Working memory
[22] Several other factors affect a person's measured span, and therefore it is difficult to pin down the capacity of short-term or working memory to a number of chunks.
[23] In the visual domain, some investigations report no fixed capacity limit with respect to the total number of items that can be held in working memory.
Instead of asking participants to report whether a change occurred between the memory and probe array, delayed reproduction tasks require them to reproduce the precise quality of a visual feature, e.g. an object's location, orientation or colour.
Resource theories have been very successful in explaining data from tests of working memory for simple visual features, such as colors or orientations of bars.
[56] Starting with work in the Neo-Piagetian tradition,[58][59] theorists have argued that the growth of working-memory capacity is a major driving force of cognitive development.
This hypothesis has received substantial empirical support from studies showing that the capacity of working memory is a strong predictor of cognitive abilities in childhood.
[61] Studies in the Neo-Piagetian tradition have added to this picture by analyzing the complexity of cognitive tasks in terms of the number of items or relations that have to be considered simultaneously for a solution.
[74] Age-related decline in working memory can be briefly reversed using low intensity transcranial stimulation to synchronize rhythms in prefrontal and temporal areas.
[76] Research has shown that aged macaques have reduced working memory-related neuronal firing in the dorsolateral prefrontal cortex, that arises in part from excessive cAMP-PKA-calcium signaling, which opens nearby potassium channels that weaken the glutamate synapses on spines needed to maintain persistent firing across the delay period when there is no sensory stimulation.
One study has shown that working memory training increases the density of prefrontal and parietal dopamine receptors (specifically, DRD1) in test subjects.
The later work of Joaquin Fuster[92] recorded the electrical activity of neurons in the PFC of monkeys while they were doing a delayed matching task.
Successful retrieval in the first attempt – something the animal can achieve after some training on the task – requires holding the location of the food in memory over the delay period.
Later research has shown similar delay-active neurons also in the posterior parietal cortex, the thalamus, the caudate, and the globus pallidus.
[98] The research described above on persistent firing of certain neurons in the delay period of working memory tasks shows that the brain has a mechanism of keeping representations active without external input.
A review of numerous studies[105] shows areas of activation during working memory tasks scattered over a large part of the cortex.
[120] Additional research conducted on patients with brain alterations due to methamphetamine use found that training working memory increases volume in the basal ganglia.
This phenomenon was first discovered in animal studies by Arnsten and colleagues,[122] who have shown that stress-induced catecholamine release in PFC rapidly decreases PFC neuronal firing and impairs working memory performance through feedforward, intracellular signaling pathways that open potassium channels to rapidly weaken prefrontal network connections.
[125] Exposure to chronic stress leads to more profound working memory deficits and additional architectural changes in PFC, including dendritic atrophy and spine loss,[126] which can be prevented by inhibition of protein kinase C signaling.
[133] Alcohol dependent young women in particular exhibit less of a BOLD response in parietal and frontal cortices when performing a spatial working memory task.
Within the theoretical framework of the multi-component model, one candidate gene has been proposed, namely ROBO1 for the hypothetical phonological loop component of working memory.
Initial evidence for this relation comes from the correlation between working-memory capacity and reading comprehension, as first observed by Daneman and Carpenter (1980)[146] and confirmed in a later meta-analytic review of several studies.
[149] A randomized controlled study of 580 children in Germany indicated that working memory training at age six had a significant positive effect in spatial working memory immediately after training, and that the effect gradually transferred to other areas, with significant and meaningful increases in reading comprehension, mathematics (geometry), and IQ (measured by Raven matrices).
Additionally, a marked increase in ability to inhibit impulses was detected in the follow-up after one year, measured as a higher score in the Go-No Go task.
Four years after the treatment, the effects persisted and was captured as a 16 percentage point higher acceptance rate to the academic track (German Gymnasium), as compared to the control group.
[152] This suggests that working memory impairments are associated with low learning outcomes and constitute a high risk factor for educational underachievement for children.
[158] One line of research suggests a link between the working memory capacities of a person and their ability to control the orientation of attention to stimuli in the environment.
[159] Such control enables people to attend to information important for their current goals, and to ignore goal-irrelevant stimuli that tend to capture their attention due to their sensory saliency (such as an ambulance siren).
The direction of attention according to one's goals is assumed to rely on "top-down" signals from the pre-frontal cortex (PFC) that biases processing in posterior cortical areas.
They wanted to find if the reduction is due to a lack of ability to focus on relevant tasks, or a low amount of memory capacity.
It found that there were certain places in the brain where most connectivity was decreased in pre-Huntington diseased patients, in comparison to the control group that remained consistently functional.
