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A groundbreaking medical procedure for those with kidney stones will soon be offered at the University of Washington after more than two decades of research.

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.

Organometallic compounds, molecules made up of metal atoms and organic molecules, are often used to accelerate chemical reactions and have played a significant role in advancing the field of chemistry.

Metallocenes, a type of organometallic compound, are known for their versatility and special “sandwich” structure. Their discovery was a significant contribution to the field of organometallic chemistry and led to the awarding of the Nobel Prize in Chemistry in 1973 to the scientists who discovered and explained their sandwich structure.

The versatility of metallocenes is due to their ability to “sandwich” many different elements to form a variety of compounds. They can be used in various applications, including the production of polymers, glucometers—used to measure the amount of glucose in the blood, perovskite solar cells, and as a catalyst, a substance that increases the rate of a chemical reaction without being consumed or changed by the reaction itself.

Metastasis is one of the main obstacles in treating cancer. Studying circulating tumor cells (CTCs) and CTC clusters at the single-cell level can help us understand the underlying mechanisms and develop better therapeutic strategies for patients. Automated solutions can vastly simplify protocols for CTC isolation for molecular characterization at the single-cell level.

What are circulating tumor cells?

CTCs are cells that break away from the primary tumor and enter the bloodstream. Once in the blood, CTCs can adapt to the microenvironment of additional sites, forming a new tumor. This process, called metastasis, is responsible for over 90% of cancer-related deaths and is an active area of research.

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.

Using a standardized assessment, researchers in the UK compared the performance of a commercially available artificial intelligence (AI) algorithm with human readers of screening mammograms. Results of their findings were published in Radiology.

Mammographic screening does not detect every breast cancer. False-positive interpretations can result in women without cancer undergoing unnecessary imaging and biopsy. To improve the sensitivity and specificity of screening mammography, one solution is to have two readers interpret every mammogram.

According to the researchers, double reading increases cancer detection rates by 6 to 15% and keeps recall rates low. However, this strategy is labor-intensive and difficult to achieve during reader shortages.

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.

Our immune system is made of various cell types responsible for fighting pathogens and disease that enter the body. There are two distinct arms or responses of the immune system: innate and adaptive. The innate immune response is the first line of defense that includes immune cells that are not specific to the invading pathogen, but recognize it is foreign and tries to kill it. Cells that are included in this response are neutrophils, basophils, eosinophils, monocytes, macrophages, mast cells, and natural killer cells. The adaptive immune response is the second line of defense and made up of cells that are more specific to the invading pathogen. The adaptive immune system includes dendritic cells, T cells, and B cells. T cells specifically have different subsets and function differently to effectively kill invading pathogens.

Although scientists know a lot about the immune system, there is still much unknown about how the cells that make up these immune responses completely function. One unclear phenomenon includes the mechanism by which immune cells know which way to travel to the site of infection. Researchers lead by Drs. Michael Sixt and Edouard Hannezo at the Institute of Science and Technology Austria (ISTA) recently reported in Science Immunology that immune cells generate their own path to navigate environments throughout the body.

One particular immune cell type, dendritic cells, are not exclusively part of the adaptive immune system. They work to bridge the innate and adaptive immune systems to help cohesively deliver a response that will efficiently kill the pathogen. More specifically, dendritic cells detect pathogens and then travel to the lymph nodes to coordinate a systemic attack. Dendritic cells move according to chemokines, or small proteins that help cells migrate to specific locations. Previously, it was believed that the chemokines produce a gradient and it was this gradient that allowed cells to migrate to specific locations. However, Sixt, Hannezo, and colleagues reported that this gradient might not be the only way for migrating cells.

This week in neuroscience, we’ve seen groundbreaking advancements ranging from a diet that can potentially extend lifespan without calorie restriction, to a new drug that could revolutionize obesity treatment.