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Category: neuroscience

Injured once, triggered forever? How the brain rewrites stress responses

A wound can leave a lasting imprint—even after it has healed. A new study in Current Biology finds that past injuries can quietly prime the body to overreact and be more sensitive to stress, pain and fear long after the damage is gone.

These findings may help explain how early injuries or trauma can set the stage for , where the remains hypersensitive long after the initial damage has healed. can set the stage for conditions, where the nervous system remains hypersensitive long after the initial damage has healed.

Researchers at the University of Toronto Mississauga discovered that mice with a history of responded more intensely to the scent of a predator, an extremely stressful event for mice. These mice showed exaggerated and developed long-lasting pain in both hind paws, including the uninjured side. Strikingly, the symptoms lasted more than six months, long after the original injury had physically healed.

Early developmental origins of cortical disorders modeled in human neural stem cells

The implications of early telencephalic development in cortical disorders remain elusive. Here, the authors define risk gene dynamics and perturbation effects in neural stem cells, revealing vulnerability phases during early human corticogenesis.

Imaging Copper Levels during Life in the Brain and beyond Using a Fluorescent Copper Sensor with Multimodal Capacity

Copper is an essential trace element for normal development and function throughout the body, including the central nervous system (CNS). Alterations to cellular copper levels result in severe neurological consequences and are linked to a range of CNS disorders, positioning treatments that restore copper balance as promising therapies for these disorders. However, despite the clear relationship between copper balance and CNS health, there are limited tools to measure copper levels in vivo in humans. This constitutes a significant challenge for both diagnosing disorders of copper imbalance and monitoring the efficacy of copper-altering treatments for these disorders. Here we report the synthesis and characterization of Fluorine-labeled Naphthalimide Copper sensor 1 (F-NpCu1), a fluorescent sensor for copper that contains a fluorine atom for future radiolabeling for clinical application. We demonstrate that the probe exhibits good stability and is highly selective for copper above other transition metals present in biological tissues. Copper binding promotes covalent bond formation between the sensor and proximal cellular proteins. F-NpCu1 is nontoxic and can be measured using fluorescence microscopy in living cells and fixed tissue sections from both mouse brain and pancreas. Furthermore, F-NpCu1 exhibits good blood-brain-barrier permeability and can report differences in brain copper levels induced by copper modulating therapies in living mice using intravital fluorescence microscopy. This study represents a promising advance toward the development of the first clinical tool for measuring copper in living humans, including in the CNS, with radiolabeling studies underway to develop 18F-NpCu1 for PET imaging of copper in vivo.

Scientists Find 2 Existing Drugs Can Reverse Alzheimer’s Brain Damage in Mice

In efforts to beat Alzheimer’s disease, researchers are looking at existing drugs that could tackle the condition, and a new study identifies two promising candidates that are currently used to treat cancer.

Already approved by regulators in the US – meaning potential clinical trials for Alzheimer’s could start sooner – the drugs are letrozole (usually used to treat breast cancer) and irinotecan (usually used to treat colon and lung cancer).

Researchers from the University of California, San Francisco (UCSF) and Gladstone Institutes started by looking at how Alzheimer’s altered gene expression in the brain.

Brain peptide ODN reduces hunger and boosts glucose regulation in rat study

University of Pennsylvania and Syracuse University scientists have discovered that a hindbrain-derived peptide, octadecaneuropeptide (ODN), can suppress appetite and improve glucose regulation without causing nausea or vomiting. Results suggest a glia-to-neuron signaling axis in the dorsal vagal complex that may be harnessed for treating obesity and type 2 diabetes.

Glial cells in the brainstem produce ODN, a signaling peptide whose physiological role in energy homeostasis has remained obscure. Researchers now find that directly activating this peptide system in the hindbrain induces weight loss, enhances glucose disposal, and lowers in obese animals.

Unlike existing therapies targeting GLP-1 receptors, ODN achieves these effects without triggering nausea-related behaviors or emesis in vomiting-competent models.