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New MRI approach maps brain metabolism, revealing disease signatures

A new technology that uses clinical MRI machines to image metabolic activity in the brain could give researchers and clinicians unique insight into brain function and disease, researchers at the University of Illinois Urbana-Champaign report. The non-invasive, high-resolution metabolic imaging of the whole brain revealed differences in metabolic activity and neurotransmitter levels among brain regions; found metabolic alterations in brain tumors; and mapped and characterized multiple sclerosis lesions—with patients only spending minutes in an MRI scanner.

Led by Zhi-Pei Liang, a professor of electrical and computer engineering and a member of the Beckman Institute for Advanced Science and Technology at the U. of I., the team reported its findings in the journal Nature Biomedical Engineering.

“Understanding the brain, how it works and what goes wrong when it is injured or diseased is considered one of the most exciting and challenging scientific endeavors of our time,” Liang said. “MRI has played major roles in unlocking the mysteries of the brain over the past four decades. Our new technology adds another dimension to MRI’s capability for brain imaging: visualization of brain metabolism and detection of metabolic alterations associated with brain diseases.”

Cerebellum may set the stage for development of mental empathy in early childhood

We can’t see what other people are thinking, so we have to infer it and that’s very crucial for our communication as humans. That’s how we create shared meaning and that’s how we choose our words to be understood, a kind of mental empathy.

A pivotal milestone in the development of Theory of Mind reasoning occurs between the ages of 3 and 5 years, a breakthrough period in which children typically start succeeding in false-belief tasks, widely regarded as a critical test of Theory of Mind abilities. These tasks require children to recognize false beliefs held by a story character, typically in the context of the character’s mental misrepresentations regarding an object’s location, content, or nature. Successfully passing false-belief tasks is argued to reflect the emergence of representations of others’ mental states.

To find out more about this critical period where evolves, scientists from the Max Planck Institute for Human Cognitive and Brain Sciences used collected data from 41 children between 3 and 12 years old.

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.

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