A team led by Northwestern University and Shirley Ryan AbilityLab scientists have developed a new technology that can eavesdrop on the hidden electrical dialogues unfolding inside miniature, lab-grown human brain-like tissues. Known as human neural organoids—and sometimes called “mini brains”—these millimeter-sized structures are powerful models of brain development and disease. But until now, scientists could only record and stimulate activity from a small fraction of their neurons—missing network-wide dynamics that give rise to coordinated rhythms, information processing and the complex patterns of activity that define brain function.

For the first time, the new technology overcomes that stubborn limitation. The soft, three-dimensional (3D) electronic framework wraps around an organoid like a breathable, high-tech mesh. Rather than sampling select regions, it delivers near-complete, shape-conforming coverage with hundreds of miniaturized electrodes. That dense, three-dimensional interfacing enables scientists to map and manipulate neural activity across almost the entire organoid.

By moving from localized probing to true whole-network mapping, the work brings organoid research closer to capturing how real human brains develop, function and even fail.

In a large US-based brain imaging study, researchers found that these drugs do not primarily affect attention networks, but instead act on systems linked to arousal, sleep, and motivation.

The puzzle of ADHD stimulants

Prescription stimulants such as methylphenidate and amphetamines are among the most used psychoactive drugs in children and adolescents with ADHD, where they remain a first-line treatment. Estimates for receiving a prescription for ADHD medication among diagnosed children vary from 38–81%. Despite their widespread use, there is still disagreement about how these drugs work in the brain.

Tumor-immune-neural circuit in cancer cachexia.

The mechanisms involved in cancer-mediated cachexia and anorexia are not well understood.

The researchers in this study delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia.

The authors show thay loss of GDF15 protects against appetite loss, muscle wasting, and fat loss in pancreatic, lung, and skin cancers.

Disrupting this feedforward loop with GDF15-neutralizing antibody, anti-CSF1R antibody, or Rearranged during Transfection (RET) inhibitor alleviates cachexia and anorexia across cancer models. sciencenewshighlights ScienceMission https://sciencemission.com/Tumor-immune-neural-circuit

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Shi et al. delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia. Specifically, tumor-derived CSF1 induces macrophage GDF15, which signals through the GFRAL-RET neural axis to enhance β-adrenergic activity and systemic wasting. Disrupting this feedforward loop alleviates cachexia across cancer models.

Researchers at UT Southwestern Medical Center have discovered that a crucial developmental process in the brain’s hypothalamus may influence how susceptible individuals are to obesity. Their preclinical findings, published in Neuron, show that a transcription factor called Otp acts as a molecular “switch” that directs immature hypothalamic neurons toward either appetite-suppressing or appetite-stimulating fates—their ultimate identities as specialized cells. The researchers found that disrupting this switch alters feeding behavior and protects mice from diet-induced obesity.

“These findings show that early developmental decisions in the hypothalamus have a long-lasting impact on energy balance,” said senior author Chen Liu, Ph.D., Associate Professor of Internal Medicine and Neuroscience and an Investigator in the Peter O’Donnell Jr. Brain Institute at UT Southwestern.

“By uncovering this fate-switching program, we can begin to understand how the brain establishes lifelong metabolic set points.”