The use of “smart drugs” to enhance productivity in academic and workplace settings is on the rise. A recent study published in Science Advances examined the effects of three popular smart drugs – methylphenidate, modafinil, and dextroamphetamine – on real-life tasks. The researchers hypothesized that these drugs, which affect dopamine and norepinephrine, would influence motivation and effort, ultimately leading to improved performance.

The study involved forty participants between the ages of 18 and 35. The participants were randomly assigned to four groups and attended four testing sessions. In each session, they were given one of three popular smart drugs or a placebo. The drugs were administered in a double-blinded manner, meaning neither the participants nor the researchers knew which drug was being given.

The researchers used a task called the “knapsack task” to evaluate the participants’ cognitive performance. This task involves solving a complex optimization problem where participants have to select items with certain weights and values to maximize the overall value while staying within a weight limit. The difficulty of the task was designed to simulate real-life complex tasks that people encounter.

Maintenance of mRNA and protein localization in motor neurons is a potential therapeutic avenue for Amyotrophic lateral sclerosis (ALS), report researchers from The Francis Crick Institute and the University College London (UCL). A new study shows how the extensive changes in mRNA and protein in ALS motor neurons are linked to mutations in an ATPase called VCP. These mutations may contribute to the mislocalization of RNA binding proteins (RBPs) that tend to clump together and the redistribution of the mRNAs they are bound to. Inhibition of VCP partly restored mRNA and protein localization and other ALS phenotypes. These results show how RBP mislocalization and mRNA redistribution in motor neurons are linked to ALS and how VCP inhibition could be used as a treatment.

The study “Nucleocytoplasmic mRNA redistribution accompanies RNA binding protein mislocalization in ALS motor neurons and is restored by VCP ATPase inhibition” was published today in Neuron.

“For the patients I see, it’s devastating that there aren’t yet impactful treatments available for ALS,” said Rickie Patani, PhD, senior group leader of the Human Stem Cells and Neurodegeneration Laboratory at the Crick, professor at UCL, and consultant neurologist at the National Hospital for Neurology. “This research represents a shift in our thinking about what causes ALS—it doesn’t involve abnormal movement of just a few proteins, but the abnormal localization of hundreds of proteins and mRNAs. This opens new avenues for research and potential therapies.

Researchers have transplanted cells capable of forming specialized brain support cells into mice brains and found that they not only competed with and replaced unhealthy cells but aged ones, too. The findings open the door to developing an effective treatment for a range of conditions like multiple sclerosis, ALS, Alzheimer’s disease, autism and schizophrenia.

‘Glial cells’ is an umbrella term for the cells that are a support system to nerve cells (neurons). Progenitor cells are descendants of stem cells that can differentiate into specific cell types, and, in the case of glial cells, human glial progenitor cells (hGPCs) differentiate into subtypes, including astrocytes and oligodendrocytes, specialized for particular functions.

Astrocytes comprise most of our central nervous system cells, providing support and protection for neurons, transporting nutrients and removing waste. Oligodendrocytes lay down and maintain the lipid-rich, insulating wrapping called myelin around some axons, the part of the neuron that connects with another neuron and allows the transmission of nerve impulses.