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.
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.
The lateral septum encodes speed and acceleration information as an animal navigates and learns how to obtain a reward from its environment.
Artificially prolonging hippocampal sharp wave ripples improves working memory.
A recurrent neural network algorithm demonstrates short-term synaptic plasticity can support short term maintenance of information, providing the memory delay period is sufficiently short.
Exposure to air pollution during pregnancy or during early life is linked to a reduction in cognitive abilities during child development. Greater fine particulate matter 2.5 exposure between fetal stage and 7 years old was associated with lower working memory scores in boys at age 10. Early life exposure to PM2.5 was also correlated with attention problems in both boys and girls.
Researchers present a new model that may explain the flexibility of working memory.
Females offspring whose mothers experienced maternal immune activation while pregnant displayed an array of behavioral abnormalities associated with schizophrenia.