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In a small study, researchers at the National Institutes of Health have found that positron emission tomography (PET) scans of the heart may identify people who will go on to develop Parkinson’s disease or Lewy body dementia among those at-risk for these diseases.

The findings, published in the Journal of Clinical Investigation and led by scientists at the National Institute of Neurological Disorders and Stroke (NINDS), part of NIH, may advance efforts to detect the earliest changes that years later lead to Parkinson’s disease and Lewy body dementia.

In 34 people with Parkinson’s disease risk factors, researchers conducted PET scans of the heart to gain insight into levels of the neurotransmitter norepinephrine. They found that the scans could distinguish individuals who would later be diagnosed with Parkinson’s or Lewy body dementia—both are brain diseases caused by abnormal deposits of the protein alpha-synuclein that form clumps known as Lewy bodies. The research was conducted at the NIH Clinical Center, currently the only location for 18 F-dopamine PET scanning.

Squamous cell lung cancer is a lung cancer subtype that is particularly difficult to treat. A new study now has revealed a novel genetic alteration that occurs in some cases in this type of tumor and that may expose a weakness of the tumor for therapeutic intervention.

The University of Cologne researchers led by Professor Roman Thomas, director of the Department of Translational Genomics, was able to show that a certain genetic change occurs during tumor formation and that a previously unknown oncogene is produced. Oncogenes are genes that promote the growth of tumors. In some cases, they can be inhibited by targeted drug treatments.

This approach is often accompanied by a higher success rate and lower side effects compared to conventional chemotherapy. The scientists’ discovery could therefore be a first step toward a more successful therapy of this particular type of cancer.

Stem cell biologist Helen Blau of Stanford University School of Medicine and colleagues previously found that blocking 15-PGDH in old mice restored their withered muscles and improved their strength after a month of treatment. On the flip side, young mice lost muscle and became weaker after their levels of this enzyme were increased for a month.

Blau’s team has now found that 15-PGDH accumulates in the muscles of old mice as the connections that allow communication between muscles and nerves are lost, another consequence of aging. Treating old mice for one month with a drug that inhibits 15-PGDH restored these connections, called synapses, between muscle fibers and motor nerve cells, and boosted the animals’ strength, the team reports in the Oct. 11 Science Translational Medicine. Those synapses are how the brain directs muscles to move.

The findings suggest that blocking the gerozyme 15-PGDH may be a way to help recover strength that has diminished due to nerve injuries, motor nerve cell diseases or aging.

A susceptibility to gain weight may be written into molecular processes of human cells, a Washington State University study indicates.

The proof-of-concept study with a set of 22 found an epigenetic signature in buccal or cheek cells appearing only for the twins who were obese compared to their thinner siblings. With more research, the findings could lead to a simple cheek swab test for an obesity biomarker and enable earlier prevention methods for a condition that effects 50% of U.S. adults, the researchers said.

“Obesity appears to be more complex than simple consumption of food. Our work indicates there’s a susceptibility for this disease and molecular markers that are changing for it,” said Michael Skinner, a WSU professor of biology and corresponding author of the study published in the journal Epigenetics.

The device shows promise in a 62-year-old advanced-stage Parkinson’s patient.

In a major medical development, a man battling Parkinson’s disease has defied the odds and regained the ability to walk, thanks to a pioneering implanted device in his spinal cord.

The remarkable breakthrough promises new hope for countless individuals worldwide who have been affected by Parkinson’s disease and its associated debilitating walking difficulties.

An enzyme that may help some breast cancers spread can be stopped with an antibody created in the lab of Cold Spring Harbor Laboratory Professor Nicholas Tonks. With further development, the antibody might offer an effective drug treatment for those same breast cancers.

The new antibody targets an enzyme called PTPRD that is overabundant in some breast cancers. PTPRD belongs to a family of known as protein tyrosine phosphatases (PTPs), which help regulate many cellular processes. They do this by working in concert with enzymes called to control how other proteins inside cells behave. Kinases add small chemical regulators called phosphates to proteins. PTPs take them off.

Disruptions in the addition or removal of phosphates can contribute to inflammation, diabetes, and . Some disruptions can be corrected with kinase-blocking drugs.

Researchers led by Mroj Alassaf at the Fred Hutchinson Cancer Research Center in the United States have discovered a link between obesity and neurodegenerative disorders like Alzheimer’s disease.

Using the common fruit fly, the research shows that a high-sugar diet—a hallmark of obesity—causes in the brain, which in turn reduces the ability to remove neuronal debris, thus increasing the risk of neurodegeneration.

Publishing November 7 in the open access journal PLOS Biology, the research will impact therapies designed to reduce the risk of developing .