Researchers measured how brain waves travel in the prefrontal cortex during working memory tasks.
Long-term memory consolidation and short-term memory processes that occur during sleep do so at a cost to one another.
Brain areas associated with working memory also gauge the quality and uncertainty of memories. Researchers reveal details about the neural mechanisms of working memory that allow us to make decisions based on our certainty of memories.
A new computational algorithm shows how the brain maintains information in the short term using specific types of neurons.
Working memory isn't confined to one area of the brain. It requires synchronous activity of at least two brain areas.
Activity in the frontoparietal network during memory tasks reflected the individual working memory capabilities of children, with an activity pattern unique to working memory.
Suppressing TLR4 activity following a traumatic brain injury, such as concussion, reduces excitability, and improves working memory performance up-to a month later.
Acetylcholine helps muscarinic M1 receptors in the prefrontal cortex to maintain information in working memory. As acetylcholine actions at M1 receptors are reduced in conditions which affect working memory, such as schizophrenia and Alzheimer's disease, researchers report the M1 receptor may serve as a potential therapeutic target to restore working memory.
200mg of caffeine, the equivalent of a strong cup of coffee, helps boost problem solving skills, but has no effect on creative thinking.
Short bouts of aerobic exercise can improve working memory as much as caffeine can. Additionally, exercise can help curb the negative effects of caffeine withdrawal, such as fatigue, headaches, and bad moods.
Obese children tend to have a thinner prefrontal cortex and cerebral cortex. The findings could explain why there is a correlation between obesity in children and decreased executive function.
SETD1A, a gene associated with schizophrenia, stunts the growth and branching of dendrites and reduces the number of dendritic spines. Reinstating the normal expression of SETD1A in mouse models restored working memory function.
