Researchers at Johns Hopkins Medicine say they have successfully demonstrated that disrupting an eye structure long suspected of blocking the growth and survival of transplanted nerve cells may help restore vision in people with optic nerve damage.

A report on the experiments with animals, stem cells and donated eye tissue was published in Science Translational Medicine. It suggests that altering or removing a thin layer of tissue called the internal limiting membrane, which separates the light-sensing retinal tissue at the back of the eye from the gel-like vitreous fluid that fills the eye, could help transplanted retinal ganglion cells (RGCs) survive and grow in people with blinding optic nerve damage.

Such damage, also known as optic neuropathy, occurs when retinal ganglion cells die of disease, inflammation or injury and stop carrying electrical signals to the brain. Common causes of damage include glaucoma, optic nerve inflammation (optic neuritis) and ischemic optic neuropathy (sudden loss of blood flow to the optic nerve).

Gait impairments such as freezing, weakness and imbalance remain resistant to standard therapies across neurological disorders. This Review examines advances in neuromodulation, from refining deep brain stimulation to integrating spinal and distributed strategies. It discusses adaptive neurotechnologies, mechanistic insights and a framework for tailoring spatiotemporally precise interventions to restore gait control.

Glioblastoma, the most common and most aggressive brain tumor type in adults, remains difficult to treat because it can infiltrate surrounding brain tissue and spread far beyond the main tumor. Researchers have captured this infiltration process in the living brain with advanced microscopy. Their study is based on observations in mice affected by a brain cancer very similar to human glioblastoma.

The results, published in the scientific journal Immunity, reveal complex and situation-dependent interactions between glioblastoma cells and the brain’s resident immune cells, also known as “microglia”. These cells patrol the brain in search of threats. The current findings suggest that microglia are not passive bystanders, but actively influence both the containment and the spread of the tumor.

The scientists observed these processes by means of so-called three-photon microscopy that employs infrared light. Focus was on the “far infiltration zone”, which designates a tissue region located several millimeters away from the primary tumor.

Among other things, the team discovered that the behavior of microglia changed as a tumor spread. Specifically, microglia showed increased motility and surveillance activity when only a few glioblastoma cells were present. However, as tumor infiltration intensified, this immune response declined.

Besides, the scientists investigated the effects of disabling a certain receptor that microglia use to sense their environment. The authors show that CX3CR1 deficiency enhanced microglial reactivity while limiting GB cell migration.

Furthermore, they looked into pharmacological depletion, i.e., drastically reducing the number of immune cells. Microglia depletion with the CSF1R inhibitor PLX5622 reduced GB cell migration and constrained tumor microtube ™ plasticity. ScienceMission sciencenewshighlights.

In a groundbreaking study, scientists have unlocked a major piece of the obesity puzzle, discovering that a naturally occurring hormone can reverse weight gain by targeting the same control center in the brain as popular weight-loss drugs like Ozempic and Wegovy.

The study, led by researchers at the University of Oklahoma and published in Cell Reports, highlighted the hormone FGF21 as a powerful tool in regulating metabolism and appetite.

For years, scientists assumed that weight-regulating signals primarily targeted the hypothalamus. However, Dr. Matthew Potthoff and his team were surprised to find that FGF21 actually bypasses that area, sending signals instead to the hindbrain-the lower back portion of the brain.

Neuroblastoma is an unusual tumor disease of the nervous system that almost exclusively affects children, mainly younger than two years old. About half of the children have high-risk tumors with a lower chance of being cured. N-MYC is linked to poorer prognosis in neuroblastoma.

Most proteins have a definite three-dimensional structure that usually contributes to their function and how they interact with other proteins. MYC is different and does not really have a fixed three-dimensional structure. The protein is flexible and constantly changes shape, which poses a challenge to researchers seeking to understand how MYC proteins work.

Also, MYC proteins are involved in the processes necessary for healthy cells to grow and divide. To prevent all cells in the body being harmed, it is important that a drug inhibits only the MYC function that is the problem in cancer cells, and nothing else. In other words, it takes a molecule that specifically affects a certain interaction between N-MYC and another protein.

In the current study, the researchers focused on the protein Aurora A, which also has a role in neuroblastoma and many other tumor forms. Preventing these proteins from interacting with each other has been suggested as a way to treat childhood tumors.

“To stop an interaction, you need to know where it’s happening. Despite the fact that N-MYC constantly changes shape, we now know where the two proteins anchor to each other. This provided clues as to what the medication should look like. We’ve also found a small molecule that manages to break apart the proteins, which lays a good foundation for future clinical trials,” says the first author.

The authors show that N-Myc binding to the Aurora A N-lobe can be inhibited by the small-molecule AurkinA, providing opportunity for therapeutical strategies to disrupt this interaction. ScienceMission sciencenewshighlights.

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