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Rare Gene Mutation Delays Alzheimer’s by Damping Immune Cell Inflammatory Signaling

Researchers at Weill Cornell Medicine report that a rare gene mutation that delays Alzheimer’s disease does so by damping inflammatory signaling in brain-resident immune cells in a preclinical study. The finding adds to growing evidence that brain inflammation is a major driver of neurodegenerative disorders such as Alzheimer’s—and that it may be a key therapeutic target for these disorders.

In their study “The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway,” in Immunity, the investigators examined the effects of the mutation APOE3-R136S—known as the “Christchurch mutation”—which was recently found to delay hereditary early-onset Alzheimer’s. The scientists showed that the mutation inhibits the cGAS-STING pathway, an innate immune signaling cascade that is abnormally activated in Alzheimer’s and other neurodegenerative diseases. The researchers found that pharmacologically blocking the cGAS-STING pathway with a drug-like inhibitor replicated key protective effects of the mutation in a preclinical model.

“This is an exciting study because it suggests that inhibiting this cGAS-STING pathway could make the brain more resistant to the Alzheimer’s process, even in the face of significant tau accumulation,” said study senior author Li Gan, PhD, the Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases and director of the Helen and Robert Appel Alzheimer’s Disease Research Institute at Weill Cornell Medicine.

Connected Minds: Preparing For The Cognitive Gig Economy

There’s also the risk of neuro-exploitation. In a world where disadvantaged individuals might rent out their mental processing to make ends meet, new forms of inequality could emerge. The cognitive gig economy might empower people to earn money with their minds, but it could also commoditize human cognition, treating thoughts as labor units. If the “main products of the 21st-century economy” indeed become “bodies, brains and minds,” as Yuval Noah Harari suggests, society must grapple with how to value and protect those minds in the marketplace.

Final Thoughts

What steam power and electricity were to past centuries, neural interfaces might be to this one—a general-purpose technology that could transform economies and lives. For forward-looking investors and executives, I recommend keeping a close eye on your head because it may also be your next capital asset. If the next era becomes one of connected minds, those who can balance bold innovation with human-centered ethics might shape a future where brainpower for hire could truly benefit humanity.

Toxoplasma gondii infection of neurons alters the production and content of extracellular vesicles directing astrocyte phenotype and contributing to the loss of GLT-1 in the infected brain

Infection with the obligate intracellular parasite, Toxoplasma gondii, leads to neuronal cysts in the brain for the lifetime of the host. Our lab has previously determined that chronic infection leads to loss of astrocytic glutamate transported, GLT-1, leading to neuronal excitotoxicity. GLT-1 can be regulated by neuronal derived extracellular vesicles (EVs). We wanted to determine if cyst infection of neurons altered EV production and content and if EVs derived from cyst-containing neurons changed astrocyte function. Our study found that Toxoplasma cyst infection decreased EV production by neurons and altered EV host protein and miRNA content. In addition, EVs from infected neurons contained parasite derived proteins including the secreted dense granule protein GRA7. Incubation of these EVs with astrocytes led to EV uptake, GRA7 localization to the nucleus, a decrease in GLT-1 expression, and changes in the transcriptional signature of astrocytes to a pro-inflammatory response. Finally, these changes in astrocytic gene expression could be seen in vivo following infection using scRNAseq. This study demonstrates that Toxoplasma cysts alter neuron-astrocyte communication bypassing traditional immune mechanisms of recognition and leading to changes in astrocyte function.

Citation: Tabaie EZ, Gao Z, Kachour N, Ulu A, Gomez S, Figueroa ZA, et al. (2025) PLoS Pathog 21: e1012733. https://doi.org/10.1371/journal.ppat.

Editor: Eric Y. Denkers, University of New Mexico—Albuquerque: The University of New Mexico, UNITED STATES OF AMERICA.

Your Brain Has a Hidden Rhythm, And It May Reveal How Smart You Are

The smarter you are, the more your brain is in sync with its own secret rhythm, a new study has found.

When your brain works particularly hard, different regions of the brain sync up as they work together to perform tasks that require a higher cognitive load. This is called theta connectivity, and a new study has found that not only is it highly flexible, adapting quickly to changing situations, but better brain coordination strongly correlates with cognitive ability.

“Specific signals in the midfrontal brain region are better synchronized in people with higher cognitive ability – especially during demanding phases of reasoning,” says psychologist Anna-Lena Schubert of Johannes Gutenberg University Mainz in Germany.

New study locates neuron clusters that help the brain repay sleep debt

Sleeping deeply into the afternoon after an all-nighter or a late night out is one way the body repays its sleep debt. The sleep-wake cycle is regulated by a homeostatic process in which the body continuously adjusts its physiological systems to maintain a balanced state of rest and alertness.

A new study identified a specific group of neurons called REVglut2 located in the center of the brain, in the thalamus, that may help us uncover how lost sleep is recovered in animals.

The researchers found that in mice, this circuit, consisting of excitatory neurons, is triggered during and induces drowsy behavior, followed by that can last for hours.

Zoning out could be beneficial—and may actually help us learn faster

Aimlessly wandering around a city or exploring the new mall may seem unproductive, but new research from HHMI’s Janelia Research Campus suggests it could play an important role in how our brains learn.

By simultaneously recording the activity of tens of thousands of neurons, a team of scientists from the Pachitariu and Stringer labs discovered that learning may occur even when there are no specific tasks or goals involved.

Published in Nature, the new research finds that as animals explore their environment, neurons in the visual cortex—the brain area responsible for processing —encode visual features to build an internal model of the world. This information can speed up learning when a more concrete task arises.

A universal sleep pattern could help strengthen and separate memories

Although we know sleep is essential to our physical and mental well-being, it remains an incredibly enigmatic behavior, scientifically speaking. Researchers at the University of Michigan, however, may have developed a new hypothesis to account for one of sleep’s looming mysteries.

Every living thing that sleeps appears to follow the same basic pattern. From wakefulness, organisms transition to a repeating cycle of sleep with low followed by a stage where our brains are harder at work, among other things, generating vivid dreams. Humans’ eyes also dance around behind our eyelids during that high-activity stage, which is why it’s referred to as (REM) sleep.

Although there are a few notable exceptions—including people with narcolepsy and people who haven’t slept in days—this repeating non-REM to REM sleep cycle is remarkably prevalent across the .