Lymphoid gene expression supports neuroprotective microglia function
TL;DR
Brain immune cells called microglia can either protect against or worsen Alzheimer's disease, and scientists found that a specific protein called CD28 helps these cells stay in "protective mode" by reducing harmful brain inflammation. This discovery could lead to new treatments that boost the brain's natural defenses against Alzheimer's.
Abstract Microglia, the innate immune cells of the brain, play a defining role in the progression of Alzheimer’s disease (AD) 1 . The microglial response to amyloid plaques in AD can range from neuroprotective to neurotoxic 2 . Here we show that the protective function of microglia is governed by the transcription factor PU.1, which becomes downregulated following microglial contact with plaques. Lowering PU.1 expression in microglia reduces the severity of amyloid disease pathology in mice and is linked to the expression of immunoregulatory lymphoid receptor proteins, particularly CD28, a surface receptor that is critical for T cell activation 3,4 . Microglia-specific deficiency in CD28, which is expressed by a small subset of plaque-associated PU.1 low microglia, promotes a broad inflammatory microglial state that is associated with increased amyloid plaque load. Our findings indicate that PU.1 low CD28-expressing microglia may operate as suppressive microglia that mitigate the progression of AD by reducing the severity of neuroinflammation. This role of CD28 and potentially other lymphoid co-stimulatory and co-inhibitory receptor proteins in governing microglial responses in AD points to possible immunotherapy approaches for treating the disease by promoting protective microglial functions.
- 1Microglia brain immune cells have both protective and harmful responses to amyloid plaques in Alzheimer's disease
- 2The transcription factor PU.1 controls protective microglial function but gets turned down when microglia encounter amyloid plaques
- 3CD28, a receptor protein normally found on immune T cells, is expressed by a small subset of protective microglia near plaques
- 4Mice lacking CD28 in their microglia showed increased brain inflammation and more amyloid plaque buildup
- 5PU.1-low, CD28-expressing microglia act as suppressive cells that reduce neuroinflammation and slow Alzheimer's progression
M87's black hole flipped its magnetic field
Imagine a bar magnet with a north and south pole. Now imagine that magnet suddenly flipping so north becomes south and vice versa. That's essentially what happened with the magnetic field around the giant black hole at the center of galaxy M87 — except this black hole is 6.5 billion times heavier than our Sun. Scientists noticed this flip by watching the powerful beam of energy, called a jet, that shoots out from the black hole. The direction and behavior of that beam changed in a way that revealed the magnetic field had reversed. It's a big deal because those magnetic fields are thought to act like the engine that powers and steers these cosmic jets, and we've rarely caught one flipping in action.
The 2026 World Cup's grass is an engineering problem
Imagine you're trying to play soccer in 16 different places across the United States, Canada, and Mexico — some in freezing cold, some blazing hot, some in stadiums with roofs that block sunlight. Half of those stadiums normally use fake grass. Now FIFA, the organization that runs the World Cup, wants every single pitch to feel and play exactly the same way, like a video game where every level has identical physics. To do that, they hired grass scientists — yes, that's a real job — who figured out how to grow special grass on thin mats with plastic underneath so it can be transported like a carpet, stitched with synthetic fibers so it doesn't rip when players sprint and tackle, and tested by literally shooting balls at it with a cannon to make sure it bounces right. Different grass species are used depending on whether a stadium is hot, cool, or dark. It's basically a giant, living, high-tech floor installation that has to survive the world's best athletes running on it.
Non-Mendelian inheritance of DNA methylation patterns in mice
Imagine your DNA is like a huge book of instructions. Mendel's laws are the normal rules for how chapters of that book get passed from parents to children. But there's also a layer of sticky notes on top of the book—called epigenetic marks—that tell cells which chapters to read and which to ignore. This study found that most of the time (about 93%), these sticky notes follow the normal inheritance rules. But about 7% of the time, they do something unexpected: new patterns appear that neither parent had, or a mark from one parent somehow silences the same mark from the other parent (called paramutation), or males and females end up with completely different sticky notes even when they inherit the same DNA. Scientists discovered this by using a new ultra-precise DNA reading technology in mice, and it opens the door to understanding hidden layers of how traits—and possibly diseases—are passed down through generations.
Digital twin–guided ablation for ventricular tachycardia
Imagine your heart is a city, and ventricular tachycardia is like a traffic jam caused by a broken road — electrical signals get stuck going in circles instead of flowing properly, causing the heart to beat dangerously fast. Doctors can fix this by burning away the broken road using a procedure called ablation. The problem is, finding the exact broken road inside a beating heart is like navigating a city you've never visited before, while driving, in the dark. What these researchers did is take detailed MRI pictures of each patient's heart, build a 3D computer copy — a 'digital twin' — and then simulate where the electrical problem was happening inside that virtual heart. They tested their fix on the computer model first, figured out exactly where to go, and THEN performed the real procedure. What used to take three hours of exploratory surgery was done in about 30 minutes, because the doctors already had a GPS map before they started.
