Tetris and cravings; molecular origins of Parkinson’s disease; targets for ALS, and more.
Languages are constantly evolving – and grammar is no exception. The way in which the brain processes language triggers adjustments. If the brain has to exert itself too much to cope with difficult case constructions, it usually simplifies them over time, as linguists from the University of Zurich demonstrate in a study on languages all over the world.
Playing Tetris for as little as three minutes at a time can weaken cravings for drugs, food and activities such as sex and sleeping by approximately one fifth, according to new research. In the first test of its kind to study people in natural settings outside of a laboratory, participants were monitored for levels of craving and prompted to play the block-shifting puzzle game at random intervals during the day.
As Parkinson’s disease progresses in patients, a puzzling dichotomy plays out in their brains. One set of neurons degenerates, while a similar population nearby is spared the same degree of damage. Why the difference? An answer to this question could clear the way for preventions and treatments for this disease. Using a new strategy they have devised to identify the molecular changes that drive the loss of neurons, researchers at The Rockefeller University and colleagues at Columbia University have identified two proteins they report may be important to Parkinson’s.
The loss of a critical receptor in a special class of inhibitory neurons in the brain may be responsible for neurodevelopmental disorders including autism and schizophrenia, according to new research by Salk Institute scientists. The importance of the receptor, called mGluR5, in other areas of the brain had been previously established. Until now, however, no one had studied their specific role in a cell type known as parvalbumin-positive interneurons, thought to be important in general cognition and generating certain types of oscillatory wave patterns in the brain.
Cells are powered by tiny energy reactors called mitochondria. When damaged, they leak destructive molecules that can cause substantial harm and eventually kill brain cells. Scientists at the National Institute of Health's National Institute of Neurological Disorders and Stroke showed that a protein called PINK1 that is implicated in Parkinson’s disease is critical for helping cells get rid of dysfunctional mitochondria. According to the new research, published in the journal Nature, PINK1 does this by triggering an intricate process called mitophagy that breaks down and removes damaged mitochondria from the cell.