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This Week on NeuroScientistNews: 9 February – 13 February

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Decoding neuronal diversity; smoking thins the brain; pathological progression of multiple sclerosis, and more.

Decoding the Building Blocks of Neuronal Diversity

This publication review examines a recent study by Molyneaux et al. describing their research to resolve the molecular instructions driving pyramidal neuron specification. Purified neuronal subtypes were subjected to whole-transcriptome analyses by high-throughput RNA-sequencing to delineate the transcriptional dynamics that influence and refine neuronal identity during development.

Smoking thins vital part of brain

Years ago, children were warned that smoking could stunt their growth, but now a major study shows new evidence that long-term smoking could cause thinning of the brain’s cortex, the brain layer in which critical cognitive functions such as memory, language and perception take place. Interestingly, the findings also suggest that stopping smoking helps to restore at least part of the cortex’s thickness.

Pathological progression of multiple sclerosis documented for the first time

An international team of researchers has for the first time documented the pathological progress of multiple sclerosis from its early to late stage and also shown that inflammatory and neurodegenerative processes have a role to play. This raises the possibility of new treatment options.

Brain develops abnormally over lifespan of people who stutter

A region of the brain thought to control speech production develops abnormally in children who stutter--a pattern that persists into adulthood, according to new research. In this first study to use MRI imaging to examine brain development in both children and adults who stutter, researchers found abnormal development of gray matter in Broca's area, the region of the frontal lobe responsible for speech. It was the only abnormality found in the 30 regions of the brain the research team investigated.

Serotonin-deficient brains are more vulnerable to social stress

Mice genetically deficient in serotonin are more vulnerable than their normal littermates to social stressors, according to a new study. Following exposure to stress, the serotonin-deficient mice also did not respond to a standard antidepressant, fluoxetine (Prozac), which works by boosting serotonin transmission between neighboring neurons.