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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.
Portions of the internet have also been visualized in similar ways, such as this image produced in 2010 by AT&T Labs.
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.
There is increased interest in brain and cognitive rehabilitation to treat people with mild thinking and memory problems. Parkinson’s disease, while typically viewed as a neurodegenerative motor disorder, also affects thinking and memory. In a small clinical trial with Parkinson’s disease patients, patients received either occupational therapy or cognitive rehabilitation. Those who had cognitive rehabilitation showed increases in functional connectivity (a measure of time-linked correlations between changes in blood flow in different parts of the brain) between the left inferior temporal lobe and the left and right dorsolateral prefrontal cortex. These are brain areas important for a number of cognitive functions including memory, planning, and mental manipulation of information. Those who did not receive cognitive intervention did not have increases in connectivity.
What does this mean for Parkinson’s disease and for cognitive rehabilitation? It’s difficult to say with this small study. It’s also unknown how long the changes last. Without a restructuring of the brain and continued cognitive rehabilitation it is not likely that the effects will last more than weeks or months after the rehabilitation ends.
To expand on this study (to bring in other research) and put things in simple terms, if people want to protect their brains they best they can as they age, they need to remain physically and mentally active and in good physical and mental shape. Learn new things. Travel to new locations. Take up a physically demanding hobby or dedicated exercise. This won’t solve all our aging problems but it will help a lot.
Díez-Cirarda, M., Ojeda, N., Peña, J. et al. Brain Imaging and Behavior (2016). doi:10.1007/s11682-016-9639-x
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.
A new study by Hall and colleagues (2015) demonstrated that a low fat diet is slightly better for reducing body fat than a low carb diet ( both were effective though).
Abstract: Summary Dietary carbohydrate restriction has been purported to cause endocrine adaptations that promote body fat loss more than dietary fat restriction. We selectively restricted dietary carbohydrate versus fat for 6 days following a 5-day baseline diet in 19 adults with obesity confined to a metabolic ward where they exercised daily. Subjects received both isocaloric diets in random order during each of two inpatient stays. Body fat loss was calculated as the difference between daily fat intake and net fat oxidation measured while residing in a metabolic chamber. Whereas carbohydrate restriction led to sustained increases in fat oxidation and loss of 53 ± 6 g/day of body fat, fat oxidation was unchanged by fat restriction, leading to 89 ± 6 g/day of fat loss, and was significantly greater than carbohydrate restriction (p = 0.002). Mathematical model simulations agreed with these data, but predicted that the body acts to minimize body fat differences with prolonged isocaloric diets varying in carbohydrate and fat.
What does this mean? It means that if you need to lose weight, you’ll probably do better with cutting back on your calories rather than changing what you’re eating. It’s easier to eat less of the same rather than less of something different. Of course, if your diet lacks your basic nutritional needs, you’ll have to change (add vegetables and some fruits), but in general just eat less.
I burn about 2000 calories per day with just normal activities (based on my height, weight, gender, etc). This means if I wanted to lose weight I’d need to consume fewer than 2000 calories per day. It takes about 3500 calories to lose a pound. That’s not exact and isn’t exactly true because if you consume fewer calories, your body tries to maintain weight by burning fewer calories. However, at some point if you restrict your caloric intake under your daily “burning” of calories, you will lose weight. The other thing you can (and probably should) do is exercise.
Men burn about 120 kilocalories per mile while running (this is weight and speed dependent) but only burn about 85 per mile walking. Women burn about 100 per mile running (again, weight and speed dependent) and about 75 per mile walking (source: http://www.runnersworld.com/weight-loss/how-many-calories-are-you-really-burning). Factor in how much you burn throughout the day (sex and weight-dependent in addition to how active you are) and there’s your caloric target to be under.
- Eat less (particularly fat)
- Exercise more
Kevin D. Hall, Thomas Bemis, Robert Brychta, Kong Y. Chen, Amber Courville, Emma J. Crayner, Stephanie Goodwin, Juen Guo, Lilian Howard, Nicolas D. Knuth, Bernard V. Miller III, Carla M. Prado, Mario Siervo, Monica C. Skarulis, Mary Walter, Peter J. Walter, Laura Yannai, Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss than Carbohydrate Restriction in People with Obesity, Cell Metabolism, Available online 13 August 2015, ISSN 1550-4131, http://dx.doi.org/10.1016/j.cmet.2015.07.021. (http://www.sciencedirect.com/science/article/pii/S1550413115003502)
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.
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).
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 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.
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 is what is known as a slowly progressing neurological disorder. It usually has an onset around or after age 60 with an average of 14 years between diagnosis and death (which means that there is a slightly reduced lifespan compared to peers without Parkinson’s disease). While symptoms vary – resting tremor, gait disturbances, flattened emotions – there are some early signs that indicate that someone might have or be developing Parkinson’s disease. If you or someone you know is experiencing a number of these symptoms, contact your primary care physician. Having one or all of these symptoms does not mean you have Parkinson’s disease (I know individuals with a number of these symptoms but they do not have Parkinson’s disease) but if you are experiencing some of them and are concerned, talk with your doctor.
- Shaking when at rest. This usually occurs on one side of the body, often in your extremities, such as a finger or foot or a hand. The shaking might also be worse when you are tired or stressed.
- Reduction in sense of smell.
- Stooped posture where you feel like you cannot stand up straight.
- Changes in your walking – tripping more, difficulty picking up your feet, reduced arm swing (typically on one side).
- Balance problems – you feel like you are more unsteady on your feet; you might not have fallen but you feel like you might.
- Lightheadedness when arising from a sitting position. This is called orthostatic hypotension (drop in blood pressure that occurs when changing from a non-moving state). Again, this is only one of many potential signs; by itself it is not concerning.
- Changes in your handwriting, particularly if it seems sloppier, smaller, or slower.
- Changes in your fine finger dexterity – difficulty with small buttons, for example.
- Stiffness in joints or pain in parts of your body. This can seem like arthritis (and might coexist with arthritis) but is a symptom of Parkinson’s disease.
- Have people telling you that you do not seem as engaged in life as you used to be (i.e., emotionally). This is one way I’ve heard people talk about how the “masked face” of Parkinson’s appears. A person might appear less emotional than he used to (or even more sad).
- Feeling like your thinking has slowed down.
- Feelings of depression or just that you do not have the energy or desire to do as much as you used to do. What is often mistaken as depression is apathy, which is quite common in Parkinson’s disease. Apathy can be a sign of depression but someone can be apathetic without being depressed.
There are other signs of Parkinson’s disease but this list covers the major and some of the minor ones. Which ones are major? Loss (reduction) of sense of smell, constipation, and resting tremor are all very common in Parkinson’s disease; loss of smell and constipation often occur before tremor so they are often missed as signs of potential Parkinson’s disease. Having none, one, or all of the above symptoms does not mean you do or do not have Parkinson’s disease. Many of the symptoms above can be signs of other disorders or can be part of the ‘normal’ aging process (e.g., slightly stooped posture, slowed thinking). However, if you are experiencing some of these symptoms, please talk to your doctor, even if for nothing more than ease of mind.