thirds of states said cost is a hurdle to approving coverage of the meds through Medicaid. “Expanding Medicaid coverage of these drugs could increase access for the almost 40% of adults and 26% of children with obesity in Medicaid,” wrote the research team led by senior investigator Clea Bell, a research assistant in state health reform for KFF. “At the same time, expanded coverage could also increase Medicaid drug spending and put pressure on overall state budgets.” Glucagon-like peptide-1 (GLP-1) drugs mimic the GLP-1 hormone, which helps control insulin and blood sugar levels, decreases appetite and slows digestion of food. However, the drugs are costly — people without insurance face paying more than $1,000 a month to take them. The 13 states where Medicaid covers GLP-1 drugs for obesity are California,…  read on >  read on >

Current treatments sometimes fail to help people with “wet” age-related macular degeneration — and researchers now think they know why. Wet AMD is caused by an overgrowth of blood vessels in the retina, the light-sensing tissue at the back of the eye. The vessels leak fluid or bleed, damaging the retina and causing vision loss. To combat this, doctors prescribe medications that slow the growth of new blood vessels, called anti-VEGF (vascular endothelial growth factor) drugs. Unfortunately, these anti-VEGF drugs might actually hamper vision improvements by triggering the over-expression of a second blood-vessel-related protein, researchers have discovered. This second protein, ANGPTL4, also can stimulate overproduction of abnormal blood vessels in the retina, researchers reported Nov. 4 in the Proceedings of the National Academy of Sciences. These findings could explain why fewer than half of patients who receive monthly anti-VEGF eye injections wind up showing any major improvements in their vision, researchers said. “We have previously reported that ANGPTL4 was increased in patients who did not respond well to anti-VEGF treatment,” said researcher Dr. Akrit Sodhi, an associate professor of ophthalmology at the Johns Hopkins University School of Medicine, in Baltimore. “What we saw in this paper was a paradoxical increase of ANGPTL4 in patients that received anti-VEGF injections — the anti-VEGF therapy itself turned on expression of this protein,” Sodhi said in a Hopkins news…  read on >  read on >

Many people turn to mindfulness meditation to help them manage their chronic pain, a practice that’s been used for centuries. However, it’s been an open question whether meditation is simply functioning as a placebo, rather than actually quelling pain. Now, a new study involving brain scans has revealed that’s not the case. Mindfulness meditation engages distinct brain mechanisms to reduce pain, and those are not part of a placebo response, researchers reported. “These two brain responses are completely distinct, which supports the use of mindfulness meditation as a direct intervention for chronic pain rather than as a way to engage the placebo effect,” said lead researcher Fadel Zeidan, a professor of anesthesiology with the University of California, San Diego. For the study, researchers recruited 115 healthy people and randomly placed them into four different treatment groups: An actual mindfulness meditation practice that involved focusing on breath without judgment A sham meditation practice that only consisted of deep breathing A placebo cream that patients were trained to believe reduce pain A control group that listened to an audiobook The team then applied a very painful but harmless heat stimulus to the back of every person’s leg and scanned their brains, to see how each responded to the pain. Placebo cream and the sham medication practice both lowered pain, but mindfulness meditation was significantly more effective at…  read on >  read on >

Huntington’s disease is a devastating, fatal neurological illness with little means of treatment, but a new study in mice offers a glimmer of hope. Huntington’s occurs when inherited genes cause key proteins to fold and clump together within brain cells. Over time, this severely hampers brain function and patients lose the ability to talk, walk, swallow and focus. There’s no cure, and the illness is typically fatal within a decade or two of symptom onset. However, new research in mice is investigating the utility of “peptide-brush polymers” as treatment. The peptides involved in the therapy are naturally occurring proteins that may block the lethal clumping of Huntington’s-associated proteins within brain cells. In studies conducted in a mouse model of Huntington’s, use of the polymer treatment appeared to “rescue” brain cells harmed by protein clumping and reverse Huntington’s symptoms, a joint team from Northwestern University and Case Western Reserve University reported. Of course, studies in mice sometimes fail to deliver the same results in people. Nevertheless, study co-lead author Nathan Gianneschi, of Northwestern University in Chicago, said “it’s quite compelling when you see animals behave more normally than they would otherwise” after the polymer treatment. Gianneschi, a professor of chemistry at Northwestern, has a personal stake in the new research. “My childhood friend was diagnosed with Huntington’s at age 18 through a genetic test,” he said in…  read on >  read on >