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Archive - Jan 12, 2020

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Baby & Adult Brains “Sync Up” During Play, Princeton Study Shows; Findings Include Evidence That Babies’ Brains Actually Guide Adults During Certain Interactions

Have you ever played with a baby and felt a sense of connection, even though the baby couldn't yet talk to you? New research suggests that you might quite literally be "on the same wavelength," experiencing similar brain activity in the same brain regions. This is something that most mothers likely know instinctively, but it has now been proven scientifically and in great detail. A team of Princeton researchers has conducted the first study of how baby and adult brains interact during natural play, and they found measurable similarities in their neural activity. In other words, baby and adult brain activity rose and fell together as they shared toys and eye contact. The research was conducted at the Princeton Baby Lab (http://babylab.princeton.edu), where University researchers study how babies learn to see, talk, and understand the world. "Previous research has shown that adults' brains sync up when they watch movies and listen to stories, but little is known about how this 'neural synchrony' develops in the first years of life," said Elise Piazza, PhD, an Associate Research Scholar in the Princeton Neuroscience Institute (PNI) and the first author on a paper published online on December 17, 2019, in Psychological Science. The article is titled “"Infant and Adult Brains Are Coupled to the Dynamics of Natural Communication.” Dr. Piazza and her co-authors (Liat Hasenfratz, PhD, an Associate Research Scholar in PNI; Uri Hasson, PhD, a Professor of Psychology and Neuroscience and Director of Graduate Studies; and Casey Lew-Williams, PhD, an Associate Professor of Psychology) posited that neural synchrony has important implications for social development and language learning. Studying real-life, face-to-face communication between babies and adults is quite difficult.

New Work Suggests That Pancreatitis Is an FGF21-Deficient State That Can Be Corrected by FGF21 Replacement Therapy & Perhaps Also by a Second Treatment Strategy Employing a PERK Inhibitor

In work that could have clinical implications, University of Texas (UT) Southwestern (UTSW) researchers have found that humans and mice with pancreatitis are deficient in a stress hormone called fibroblast growth factor 21 (FGF21). Normally, FGF21 is more abundant in the pancreas than in any other organ in the body. The scientists also showed that replacement therapy reverses the condition in mouse models in about 24 hours and may even prevent it. The study also reports success with a second treatment strategy. A potential drug called a PERK inhibitor targets a different step in the integrated stress response, the cellular pathway affecting the amount of FGF21 available in the pancreas. “Given that several FGF21 drug candidates are, or soon will be, in clinical trials for conditions related to metabolic disease, it may be possible to test fibroblast growth factor 21 for treating human pancreatitis in the near future,” says David Mangelsdorf, PhD. In addition to being Chair of Pharmacology at UTSW, Dr. Mangelsdorf is an investigator in the Howard Hughes Medical Institute (HHMI). He adds that he knows of no current investigations of PERK inhibitors for clinical use. The new study was published online on January 8, 2020 in Science Translational Medicine and the open-access article is titled “Pancreatitis Is an FGF21-Deficient State That Is Corrected by Replacement Therapy.” Pancreatitis, a debilitating and sometimes deadly inflammation of the pancreas, can be acute or chronic. It accounts for about 275,000 U.S. hospitalizations each year, with its incidence on the rise for reasons that are unclear.

Functional Inhibition of Dopaminergic Neurons by Astrocyte GABA Identified As Core Cause of Parkinson's Disease; Findings Suggest New Form of Treatment for Patients in Early Stages of PD

As many as 7 to 10 million people in the world are thought to live with Parkinson's disease (PD). Being the second most common neurodegenerative disease, PD severely affects patients' quality of life, not just brining movement abnormalities. Despite its prevalence and negative impact, current medical treatments for PD rely on alleviating PD symptoms with little effort to explore ways to reverse the symptoms. It has been firmly believed that abnormal movements of PD begin in the brain where the production of dopamine, a neurotransmitter for movement control, is irreversibly impaired, i.e., in a state of neuronal death. Currently, L-DOPA, a potent PD medication is mainly prescribed to replenish dopamine in the deprived brain. However, such a treatment is symptomatic therapy, rather than a disease-modifying therapy. Long-term use of L-DOPA is well-known to cause serious side effects such as involuntary, erratic, and writhing movements. Led by Dr. C. Justin Lee, along with Dr. Hoon Ryu and Dr. Sang Ryong Jeon, researchers at the Center for Cognition and Sociality within the Institute for Basic Science (IBS), the Korea Institute of Science and Technology (KIST), and the Asan Medical Center (AMC) have discovered a new mechanism for PD pathology. The researchers reported that the symptoms of PD begin when dopaminergic neurons are "non-functional", even before they die off. Though the neuronal death had been till now believed to be the obvious cause of PD, the study found that the movement abnormalities of PD begin in the earlier stage when dopaminergic neurons, though being alive, cannot synthesize dopamine (they are in a “dormant” state). "Everyone has been so trapped in the conventional idea of the neuronal death as the single cause of PD.