Collaborative Learning: The Example of Quizlet

One of the benefits of the internet and world wide web are the opportunities for collaborative learning and work. The distributed structure of the internet mirrors the brain in many ways. While specific parts of the brain are specialized for specific tasks, wide areas of the brain are needed to do just about anything. The interconnectedness of major brain networks are visualized in the following image.

brain_networks

Portions of the internet have also been visualized in similar ways, such as this image produced in 2010 by AT&T Labs.

ATT_internet_map

What does this have to do with collaborative learning?

One example is the site Quizlet.com (I have no affiliation with them). Quizlet is a site billing itself as providing “Simple tools for learning anything. Search millions of study sets or create your own. Improve your grades by studying with flashcards, games and more.”

People can create study sets (digital flashcards) about just about any topic. The site is particularly helpful for middle and high school students who can access content created by others or provide their own content.

Do you need to study vocabulary words for the SAT? There is a study set with words that might appear on the test.

Do you need to study for an AP Psychology test? Here’s a set of terms that might be helpful.

Whether you are lazy and don’t want to create your own study materials, are interested in learning something new, have a big test coming up, or want to help other people, sites like Quizlet provide opportunities for collaborative learning.

Image sources

Hagmann P, Cammoun L, Gigandet X, Meuli R, Honey CJ, Wedeen VJ, Sporns O (2008) Mapping the structural core of human cerebral cortex. PLoS Biology Vol. 6, No. 7, e159.

http://www.research.att.com/export/sites/att_labs/groups/infovis/news/img/ATT_Labs_InternetMap_0730_10.pdf

Memory Problems in Some With Parkinson’s Disease

From a recent news release by Jill Pease at the University of Florida.

Using a combination of neuropsychological testing and brain imaging, University of Florida researchers have discovered that in a group of recently-diagnosed patients with Parkinson’s disease, about one quarter have significant memory problems.

Parkinson’s disease is commonly known as a movement disorder that leads to tremors and muscle rigidity, but there is growing recognition of cognitive problems associated with the disease. One of the most common is slower thinking speed that causes patients to have trouble quickly retrieving information. The UF study identifies a subset of patients who have a different kind of cognitive issue — memory problems, or difficulty learning and retaining new information.

The findings were published July 24 in the journal PLOS ONE.

“While a large proportion of people with Parkinson’s will experience slower thinking speed, which may make them less quick to speak or have difficulty doing two things at once, we now know that there are a subset of individuals with Parkinson’s disease who have memory problems,” said Catherine Price, Ph.D., the study’s senior author and an associate professor in the UF College of Public Health and Health Professions’ department of clinical and health psychology, part of UF Health. “It is important to recognize which people have issues with learning and memory so we can improve diagnostic accuracy and determine if they would benefit from certain pharmaceutical or behavioral interventions.”

For the UF study, 40 people in the early stages of Parkinson’s disease and 40 healthy older adults completed neuropsychological assessments and verbal memory tests.

About half the participants with Parkinson’s disease struggled with an aspect of memory, such as learning and retaining information, or recalling verbal information, said lead author Jared Tanner, Ph.D., an assistant research professor in the UF department of clinical and health psychology who conducted the study as part of his dissertation research for a UF doctoral degree in clinical psychology.

“And then half of those participants, or nearly one quarter of all participants with Parkinson’s, were really having a difficult time consistently with their memory, enough that it would be noticeable to other people,” said Tanner, adding that researchers were encouraged by the fact that most participants in the initial stages of Parkinson’s were not having significant memory problems.

All participants received brain scans, which used new imaging techniques that allowed the scientists to navigate the pathways of white matter fibers, the tissue through which messages travel across the brain. The methodology was developed by the research group ofThomas Mareci, Ph.D., a professor of biochemistry and molecular biology in the UF College of Medicine, and is described in a paper published July 14 in PLOS ONE.

Experts have theorized that cognitive problems in Parkinson’s are caused by a shortage of the brain chemical dopamine, which is responsible for patients’ motor issues. But with the help of imaging, the UF researchers were able to spot changes in the brain’s gray and white matter that appear unrelated to dopamine loss and are specific to those patients with Parkinson’s who have memory problems.

“Not only is gray matter important for memory, in Parkinson’s disease white matter connections between the temporal lobe and a region in the posterior portion of the brain called the retrosplenial cortex were particularly important in the recall of verbal information,” Tanner said. “People with Parkinson’s disease who had stronger connections between these areas of the brain did better at remembering information.”

Tanner’s study is part of a larger research project supported by a $2.1 million grant from the National Institute of Neurological Disorders and Stroke of the National Institutes of Health. Researchers led by Price are using imaging and cognitive testing to determine profiles for the cognitive problems that most commonly affect patients with Parkinson’s. The information gleaned from the research could help clinicians foreshadow the type of cognitive impairment a patient may experience over time, if any, and tailor treatment plans accordingly.

GABA receptor role in postoperative cognitive decline

About 20-30% of older adults (age greater than 60) undergoing major surgery experience temporary (generally reversed) memory and thinking deficits after major surgery, particularly heart and orthopedic. A small minority (<5%, probably much less) might not return to cognitive baseline (how they were before surgery). The cause of this decline in cognition is unclear, although many attribute it to the anesthesia used. So far, however, research has been inconclusive as to specific causes of cognitive difficulties after surgery. This is because surgeries are major events that affect most parts of the body, not just what is being operated upon. They are stressful – physically and emotionally.

Newly published research proposes one mechanism for causes of memory problems after surgery – anesthesia acting on ɣ-aminobutyric acid type A receptors (ɣ5GABAaR). This new research suggests that the function of these receptors does not return to baseline until much later than previously believed. This means that the normal function of chemicals in the brain, particularly ones important for memory, might be disrupted for longer than expected, and might play a role in memory problems that some individuals experience after major surgery.

Reference

Zurek, A. A., Yu, J., Wang, D. S., Haffey, S. C., Bridgwater, E. M., Penna, A., … & Orser, B. A. (2014). Sustained increase in ?5GABA A receptor function impairs memory after anesthesia. The Journal of clinical investigation, 124(12).

Modeling the Human Brain

Wired has an article about Dr. Henry Markram’s goal to simulate an entire human brain within 10 years. While his goal will not be met within that time-frame, this is important work to do. If we can have a way to simulate brain development or function, it can help us understand how brain disorders occur and help with the treatment of them.

One of the great things about the project is the collaborative nature of it: “‘But the only way you can find out is by building it,’ [Markram] says, ‘and just building a brain is an incredible biological discovery process.’ This is too big a job for just one lab, so Markram envisions an estimated 6,000 researchers around the world funneling data into his model…. Neuroscientists can spend a whole career on a single cell or molecule. Markram will grant them the opportunity and encouragement to band together and pursue the big questions.”

Read the Wired article for more information about the project and the 1 billion Euro grant Markham received.

Intelligence and Neurological Conditions

Intelligence is an interesting concept. We have tests that measure what we call intelligence but such tests are limited and culture-centric (not that that is necessarily a negative thing). However, for the sake of discussion I will operationally define aptitude (i.e., intelligence) as Intelligence Quotient so as to have a standard metric as foundation for this post.

I spend time assessing people’s memory and thinking abilities. I almost always try to get some measure of baseline aptitude either by estimating it (e.g., years of education, vocabulary knowledge, word reading ability) or by formally measuring via an intelligence test. Granted, this has limitations but it allows me to estimate how well an individual’s brain should function across multiple domains of thinking (e.g., problem-solving, reasoning, memory, language, and so forth). In other words, the higher a person’s general aptitude (abilities), the better he generally will do across most cognitive domains barring brain insult. This is certainly not a rule codified in stone and in triplicate but it serves as a rubric to follow.

Intelligence as measured by IQ is generally quite stable across the lifespan but can improve modestly with  diligence in informal or formal education. Intelligence as denoted by IQ can also decrease modestly if people are intellectually inactive, although such declines are slight. What can happen though is as brains age or if damaged by a pathological process or an injury, components of IQ can decrease. My primary clinical and research focus is in understanding how brains and cognition change in old age – both naturally and in the presence of neurological (brain) insult. Remarkably, the measures we use for intelligence tend to be rather insensitive to aging and even neurological insult, at least some of the components of intelligence are generally insensitive to brain insult. However, this leads to one area where our conceptualization of intelligence as IQ starts to break down.

As they age, the brains of people almost universally slow down. Wear and tear on the brain over decades of life affects how well and quickly we can think. Blood, which is essential for life and for the functioning of the brain, happens to be toxic to brain cells. Sometimes the protections in the brain that keep blood far enough from brain cells (neurons) to protect them but near enough to feed and maintain brain cells start to break down over time. This can injure the brain and start to reduce how well the brain works, even lowering IQ. Now, does that mean that a person’s intelligence decreases? If IQ = intelligence, then yes, it does. Contrary to how I operationalized intelligence earlier, intelligence is not synonymous with IQ. IQ can be a useful concept but it is far from perfect, particularly if by using it one argues that someone is less intelligent simply because his head was injured in an accident or because she developed dementia or suffered a stroke.

This is an area that demonstrates the limitations of our current research and clinical conceptualizations of intelligence. However, understanding how IQ changes over time and how it is affected by neurological conditions is important information to have, as it can help localize areas of pathology.

The Magic of Deep Brain Stimulation Surgery

Deep brain stimulation (DBS) is a neurosurgery where an electrode (or electrodes) is implanted within the deep portions of the brain with the hope of changing an abnormally functioning brain. DBS is used to treat Parkinson’s disease, essential tremor, multiple sclerosis, and even some intractable depression and obsessive-compulsive disorder. It is an exciting area of research and clinical work. Here is a video of a neurosurgeon and a neurologist talking about their work with DBS. It almost seems like magic. Like magic, it can be dangerous without proper controls. It does wonders for many people though.

 

Parkinson’s Disease and the Brain

The Michael J. Fox Foundation has a good, basic introduction to the neurobiology of Parkinson’s disease. The brief animate video provides an overview of affected parts of the brain as well as the role that dopamine, a neurotransmitter – a chemical in the brain that allows brain cells to communicate with each other – plays in Parkinson’s disease. Click on the link below and then click on the video link titled PARKINSON’S AND THE BRAIN to learn more about how Parkinson’s disease affects the brain.

Learn More

Can We Cure Parkinson’s Disease?

The National Parkinson’s Foundation produced a series of brief videos providing overviews of Parkinson’s disease related topics by prominent clinicians and researchers in the field of Parkinson’s disease. In one video, we are provided with an overview of the questions of whether or not we can cure Parkinson’s disease and how do we treat Parkinson’s disease.

The short answer is: no, we cannot right now cure Parkinson’s disease. We have hopes that stem cell therapies will work but there are a number of issues related to stem cells that make them potentially problematic (e.g., how do we make sure they don’t turn into cancers).

We can, however, treat symptoms of Parkinson’s disease with drug, physical, and cognitive therapies. L-dopa is effective at reducing tremors in most people and well as increasing rate and speed of movement. In some cases, deep brain stimulation is warranted. It has shown to be quite effective for many people. But for now we cannot cure Parkinson’s disease.

Writing Memories In the Brains of Flies

Source for the following post: BBC NEWS | Science & Environment | Bad memories written with lasers

The brains of flies are far simpler than the brains of humans. Previously, researchers had discovered that only 12 neurons were involved in the formation of associative memories in flies. This most recent study builds on this knowledge. If these 12 neurons are involved in forming memories, could researchers trigger these neurons and create memories?

According to a recently published paper in Cell, the answer is “Yes.” Using genetically-modified flies with adenosine-5′-triphosphate (ATP) activated neurons (the ATP is triggered by lasers), the researchers were able to affect the flies such that “the flies associated the smell with a bad experience, so the laser flash gave the fly a memory of a bad experience that it never actually had.”

Here’s a link to the journal article (requires a subscription).

Here’s the abstract:

“Dopaminergic neurons are thought to drive learning by signaling changes in the expectations of salient events, such as rewards or punishments. Olfactory conditioning in Drosophila requires direct dopamine action on intrinsic mushroom body neurons, the likely storage sites of olfactory memories. Neither the cellular sources of the conditioning dopamine nor its precise postsynaptic targets are known. By optically controlling genetically circumscribed subsets of dopaminergic neurons in the behaving fly, we have mapped the origin of aversive reinforcement signals to the PPL1 cluster of 12 dopaminergic cells. PPL1 projections target restricted domains in the vertical lobes and heel of the mushroom body. Artificially evoked activity in a small number of identifiable cells thus suffices for programming behaviorally meaningful memories. The delineation of core reinforcement circuitry is an essential first step in dissecting the neural mechanisms that compute and represent valuations, store associations, and guide actions.”

You can also listen to an interview with one of the researchers on this episode of NPR’s Science Friday.

As we learn more about how memories are created we might be able to understand and fix problems when memories fail.

The Relationship Between Executive Function and Processing Speed

Understanding the relationship between brain (specifically subcortical structures) and cognitive processes is a field still in its infancy. The rise of structural and functional neuroimaging that started in the 1970s and really began to mature in the 1990s (with even greater changes and advancements being made today), led to the ability to measure the structure and function of various brain regions in vivo. This was and is important for neuropsychologists because it allowed them to more accurately assess the relationship between the brain and cognitive and behavioral functions.

Processing speed is a basic cognitive or brain processes that subserves many other higher-order cognitive domains. Among those higher domains is executive functioning, a somewhat broad construct that involves the organization of behaviors and behavior responses, selective attention of pertinent information and suppression of unnecessary information, and maintenance and shifting of cognitive sets. Thus, executive functioning is dependent on processing speed but processing speed is not dependent on executive functioning. If executive functioning is a car, processing speed is the engine. Having a faster or more powerful engine means that the car can go faster. More efficient engines allow the car to function at a higher level of efficiency. Thus, while processing speed and executive functions are distinct, they are related with processing speed as one of the basic cognitive processes driving executive functions.

As an example of the interaction between executive functions and processing speed in clinical applications we can look at the Stroop Color-Word task. A person who is not only able to read the words or name the colors quickly but also able to inhibit the undesired but automatic process (namely, word reading on the incongruent color-word task) will receive a higher score on the Stroop task. This would, in combination with other executive function tests, be evidence for intact or even good executive functioning.

Even on non-speeded executive tasks those with fast processing speed can benefit because they can sort through information more quickly and hopefully, efficiently – speed and efficiency are related but not exactly the same. However, not all tests of executive function rely on processing speed. A person, for example, could be slow on the Wisconsin Card Sort Test, yet not exhibit any “executive dysfunction” in that they could complete all the categories and not have an abnormal number of perseverative errors. This simply demonstrates that “executive functions” are diverse and varied.

As a basic process that is dependent on basic neuronal function and glial support, any sort of focal or diffuse injury to the brain can affect processing speed. An example of this is traumatic brain injury, which frequently results in diffuse axonal injury; this diffuse injury negatively affects cognitive processing speed. Any time the white matter is focally or grossly disrupted, processing speed is in danger of disruption itself. This disruption of white matter could be anything from axonal damage, loss of oligodendroglia (which form the myelin), or even low levels of neurotransmitters.

White matter disruption also occurs in multiple sclerosis where diffuse lesions are apparent in the white matter. This disruption also occurs more often in people with heightened vascular risk factors, such as hypertension, diabetes, and cardiovascular disease. People who have these vascular risk factors and subsequent damage to their white matter (this damage or disruption is frequently termed leukoaraiosis) have reduced processing speed and attention (Viana-Baptista et al., 2008). Lesions to subcortical structures, such as the caudate, also result in reduced processing speed (Benke et al., 2003) in addition to executive dysfunction.

In subcortical disease processes such as Huntington’s disease, which usually starts with atrophy of the caudate nuclei, or Parkinson’s disease, which starts with a loss of the majority of dopaminergic cells in the substantia nigra, processing speed is consistently affected. Some common symptoms of Parkinson’s disease are freezing and a shuffling gait; even though these symptoms are motoric, they can be indicative of the global cognitive slowing that also occurs. However, it seems that processing speed is heavily dependent on the integrity of white matter.

Because of the diffusivity of processing speed, I am not aware of any areas of the brain shown to be necessary for processing speed, outside of global white matter. As I mentioned above, damage to the caudate has been shown to affect processing speed but damage to almost any area of the brain, especially if the white matter is disrupted results in slowed processing speed. Neuropsychologists often talk about a patient who has executive dysfunction, slowed speed of processing, as well as some other cognitive deficits as exhibiting signs of a frontal-subcortical disruption – a frontal-subcortical profile. So far, no one has localized processing speed to a single area – many brain structures or areas affect it.

At this point, processing speed and executive functions cannot be “mapped” to separate basal ganglia structures or loops. Of the three classically recognized cortico-striato-thalamo-cortical loops involved in cognitive and emotional processes rather than basic motor processes, which were first introduced by Alexander, Delong, and Strick (1986), the dorsolateral prefrontal cortex circuit appears to be most correlated with processing speed (Mega & Cummings, 1994). This is also the circuit most strongly linked with executive functioning. It appears that rather than utilizing different circuits processing speed and executive functions utilize the same circuits; however, processing speed is much more globalized.

References

Alexander, G. E., DeLong, M. R., & Strick, P. L. (1986). Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annual Review of Neuroscience, 9, 357-381.

Benke, T., Delazer, M., Bartha, L., Auer, A. (2003). Basal ganglia lesions and the theory of fronto-subcortical loops: Neuropsychological findings in two patients with left caudate lesions. Neurocase, 9, 70-85.

Mega, M. S., & Cummings, J. L. (1994). Frontal-subcortical circuits and neuropsychiatric disorders. The Journal of Neuropsychiatry and Clinical Neurosciences, 6, 358-370.

Viana-Baptista M, Bugalho P, Jordão C, Ferreira N, Ferreira A, Forjaz Secca M, Esperança-Pina JA, Ferro JM. (2008). Cognitive function correlates with frontal white matter apparent diffusion coefficients in patients with leukoaraiosis. Journal of Neurology, 255, 360-366.