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HomeHealthRevolutionary Imaging Technique Reveals Protein Abnormalities Linked to Motor Neuron Disease

Revolutionary Imaging Technique Reveals Protein Abnormalities Linked to Motor Neuron Disease

Researchers have employed a novel technique to detect harmful changes linked to motor neurone disease.

A new technique developed at the University of Birmingham has successfully pinpointed pathological changes related to motor neurone disease.

This innovative method aims to enhance scientists’ understanding of the brain changes that contribute to motor neurone disease (MND), and it could potentially lead to new treatment options in the future. The findings result from a collaboration between the University of Birmingham and the University of Sheffield, and they have been published in Nature Communications.

Motor neurone disease—often referred to as amyotrophic lateral sclerosis or ALS—is a condition that leads to muscle degeneration because the motor neurons in the brain fail to send signals to the muscles, causing muscle weakness. Approximately 5,000 individuals in the UK are living with this disease at any given time, and there is currently no known cure.

At the University of Birmingham, researchers have created a technique that allows them to analyze specific proteins in their natural form, directly derived from brain and spinal cord tissue samples. This method, known as native ambient mass spectrometry (NAMS), provides an unprecedented ability to study the structure of proteins regarding their location within the tissue.

In collaboration with the University of Sheffield, the team discovered a deficiency of metal in a notable protein called SOD1, which accumulates in certain areas of the brain and spinal cord in mice with MND.

Although SOD1 has been linked to motor neurone disease in the past, this marks the first instance where detailed molecular imaging has illustrated how forms of the protein missing metal ions gather in the affected mice.

Helen Cooper, the lead researcher from Birmingham’s School of Biosciences, stated: “This is the first approach to demonstrate that this variant of SOD1 is related to the pathology of motor neurone disease. It represents a preliminary step toward discovering treatments for MND and opens an exciting avenue for understanding the molecular foundations of other diseases in remarkable detail.”

Richard Mead from the Sheffield Institute for Translational Neuroscience expressed his enthusiasm, saying: “We were thrilled to implement this remarkable methodology developed by Helen’s team to gain fresh insights into the biology of MND. We are eager to further utilize this technology to investigate the reasons motor neurons deteriorate and to discover new ways to assist those impacted by MND.”

The researchers plan to next investigate whether similar imbalances exist in human tissue samples and explore potential treatments for these imbalances in mice using existing drug compounds.