I just released a new book, Blame Game. How To Win It. Although it is based more on general psychological principles, one of the five chapters explains how learning and memory changes the brain, chemically and structurally, and thus provides a way to change behavior permanently. The book's thesis is a five-step program for living the good life. Think of it as "debt relief" for the high costs of excuse-making. Prominent psychologists have endorsed the pre-publication version. Check it out at Amazon or at your local bookstore (official release date is July 24).

Updating Existing Memories Also Requires Consolidation

As a newly forming memory develops (see chapter on memory consolidation in my book), it is susceptible to disruption by mind wandering, other stimuli, distractions, etc. When a new memory is retrieved, a re-consolidation process will be required if updated information needs to be incorporated. Such re-consolidation involves a new round of protein synthesis in brain cells, similar to that which is needed to make the initial learning a lasting memory. Likewise, a re-consolidation process must be protected from disruptive influences if the updated information is to be integrated and consolidated with the original learning.

There is good news and bad news here. The good news is that new information can update and be integrated with old memories. Recall also my earlier post on the possible use of this principle with treatment of Post-traumatic Stress Syndrome. The bad news is that old memories become vulnerable to corruption with each new re-consolidation, leading perhaps to false memories. My book has a whole chapter on false memory.

Source: Rodriguez-Ortiz, C. J. et al. 2005. Spatial memory undergoes post-retrieval consolidation only if updating information is acquired. Soc. Neuroscience Abstract 654.20.

Omega 3 May Reduce Odds of Alzheimer’s Disease

In mice, rats, and cultured human cells, an omega-3 fatty acid found in algae called docosahexaenoic acid, or DHA, was found to decrease an important risk factor for late-onset Alzheimer's disease. DHA increases the production of a protein vital to clearing the brain of the enzymes that make the beta amyloid plaques found in Alzheimer's disease.

Alzheimer's patients are known to have reduced levels of this protein that normally would clear the plaque-making enzymes. This data suggest that long-term use of DHA supplements might help people reduce the odds of developing Alzheimer’s disease.

The National Institutes of Health is now funding a multi-million dollar clinical study on the effects of vegetarian DHA from microalgae in slowing the progression of Alzheimer's disease. This DHA is a vegetarian form of omega-3, which supports brain, eye and cardiovascular health throughout life. I have mentioned the value for omega 3 in an earlier blog. Most people don’t get enough omega 3 in their diet. But it is not just the amount of DHA that is important, but also its ratio to another fatty acid, omega 6. A typical Western diet produces a ratio ranging from 1:10 to 1:30, where ideally it should be 1:5 to 1:3.

Fish oil is the usual source of DHA, but the algae source is vegetarian and may have fewer ocean contaminants. It is made by the Martek Biosciences Corporation (http://www.martek.com/).

Source:

Ma, Qie-Lan, et al. 2007. Omega-3 fatty acid docosahexaenoic acid increases SorLA/LR11, a sorting protein with reduced expression in sporadic Alzheimer's Disease (AD): Relevance to AD prevention. Journal of Neuroscience, 27(52):14299-14307.

Help Your Working-memory Capacity

I just read a fascinating book on increasing teacher awareness of the importance of working-memory capacity for teaching and learning strategies. Many youngsters have working memory limitations, and they usually do not grow out of them. This is a major and serious cause of low grades, poor learning skills, poor confidence, and life-long diminished motivation to learn.

Limited working-memory capacity impairs the ability to think and solve problems. I was told once by a middle-school teacher that her “special needs” students could do the same math as regular students, but they just can’t remember all the steps. This clearly reflects a limited working-memory capacity. If the demands made on working memory could be lessened, better thinking could result.

Certain strategies can help to reduce the load on working memory. Teachers should model and students should employ the following devices:

• Provide help, cues, mnemonics, reminders.

• KISS (Keep It Simple, Stupid!)(example: use short, simple sentences, present much of the instruction as pictures/diagrams).

• Don’t present so much information. Less can be more.

• Facilitate rehearsal, using only relevant information and no distractors.

• Get engaged, by taking notes, and creating diagrams and concept maps.

• Attach meaning from what is already known. (The more you know, the more you can know).

• Organize information in small categories.

• Break down tasks into small chunks. Master each chunk sequentially, one at a time.

Doing these things not only helps the thinking process, but will also promote the formation of lasting memories. The process of converting working memory into permanent form is called consolidation, and I will explain that next time.

Source:

Gathercole, Susan E., and Alloway, Tracy P. 2008. Working memory and learning. Sage Publications,. 124 pages.

Core Neuroscience Ideas

Readers of this blog who want to have a fuller understanding on how the brain achieves learning and memory may want to know about my new e-book on Core Ideas In Neuroscience.

This modular e-book is a new kind of neuroscience textbook that can liberate professors and students from the boredom of traditional lectures. The book is designed for psychology, medical, allied health, and biology students and professionals who are tired of textbooks that tell them more than they want to know and who don’t want to spend over $100 for their neuroscience book.

This is the fast and inexpensive way to get up to speed on the core ideas in neuroscience.

Benefits for students include: important things are made explicit. Less material is easier to comprehend quickly and to remember. Book’s focus on ideas promotes active learning, critical thinking, insight and understanding. Benefits for professors include: no need to worry about students missing the important information; key concepts are succinctly presented in the book. Class time can be used for more engaging material, such as discussion and debate, clinical case studies, journal club, or design of new experiments. Each of the 75 core ideas is generally treated as a 3-5 page module in which the idea is succinctly stated and explained, with key terms defined. Then, a couple of examples are given, followed by contemporary and classic references. The book has 174 study questions, 96 figures, 545 references (including 306 citation classics), and 566 e-pages. It costs only $11.95, just 16 cents per idea.

Giving Up Can Help Tip-of-the-Tongue States

All of us have had those tip-of-the-tongue (TOT) states where we just can't recall a friend's name or some fact just when we need it. I discuss this phenomenon on pages 198 to 206 of my book. I explain how to deal with this problem by staying calm and trying to recall all the cues associated with what you are trying to remember.


But what if you did not use many cues when you first formed the memory? In those cases, the remedy should perhaps be different. Two psychologists at McMaster University in Ontario recently published a study showing that trying hard to retrieve a TOT memory may be counterproductive. They studied 30 volunteers who were shown definitions to words they did not know. Some definitions were easy, some were hard, and some were fakes. When tested for recall, subjects were instructed to press a button any time they encountered a TOT state. When subjects entered a TOT state they were told to keep trying and they would be told the answer in 10 or 30 seconds if they don't get it.

Subjects were re-tested two days later by being asked to generate the word that fit each definition. Researchers found that subjects had a high probability of stumbling again on the same words they had trouble with the first time. TOTs were almost twice as likely to happen again on words that initially caused a TOT and had been followed by a long delay than on those that had been followed by a short delay. One conclusion is that failing the first time is actually an implicit learning condition wherein subjects are learning to fail again. The longer they kept trying, as in the 30-second group, the more time they had to learn to fail.

These subjects had not been instructed to make visual images of words and their definitions during initial learning. Had that been done, there might have been fewer TOTs the second time and those that did occur could probably have been resolved by thinking of the cues.

So, the next time you have a TOT for somebody's name or some fact, first think of all the cues you can. If cues don't come to mind, you probably should quickly move on mentally to something else and periodically come back to the item that caused your TOT state. When the answer finally does come to you, make as many associations as you can that can serve as cues the next time.


Soucre: Warriner, A. B., and Humphreys, K. R. 2008. Learning to fail: recurring tip-of-the-tongue states. Quaterly J. Exp. Psychol. 61: 535-542.

Learning to Learn II – Learning Can Increase the Biological Capacity to Learn

I explained in my book on memory that the hippocampus is the brain structure that promotes consolidation of (declarative) short-term memories into long-term memories. I have also reviewed studies showing that the hippocampus is the one structure in the brain that clearly receives newborn nerve cells, even in the adult. New cells can enhance the ability of the hippocampus to create lasting memories. What has not been emphasized is the importance of survival of new neurons. To be of lasting benefit, new neurons must survive beyond just being born.

Insight into the requirements for neuron survival has come in a recent study by J. R. Epp and colleagues at the University of British Columbia. They injected rats with a chemical marker for DNA that shows up in any new DNA, that is in any newly born cells. If that marker shows up in a cell, it means that that this is a new cell that has incorporated the marker along with its new DNA.

Immediately after injection of the marker, the experimenters trained the rats in a large pool of water that had a safe platform located 2 cm under the water surface where rats could learn its location from seeing cues outside of the pool (such as windows, doors, pictures on the wall, etc.). Other studies had established that learning this task is accomplished by the hippocampus. Rats were divided into groups and trained on days 1-5, 6-10, or 11-15 after injection of the DNA marker. The new-DNA marker showed up only in rats trained on days 6-10 after marker injection. This indicated that there must have been new neurons in the hippocampus of these rats that did not survive in the two groups where marker was not seen. Put another way, for new neurons to survive there is a critical period where they have to be stimulated by learning experiences. Without that stimulus, they die.

Earlier studies had shown that new neurons in rat hippocampus have a development cycle wherein 6-10 days after birth is a middle stage of development in which new neurons are rapidly sending out membrane processes in search of contacts with other neurons. When neurons make contact with targets they can survive. The stimulus of learning thus provides a stimulus for forming new synapses with other neurons, thus enabling new neurons to survive.

The data were originally pooled across all rats in each test group. However, when the data were segregated by how well rats learned (the top and bottom 50 %), it became clear that it was only the poor learners that were showing an effect on new-neuron survival by maze learning. Poor learners probably got more stimulation from the learning because their brains had to work harder at it. It wasn’t that much of a mental challenge for good learners.

We know that humans are continually producing new neurons in the hippocampus. The issue is the need to experience enough demanding learning to help these new neurons survive. The critical period for learning to influence new-neuron survival in humans is not known. So, the practical take-home message is that we need to be learning constantly, every day, so that no matter what the critical period is, we will be helping our new neurons to survive. Survival of new neurons means a greater biological capacity for learning, at least in people who are not good learners. In other words, here is a clear case where the “poor get richer.”

Source: Epp, J. D., Spritzer, M. D., and Gales, L. A. M. 2007. Hippocampus-dependent learning promotes survival of new neurons in the dentate gyrus at a specific time during cell maturation. Behavioural Neuroscience. 149: 273-285.

Learn One Movement Skill At a Time

"Motor memory" refers to a mental model (MM) that the brain constructs from past experience. In the example given by researchers Reza Shadmehr and Thomas Brashara-Krug, when a person plans to pick up a brick, a MM of the amount of force required to pick up the brick is used to execute the action.The brain does not estimate the force as if it were a feather nor if it were a sack of cement, rather it uses its memory of what a brick weighs to create a model of how much force will be needed to pick it up.

In the studies they reported, they used a robotic arm that subjects used to manipulate objects. In learning how to use the mechanical arm, subjects had to create a MM of how to make it do what they wanted. Like other kinds of learning, the MM is consolidated with practice into long-term memory.Moreover, motor performance continues to improve, even after actual practice has stopped, indicating that the MM itself may be subconsciously rehearsed, off-line so to speak.

Motor memory processes have great applicability in everything from learning to touch-type to learning to throw a football to a moving target. The study by Shadmehr and Brashara-Krug explored the finding that a recently acquired MM (MM1) can be disrupted if a second MM (MM2) was introduced too soon after MM1.That is, a MM1 has to have enough time to consolidate, just as declarative memories do.

Also, a MM1 can interfere with learning a MM2, if there is not enough time separation between learning the two motor tasks.This was demonstrated in the present study by having 60 subjects learn how to make two conflicting movements using the robotic arm. The MM for both tasks could be learned but only if the training sessions were separated by at least 5 hours. If the interval was shorter, learning of the second MM (MM2) was impaired, as was the likelihood of consolidating the first MM.

The “take home message” of this research is that learning different movement tasks should be separated in time, lest there be interference with forming long-term memory of both tasks. My explanation is the following: Once MM1 gets consolidated (that is, after about 5 hours), the circuits that sustain its short-term representation now become available for learning a second motor memory (MM2). That is, MM1 has proactive interfering after-effects that dissipate with consolidation of the MM1 and thus no longer interfere with learning an MM2.

Athletic coaches might be well advised to ponder the application of this principle.


Shadmehr, R., and Brfashers-Krug, T. 1997. Functional stages in the formation of human long-term motor memory. J. Neuroscience. 17(1): 409-419.