Lifeboat Foundation

An essential protein that acts as a gatekeeper for calcium entering cells promotes the growth of oral cancer and generates pain, according to a new study published in Science Signaling led by researchers at New York University College of Dentistry.

Targeting this protein—the ORAI1 calcium channel —could provide a new approach to treating oral cancer, which causes persistent pain that worsens as it progresses.

“Our results show that the ORAI1 channel fuels the growth of oral cancer tumors and produces an abundance of molecules that, once secreted, interact with neurons resulting in an increased sensitivity to pain,” said Ga-Yeon Son, a postdoctoral fellow in the Department of Molecular Pathobiology at NYU College of Dentistry and the study’s first author.

As scientists get better at interpreting the language of the brain, they get closer to not just treating disease, but also enhancing our senses and our intellects. Should they go there?

Summary: New findings challenge our understanding of fruit fly social behaviors. While traditionally thought to rely primarily on chemical receptors for social interactions, the fruit fly’s visual system plays a pivotal role too.

By manipulating the visual feedback neurons in male fruit flies, researchers discovered that their social inhibitions were altered, leading males to court other males. This novel insight can potentially enlighten our comprehension of social behaviors in humans, including those with bipolar disorder and autism.

Male fruit flies don’t usually like each other. Socially, they reject their fellow males and zero in on the females they discern via chemical receptors—or so scientists thought.

New research from Cornell University biologists suggests the fruit fly’s visual system, not just chemical receptors, are deeply involved with their social behaviors. The work sheds light on the possible origin of differences in human social behaviors, such as those seen in people with bipolar disorder and autism.

The paper is published in Current Biology.

A new blood-based diagnostic test could be a major advancement for the treatment of Parkinson’s, a disease that afflicts 10 million people worldwide and is the second-most common neurodegenerative disease after Alzheimer’s.

Building on the knowledge that mitochondrial dysfunction plays a prominent role in the pathogenesis of Parkinson’s a team of researchers, led by neuroscientists at Duke Health, have developed an assay that enables the accurate, real-time quantification of mitochondrial DNA damage in a scalable platform [1]. The results of the study, which received support in part from The Michael J Fox Foundation for Parkinson’s Research, have been published in the journal Science Translational Medicine.

“Currently, Parkinson’s disease is diagnosed largely based on clinical symptoms after significant neurological damage has already occurred,” said senior author Laurie Sanders, PhD, an associate professor in Duke School of Medicine’s departments of Neurology and Pathology and member of the Duke Center for Neurodegeneration and Neurotherapeutics.

Summary: Researchers provided robust evidence supporting the controversial “critical brain hypothesis” through a project called DishBrain.

This experiment, involving 800,000 human neural cells playing Pong, reveals how neurons shift into a “neural critical” state when informed about the surrounding environment, enabling cascades of brain activity. This state lies between the extremes of epileptic excitation and a comatose stall.

The findings hint at profound insights into brain function and potential treatments for neurological disorders.

A study led by researchers at the UCLA Jonsson Comprehensive Cancer Center sheds new light on why tumors that have spread to the brain from other parts of the body respond to immunotherapy while glioblastoma, an aggressive cancer that originates in the brain, does not.

In people with tumors that originated in other parts of the body but spread to the brain, treatment with a type of immunotherapy called immune checkpoint blockade appears to elicit a significant increase in both active and exhausted T cells—signs that the T cells have been triggered to fight the cancer. The reason the same thing doesn’t occur in people with glioblastoma is that anti-tumor immune responses are best initiated in draining lymph nodes outside of the brain, and that process does not occur very effectively in glioblastoma cases.

To date, immunotherapy has not been effective in treating glioblastoma, but it has been shown to slow or even eradicate other types of cancer, such as melanoma, which frequently metastasizes to the brain.

Cancer is a deadly disease with multiple risk factors. Risk factors are dependent on the type of cancer and each one is treated differently. The heterogeneity of various cancers is the main reason there is no cure. Additionally, cancer evolves and can also come back after being treated and lying dormant for years. Therefore, it is very difficult to find an effective treatment that provides high quality of life for patients.

One aggressive cancer that is difficult to treat includes glioblastoma. This brain tumor is fast-growing and results in the form of many different symptoms including headache, vomiting, and seizures. Unfortunately, there is not much known on glioblastoma. The cause of this disease is unclear and treatment options are limited. This tumor stays in the brain and does not metastasize, but because of its location, glioblastoma is hard to treat. Currently, treatment options include radiation, chemotherapy, and surgery with limited success. Even immunotherapy, a more recent treatment, which activates the body’s immune system to kill the tumor has limited efficacy in the brain.

A group of researchers led by Dr. Robert Prins at the David Geffen School of Medicine at University of California Los Angeles (UCLA) recently published an article in the Journal of Clinical Investigation (JCI) describing new research that could help overcome obstacles to glioblastoma treatment. More specifically, Prins and colleagues have reported why glioblastoma that originates from other parts of the body respond better to immunotherapy compared to glioblastoma that originates in the brain.