The brain is plastic throughout life, but never more so than from birth to young adulthood. It increases its volume by developing dendrites and axons that connect neurons in to each other, forming new pathways to process the information that it will store. Those connections require maintenance. And if a connection is unsuccessful, better to delete it than to keep it. This is known as synaptic pruning and occurs from childhood to the age of 20. Now, a group of scientists from the University of Cambridge and Fudan University has described a neuropsychopathological (NP) factor that explains why inappropriate pruning in adolescence is related to mental health disorders.

A unique characteristic of Helicobacter pylori could serve to end infections of this gastric bacterium. A group of scientists from the University of Munich have found that this pathogen has a strategic point in its mitochondrial respiratory complex I that could be targeted with inhibitors. “We did not look for respiration inhibitors in the first place,” co-senior author Wolfgang Fischer told BioWorld. “We screened libraries with a reporter assay, looking for something different, a particular protein secretion, the secretion system type (T4SS). Then, we found that a lot of compounds inhibit this process. From these compounds, we came to the point that they are actually respiration inhibitors,” he explained.

The analysis of thousands of proteins in the brain has revealed the association of astrocytes with obsessive-compulsive disorder (OCD). A proteomic study by researchers from the University of California Los Angeles (UCLA) has identified them in different cellular compartments of astrocytes and neurons. One such protein, the postsynaptic protein SAPAP3, appeared to regulate the organization of the actin cytoskeleton. Its deficit in astrocytes could cause OCD.

The editing in human cells and in mice of the survival motor neuron 1 gene (SMN1) restored the levels of SMN protein that the mutation of the SMN2 gene produces in spinal muscular atrophy (SMA). Scientists from the Broad Institute in Boston and The Ohio State University reversed the mutation using the base editing technique. “This base editing approach to treating SMA should be applicable to all SMA patients, regardless of the specific mutation that caused their SMN1 loss,” the lead author David Liu, a professor and director of the Merkin Institute of Transformative Technologies in Healthcare at the Broad Institute of Harvard and MIT, told BioWorld.