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‘Tour de force’ mouse study shows a gut microbe can promote memory loss

Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut.

In a new study, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found.


Research suggests the microbiome may contribute to cognitive decline—but its relevance in humans is unclear.

Atypical Development of Functional Brain Networks in Neonates with Congenital Heart Disease

New in JNeurosci: fMRI study from Kim et al. reveals that babies with congenital heart disease have altered sensorimotor and limbic brain networks that cardiovascular surgery improves.

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Congenital heart disease (CHD) affects approximately 1% of live births in the United States and is the most prevalent congenital disorder. Despite advances in neonatal cardiovascular surgery improving survival, neurodevelopmental impairments remain prevalent, impacting motor skills, social behavior, and executive function. Motor deficits and long-term challenges in emotional regulation and memory are particularly common. Recent research using resting-state functional MRI (rs-fMRI) has revealed disorganized brain networks in newborns with CHD. However, those few prior rs-fMRI studies examining the impact of CHD have relied on predefined brain parcellations to compare group-level connectivity, limiting the ability to capture spatial alterations in neonatal brain networks in CHD. Understanding these network-level changes is critical for elucidating mechanisms of neurodevelopmental impairment and identifying early biomarkers of risk. To address these gaps, our study introduces two conceptual advances: 1) a data-driven approach to investigate atypical brain network development in high-risk CHD and 2) the use of a population-sized, independent dataset of healthy newborns to derive a normative set of neonatal brain networks. By analyzing a large rs-fMRI of human newborns (N=448; 219 females and 229 males), we identify atypical brain activity in the sensorimotor and limbic networks of newborns with complex CHD. Notably, before cardiovascular surgery, these networks are split into left and right hemispheric subnetworks. Postoperatively, these components coalesce into a singular, symmetric pattern resembling networks observed in healthy neonates. Our study highlights the potential of rs-fMRI to detect subtle, early functional disruptions in CHD and may inform future biomarkers of neurodevelopmental risk.

Significant Statement Congenital heart disease, the most common congenital disorder, affects 1% of live births and is associated with persistent neurodevelopmental impairments despite improved surgical survival. These deficits, including motor, socio-emotional, and cognitive challenges, may stem from early brain network disruptions. Prior resting-state fMRI studies in CHD relied on predefined parcellations, limiting detection of subtle spatial alterations. In this study, we used a data-driven approach and leveraged an independent normative dataset to define resting-state networks. Comparing CHD patients and healthy controls against these independently derived networks, we reveal atypical sensorimotor and limbic network organization preoperatively, which normalizes post-surgery. These findings highlight the potential of rs-fMRI to identify early biomarkers of neurodevelopmental risk and guide targeted interventions in this high-risk population.

Potassium channels functionality is coupled to trafficking!

In a study published recently in PNAS, researchers have revealed the relationship between KCNQ2/3 channel functionality (i.e., how well they work to control electrical signals in neurons) and localization (i.e., where they are found inside a cell), with important implications for the treatment of these epileptic disorders.

For KCNQ2/3 channels to work properly in the brain, they must have full functionality and be located in the correct cellular region – specifically the axon initial segment (AIS), the site in neurons where electric signals are first triggered, controlling nerve cell activity. This led the research team to wonder: does the functionality of KCNQ2/3 channels affect their cellular localization, or are the two not linked at all?

To investigate this potential association, the research team first genetically engineered the functionality of the channels, and then used channel trafficking imaging to visualize whether the channels were taken to their location in the AIS. In this way, they demonstrated that KCNQ2/3 functionality was indeed linked to its trafficking to the correct cellular localization. What’s more, when they used single-molecule imaging, they could see that reduced KCNQ3 functionality actually reduced the AIS localization of KCNQ2/3 by altering the entire trafficking pathway.

“Because we already knew that the localization of KCNQ2/3 to the AIS is regulated by a protein known as ankyrinG, or ankG, we next decided to explore the interactions between full-length KCNQ3 and ankG,” explains lead author of the study. “We found that the active conformation of KCNQ3 was essential for its stable binding to ankG, further confirming that functional KCNQ2/3 is needed to ensure its proper accumulation at the AIS.”

Together, these findings highlight the mechanisms underlying the important link between KCNQ2/3 functionality and localization, and provide clues about how their alterations might affect neuronal excitability. ScienceMission sciencenewshighlights.


Potassium KCNQ2/3 channels are crucial for suppressing the excitability of brain cells, or neurons. When these channels don’t work properly, they can cause specific types of epilepsy like benign familial neonatal convulsions and early infantile epileptic encephalopathy.

Developmental reprogramming in melanocortin neurons modulates diet-induced obesity in mice

Reprogramming in melanocortin modulates diet-induced obesity.

Hypothalamic proopiomelanocortin (POMC) neurons promote satiety, while agouti-related peptide (AgRP) neurons drive hunger and maintain energy balance.

However, it is not clear how the system is diversified developmentally.

The researchers in this study show that transcription factor Otp act as a developmental ‘‘switch’’ in the hypothalamus and determines whether immature neurons become appetite suppressing (POMC) or appetite stimulating (AgRP).

Disrupting this switch reshapes feeding behavior and protects mice from obesity, revealing how early life programming shapes lifelong metabolic health. sciencenewshighlights ScienceMission https://sciencemission.com/melanocortin-neurons-modulates-diet-induced-obesity


Xu et al. show that a developmental “switch” in the hypothalamus determines whether immature neurons become appetite suppressing or appetite stimulating. Disrupting this switch reshapes feeding behavior and protects mice from obesity, revealing how early-life programming shapes lifelong metabolic health.

Immune cells in the brain may tune fertility hormones, animal study suggests

The kick-off signal for puberty begins in the brain. Specifically, in the hypothalamus, where specific neurons release a hormone that activates the hypophysis, at the base of the skull, which then releases other hormones to start gonad—ovaries or testicles—maturation. This mechanism leading to a fertile organism is the hypothalamic-pituitary-gonadal (HPG) axis.

A study by Spain’s National Cancer Research Center (CNIO) has discovered in animal models that two previously unsuspected elements are also involved in this hormone regulating system: microglia—defensive cells of the nervous system—and the protein RANK, which contributes to bone remodeling and is essential in the functioning of the mammary glands.

The work is published in the journal Science. It is led by Eva González-Suárez, head of the CNIO Transformation and Metastasis Group, who discovered in 2010 the key role played by RANK in the development of breast cancer. The first author is Alejandro Collado, a researcher from the same group and co-corresponding author.

A new reagent makes living brains transparent for deeper, non-invasive imaging

Making a living brain transparent and watching its neurons fire without disturbing their function—sounds like science fiction, doesn’t it? Yet the solution may already exist within our own bodies. In a paper published in Nature Methods, a research team led by Kyushu University introduces a new reagent called SeeDB-Live.

SeeDB-Live uses albumin—a common protein in blood serum—to clear tissue while preserving cellular function. The technique allows scientists to see deeper, brighter structures in both brain slices in a dish and living mice, achieving neural activity that was previously out of sight.

“This is the first time tissue clearing has been achieved without altering its biology,” says Takeshi Imai, professor at Kyushu University’s Faculty of Medical Sciences and the study’s senior author.

Plasma Phosphorylated Tau 217 and Incident MCI and Dementia in Older Women

In this cohort study of cognitively unimpaired older women, p-tau217 was associated with incident MCI or dementia up to 25 years later.


This cohort study examines associations of baseline plasma phosphorylated tau 217 with incident mild cognitive impairment (MCI) or dementia and whether associations vary by age, race, APOE ε4 carrier status, or hormone therapy use among older men and women.

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