News of Note—Fixing a misfolded Parkinson’s protein; understanding the brain's appetite center

3D brain against purple background
Canadian researchers are examining how a misfolded protein that causes Parkinson's disease can be corrected by a molecule inside nerve cells.

A potential new target in Parkinson’s disease

 

One of the causes of the degenerative brain disorder Parkinson’s disease is the misfolding of a protein called alpha-synuclein. When the protein misfolds, it leaves toxic deposits that cause nerve cells to die. Researchers at the University of Guelph in Canada used stem cells from people suffering from the disease to study how nerve cells react to misfolded alpha-synuclein. They discovered that a molecule inside of nerve cells called cardiolipin pulls alpha-synuclein out of the toxic brain deposits and re-folds it into the proper shape—but that process is disrupted in Parkinson’s, the researchers reported in the journal Nature Communications. That understanding of cardiolipin’s role could inspire new treatments for the disease, they believe. (Release)

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How the brain’s appetite-control system governs obesity

 

The hormone pro-opiomelanocortin (POMC) is often referred to as a “grandfather” hormone, because after it’s produced in the brain’s hypothalamus, it’s broken up into several hormones that regulate appetite. Researchers at the University of Michigan Medical School have identified a mechanism by which this process can go awry—leading to overeating and obesity. Before POMC can leave the cells that produce it, they reported in the Journal of Clinical Investigation, the hormone goes through an inspection process. When that process is too tightly regulated, the hormone clumps up inside cells, leading to a shortage of appetite-regulating hormones in the body. The researchers found that mice with a defective POMC-regulating system ate more and gained weight rapidly, even when fed a low-calorie diet. (Release)

 

Therapeutic gel could improve delivery of cancer drugs

 

Scientists at the University of North Carolina School of Medicine and North Carolina State University have created an injectable gel scaffold designed to deliver combinations of chemotherapy and immunotherapy drugs directly into tumors. Their idea is to deliver the chemo first, killing some cancer cells while making others vulnerable to immunotherapy drugs like checkpoint inhibitors. They developed a polymer gel that can carry both gemcitabine, a chemo drug, and a PD-1 blocker. As the gel breaks down, it releases the chemo first, followed by the PD-1 inhibitor. When they tested the gel in animal models of melanoma and breast cancer, they observed significant tumor shrinkage, they reported in the journal Science Translational Medicine. (Release)