Posts Tagged plasticity

[BLOG POST] 6 Basic Principles of Neuroplasticity – The Best Brain Possible

6 Basic Principles of Neuroplasticity

Neuroplasticity is an umbrella term referring to the various capabilities of your brain to reorganize itself throughout life due to your environment, behavior, and internal experiences. To ensure the survival of the species, the human nervous system evolved to adapt to its environment — based on learning from past experiences. This is true for all organisms with a nervous system.

According to the book Neuroplasticity from The MIT Press Essential Knowledge Series,  by Moheb Constandi:

But what does ‘rewiring your brain’ actually mean? It refers to the concept of neuroplasticity, a very loosely defined term that simply means some kind of change in the nervous system. Just 50 years ago, the idea that the adult brain can change in any way was heretical. Researchers accepted that the immature brain is malleable, but also believed that it gradually hardens, like clay poured into a mold, into a permanently fixed structure by the time childhood ended. It was also believed that we were born with all the brain cells we will ever have, that the brain is incapable of regenerating itself, and therefore any damage or injuries it sustains cannot be fixed.

In fact, nothing could be further from the truth.”

In the 1980s, researchers at The University of California at San Francisco (UCSF) confirmed that the human brain remodels itself following the “Hebbian rule.” Donald Hebb, a Canadian psychologist, first proposed that “Neurons that fire together, wire together” meaning that the brain continually alters itself physically and operationally based on incoming stimuli.

Types of Neuroplasticity

Although the definition of the word “neuroplasticity” is vague without further qualification, there are basically two types of neuroplasticity:

  • Functional plasticity: The brain’s ability to move functions from one area of the brain to another area.
  • Structural plasticity: The brain’s ability to actually change its physical structure as a result of learning.

Plasticity occurs throughout the brain and can involve many different physical structures, for instance, neurons, synapses, vascular cells, and glial cells.

Your Brain Never Stops Changing

Far from being fixed, your brain is a highly dynamic structure, which undergoes significant change, not only as it develops, but also throughout your entire lifespan. As mentioned above, science used to believe that the brain only changed during certain periods in youth. While it’s true that your brain is much more plastic in the younger years and capacity declines with age, plasticity happens from birth until death.

The human brain reaches about 80 percent of its adult size by two years of age, and growth is nearly complete by age ten. We now know that extensive plastic changes continue to take place in late adolescence and beyond. Harnessing the process of neuroplasticity in adulthood isn’t quite as simple as some of the neuro-hype would have you believe, but it can be accomplished under specific circumstances.

You are not stuck with the brain you were born with or even the one you have right now.

Plasticity Is How All Learning and Memory Happen

Learning and memory are neuroplastic processes in your brain, involving chemical and structural changes. By altering the number or strength of connections between brain cells, information gets written into memory. It’s not really known exactly where or how the recording and recalling of memories happen, but the most popular candidate site for memory storage is the synapse, the space between neurons, where they communicate.

This means that when you repeatedly practice an activity or access a memory, your neural networks are physically shaped accordingly. When you cease a behavior or recalling a specific memory, your brain eventually disconnects the cells no longer in use for that pattern. This can work to your advantage and disadvantage. For example, it’s how bad habits are createdAll addiction happens because of neuroplasticity. However, it’s also how you can weaken painful traumatic memories and reduce anxiety and depression.

6 Basic Principles of Neuroplasticity

Plasticity Allows For Amazing Adaptability

Regions that are normally specialized to perform specific functions can switch roles and process other kinds of information.

Plasticity was first demonstrated in an experiment with ferrets, who have identical wiring to the auditory cortex and visual cortex as humans except for one important factor. The basic human wiring exists at birth while ferrets grow the circuit after birth. Scientist interrupted the pathway in the ferrets so that nerves from the eye grew into the auditory cortex. The ferrets were then trained to respond to sounds and lights. They “heard” the lights with parts of the brain that would normally process sound. 

In a later experiment, sighted adults were blindfolded 24 hours a day for five days. The subjects spent their time learning Braille and performing various tactile and auditory activities. They had their brains scanned before and at the end of the experiment. In the earlier scans, their auditory cortex showed normal activity upon hearing sounds. As expected, their visual cortices lit up when seeing and their somatosensory cortices buzzed when fingering Braille symbols. After five days of being blindfolded, cortical brain regions that had been dedicated to seeing were now hearing and feeling.

You Encourage or Discourage Neuroplasticity With Your Lifestyle Habits

Neuroplastic change occurs in response to stimuli processed in the brain originating either internally or externally.  External stimuli, including things like exercise and cognitive stimulation, enhance the production of neural stem cells and promote the survival of newborn neurons. Internal stimuli originating from your own mind, such as meditation and visualization have also been shown to increase neuroplasticity.  Certain types of neuroinflammationinsufficient sleep, and stress and depression have proven to decrease neuroplasticity.

You can support your brain and encourage neuroplasticity through your lifestyle habits as follows:

  1. Sleep — and lots of it — is absolutely essential for an optimally functioning brain.
  2. Exercise is fertilizer for your brain and promotes the birth and preservation of new brain cells (neurogenesis).
  3. Learn how to feed your brain the nutrients it needs to be in top form.
  4. Make your mental health a priority. Take steps to decrease stress and depression.

As for specific activities you can do, Dr. Michael Merzenich, one of the original researchers confirming plasticity at UCSF and the co-founder of Posit Science Corporation, gives this advice in the article 8 Practical Ways to Keep Your Mind Sharp:

Look for activities that are attentionally demanding and inherently rewarding, and that continuously involve new elements to master. Those types of activities engage brain chemistry that’s beneficial for learning, remembering and mood — by stimulating the production of acetylcholine (when paying attention), norepinephrine (when encountering something new), and dopamine (when feeling rewarded).”

Brain Change Is Specific

The nature of change in your brain is specific to the experience. Experience-dependent changes are usually focal and time-dependant. Plastic change doesn’t typically occur widespread across the brain.

Research has proven that the biggest changes occurring in the brain as a result of learning new skills. For example, in animal studies, research has shown that learning new motor skills yields more dramatic changes in the brain than does the repetition of previously acquired motor movements.

This doesn’t mean that working on existing skills is not beneficial. Repetition is absolutely necessary for neuroplastic alterations to last. Most initial changes are temporary. Your brain first records the change, then determines whether it should make it permanent or not. It only sticks if your brain judges the experience to be novel enough or if the outcome is important enough.

Neuroplastic change is also regionally specific. For example, if you’re learning a skill using your right hand, the changes will be greatest in the areas responsible for that movement. The right and left sides of your body are controlled by the opposite side of your brain. Hence, training with your right hand will make the most changes to the left side of your brain, and vice versa.

Neuroplasticity can help you or hurt you.

6 Basic Principles of Neuroplasticity

Neuroplasticity Is Both Positive and Negative

When you hear about neuroplasticity, it’s usually in conjunction with remarkable, positive brain and life change — almost like science fiction. And like science fiction, it has a dark side. It’s because of neuroplasticity that addictions become ingrained in your brain, valuable skills are lost as your brain ages, and some brain illnesses and conditions show up in humans.

Bad habits and addictions

Forming a habit involves neuroplastic change in your brain. A person desires something because their plastic brain has become sensitized to the substance or experience and craves it. When an urge is satisfied, dopamine, a feel-good neurotransmitter, is released. The same shot of dopamine that gives pleasure is also an essential component of neuroplastic change. Dopamine assists in building neuronal connections that reinforce the habit.

Every time you act in the same way, a specific neuronal pattern is stimulated and strengthened. We know that neurons that fire together wire together. Your brain, wanting to be efficient, takes the path of least resistance each time and a habit — or a full-blown addiction — is born. Fortunately, breaking habits and addictions is accomplished via the same neuroplastic process in reverse

Brain Decline

A lot of the ways in which our brain function degrades that we typically think of as part of “just getting old” is really negative neuroplastic change. As people age, they unknowingly contribute to their brain’s decline by not using and challenging it as much.

You’ve got a “use it or lose it” brain. Information rarely accessed and behaviors seldom practiced cause neural pathways to weaken until connections may be completely lost in a process called “synaptic pruning.” In his book, Soft-Wired: How the New Science of Brain Plasticity Can Change Your Life, Dr. Michael Merzenich calls backward neuroplastic change “negative learning”.

Negative learning can happen at any age — especially with technology doing so much brain work for us these days. Using a GPS consistently, staring straight ahead at a screen for hours a day, texting and not talking to people face-to-face, and many more habits of the modern lifestyle can contribute to undesirable brain changes.

Mental Illness

It’s also because of neuroplasticity that some of the major brain illnesses and conditions show up in humans. Schizophrenia, bipolar disorder, depression, anxiety, obsessive-compulsive and phobic behaviors, epilepsy, and more occur because of neuroplastic change. For example, depression can develop from neuroplastic changes brought about by many things, such as adverse childhood experiences, life circumstances, trauma, lack of emotional support, and stress.

Fortunately for us, neuroplastic change is reversible. You can improve your brain’s function — through the same neuroplastic processes. It’s possible to overcome a mental health condition by driving a brain back towards normal operation through neuroplastic change. Many studies on brain plasticity have demonstrated that many aspects of your brain power, intelligence, or control – in normal and neurologically impaired individuals – can be improved by intense and appropriately targeted behavioral training.


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[WEB PAGE] Reversing SCI and Stroke Damage is Like Finding a Needle in a Haystack

Reversing SCI and Stroke Damage is Like Finding a Needle in a Haystack

A team of researchers from University of Toronto Engineering and the University of Michigan has redesigned and enhanced a natural enzyme that they suggest shows promise in promoting the regrowth of nerve tissue following spinal cord injury or stroke.

Their new version is more stable than the protein that occurs in nature, and could lead to new treatments for reversing nerve damage resulting from the traumatic injury, according to a media release from University of Toronto Faculty of Applied Science & Engineering.

The study is published in the journal Science Advances.

“When we started this project, we were advised not to try as it would be like looking for a needle in a haystack. Having found that needle, we are investigating this form of the enzyme in our models of stroke and spinal cord injury to better understand its potential as a therapeutic, either alone or in combination with other strategies.”

— University of Toronto Engineering professor Molly Shoichet, the study’s senior author

How a Glial Scar Inhibits Nerve Repair

One of the major challenges to healing after spinal cord injury or stroke is the formation of a glial scar. It is formed by cells and biochemicals that knit together tightly around the damaged nerve. In the short term, this protective environment shields the nerve cells from further injury, but in the long term it can inhibit nerve repair.

About two decades ago, scientists discovered that a natural enzyme known as chondroitinase ABC — produced by a bacterium called Proteus vulgaris — can selectively degrade some of the biomolecules that make up the glial scar.

By changing the environment around the damaged nerve, chondroitinase ABC has been shown to promote regrowth of nerve cells. In animal models, it can even lead to regaining some lost function.

But progress has been limited by the fact that chondroitinase ABC is not very stable in the places where researchers want to use it, according to the release.

“It’s stable enough for the environment that the bacteria live in, but inside the body it is very fragile. It aggregates, or clumps together, which causes it to lose activity. This happens faster at body temperature than at room temperature. It is also difficult to deliver chondroitinase ABC because it is susceptible to chemical degradation and shear forces typically used in formulations.”

— Molly Shoichet

Various teams, including Shoichet’s, have experimented with techniques to overcome this instability. Some have tried wrapping the enzyme in biocompatible polymers or attaching it to nanoparticles to prevent it from aggregating. Others have tried infusing it into damaged tissue slowly and gradually, in order to ensure a consistent concentration at the injury site.

But all of these approaches are mere Band-Aids — they don’t address the fundamental problem of instability, per the release.

A New Approach

In this recent study, Shoichet and her collaborators tried a new approach: they altered the biochemical structure of the enzyme in order to create a more stable version.

“Like any protein, chondroitinase ABC is made up of building blocks called amino acids. We used computational chemistry to predict the effect of swapping out some building blocks for others, with a goal of increasing the overall stability while maintaining or improving the enzyme’s activity.”

— Molly Shoichet

“The idea was probably a little crazy, because just like in nature, a single bad mutation can wreck the structure. There are more than 1,000 links in the chain that forms this enzyme, and for each link you have 20 amino acids to choose from. There are too many choices to simulate them all.”

— Mathew O’Meara, a professor of computational medicine and bioinformatics at the University of Michigan, and co-lead author

To narrow down the search space, the team applied computer algorithms that mimicked the types of amino acid substitutions found in real organisms. This approach — known as consensus design — produces mutant forms of the enzyme that don’t exist in nature, but are plausibly like those that do.

In the end, the team ended up with three new candidate forms of the enzyme that were then produced and tested in the lab. All three were more stable than the wild type, but only one, which had 37 amino acid substitutions out of more than 1,000 links in the chain, was both more stable and more active, the release continues.

“The wild type chondroitinase ABC loses most of its activity within 24 hours, whereas our re-engineered enzyme is active for seven days. This is a huge difference. Our improved enzyme is expected to even more effectively degrade the glial scar than the version commonly used by other research groups.”

–Marian Hettiaratchi, co-lead author

A former postdoctoral fellow in Shoichet’s lab, Hettiaratchi is now a professor of bioengineering at the University of Oregon’s Phil and Penny Knight Campus for Accelerating Scientific Impact.

The next step will be to deploy the enzyme in the same kinds of experiments where the wild type was previously used.

Shoichet points to the multidisciplinary nature of the project as a key to its success, the release concludes.

“We were able to take advantage of the complementary expertise of the authors to bring this project to fruition, and we were shocked and overjoyed to be so successful,” she says. “It went well beyond our expectations.”

[Source(s): University of Toronto Faculty of Applied Science & Engineering, EurekAlert]

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[Abstract + References] A Novel Wearable Device for Motor Recovery of Hand Function in Chronic Stroke Survivors


Background. In monkey, reticulospinal connections to hand and forearm muscles are spontaneously strengthened following corticospinal lesions, likely contributing to recovery of function. In healthy humans, pairing auditory clicks with electrical stimulation of a muscle induces plastic changes in motor pathways (probably including the reticulospinal tract), with features reminiscent of spike-timing dependent plasticity. In this study, we tested whether pairing clicks with muscle stimulation could improve hand function in chronic stroke survivors. 

Methods. Clicks were delivered via a miniature earpiece; transcutaneous electrical stimuli at motor threshold targeted forearm extensor muscles. A wearable electronic device (WD) allowed patients to receive stimulation at home while performing normal daily activities. A total of 95 patients >6 months poststroke were randomized to 3 groups: WD with shock paired 12 ms before click; WD with clicks and shocks delivered independently; standard care. Those allocated to the device used it for at least 4 h/d, every day for 4 weeks. Upper-limb function was assessed at baseline and weeks 2, 4, and 8 using the Action Research Arm Test (ARAT), which has 4 subdomains (Grasp, Grip, Pinch, and Gross). 

Results. Severity across the 3 groups was comparable at baseline. Only the paired stimulation group showed significant improvement in total ARAT (median baseline: 7.5; week 8: 11.5; P = .019) and the Grasp subscore (median baseline: 1; week 8: 4; P = .004). 

Conclusion. A wearable device delivering paired clicks and shocks over 4 weeks can produce a small but significant improvement in upper-limb function in stroke survivors.


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[Abstract] Robot-assisted gait training promotes brain reorganization after stroke: A randomized controlled pilot study


Background: Robot-assisted gait training (RAGT) can improve walking ability after stroke but the underlying mechanisms are unknown.

Objective: We evaluated the changes in the injured brain after RAGT and compared the effects of early start and late start of RAGT.

Methods: Eleven patients with hemiplegia after stroke undergoing inpatient rehabilitation were examined within 3 months of stroke onset and were randomly assigned into two groups. Group 1 started RAGT with conventional physiotherapy immediately after enrollment, whereas Group 2 underwent conventional physiotherapy for 4 weeks before starting RAGT. We acquired diffusion tensor imaging data after enrollment and at 4 and 8 weeks after treatment. Fractional anisotropy (FA) and mean diffusivity (MD) maps were used to analyze the neural changes.

Results: Repeated measures analysis of variance of the data at 4 weeks after treatment showed a significant interaction between time and groups (RAGT versus control) for the FA and MD values in the non-lesioned hemisphere, indicating that the non-lesioned hemisphere was significantly reorganized by RAGT compared with conventional physiotherapy. Analysis of the data at 8 weeks after treatment showed a significant interaction between time and groups (early and late start of RAGT) for the MD values in the motor-related areas bilaterally, indicating that early start of RAGT significantly accelerated bi-hemispheric reorganization as compared with late start of RAGT.

Conclusions: Our findings indicate that RAGT can facilitate reorganization in the intact superior temporal, cingulate, and postcentral gyri. Furthermore, early start of RAGT can accelerate bi-hemispheric reorganization in the motor-related brain regions.

via Robot-assisted gait training promotes brain reorganization after stroke: A randomized controlled pilot study – PubMed

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[Abstract] The Effect of Priming on Outcomes of Task-Oriented Training for the Upper Extremity in Chronic Stroke: A Systematic Review and Meta-analysis

Background. Priming results in a type of implicit memory that prepares the brain for a more plastic response, thereby changing behavior. New evidence in neurorehabilitation points to the use of priming interventions to optimize functional gains of the upper extremity in poststroke individuals. Objective. To determine the effects of priming on task-oriented training on upper extremity outcomes (body function and activity) in chronic stroke.

Methods. The PubMed, CINAHL, Web of Science, EMBASE, and PEDro databases were searched in October 2019. Outcome data were pooled into categories of measures considering the International Classification Functional (ICF) classifications of body function and activity. Means and standard deviations for each group were used to determine group effect sizes by calculating mean differences (MDs) and 95% confidence intervals via a fixed effects model. Heterogeneity among the included studies for each factor evaluated was measured using the I2 statistic.

Results. Thirty-six studies with 814 patients undergoing various types of task-oriented training were included in the analysis. Of these studies, 17 were associated with stimulation priming, 12 with sensory priming, 4 with movement priming, and 3 with action observation priming. Stimulation priming showed moderate-quality evidence of body function. Only the Wolf Motor Function Test (time) in the activity domain showed low-quality evidence. However, gains in motor function and in use of extremity members were measured by the Fugl-Meyer Assessment (UE-FMA). Regarding sensory priming, we found moderate-quality evidence and effect size for UE-FMA, corresponding to the body function domain (MD 4.77, 95% CI 3.25-6.29, Z = 6.15, P < .0001), and for the Action Research Arm Test, corresponding to the activity domain (MD 7.47, 95% CI 4.52-10.42, Z = 4.96, P < .0001). Despite the low-quality evidence, we found an effect size (MD 8.64, 95% CI 10.85-16.43, Z = 2.17, P = .003) in movement priming. Evidence for action observation priming was inconclusive.

Conclusion. Combining priming and task-oriented training for the upper extremities of chronic stroke patients can be a promising intervention strategy. Studies that identify which priming techniques combined with task-oriented training for upper extremity function in chronic stroke yield effective outcomes in each ICF domain are needed and may be beneficial for the recovery of upper extremities poststroke.

via The Effect of Priming on Outcomes of Task-Oriented Training for the Upper Extremity in Chronic Stroke: A Systematic Review and Meta-analysis – Erika Shirley Moreira da Silva, Gabriela Nagai Ocamoto, Gabriela Lopes dos Santos-Maia, Roberta de Fátima Carreira Moreira Padovez, Claudia Trevisan, Marcos Amaral de Noronha, Natalia Duarte Pereira, Alexandra Borstad, Thiago Luiz Russo,

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[Abstract] A Novel Wearable Device for Motor Recovery of Hand Function in Chronic Stroke Survivors

Background. In monkey, reticulospinal connections to hand and forearm muscles are spontaneously strengthened following corticospinal lesions, likely contributing to recovery of function. In healthy humans, pairing auditory clicks with electrical stimulation of a muscle induces plastic changes in motor pathways (probably including the reticulospinal tract), with features reminiscent of spike-timing dependent plasticity. In this study, we tested whether pairing clicks with muscle stimulation could improve hand function in chronic stroke survivors.

Methods. Clicks were delivered via a miniature earpiece; transcutaneous electrical stimuli at motor threshold targeted forearm extensor muscles. A wearable electronic device (WD) allowed patients to receive stimulation at home while performing normal daily activities. A total of 95 patients >6 months poststroke were randomized to 3 groups: WD with shock paired 12 ms before click; WD with clicks and shocks delivered independently; standard care. Those allocated to the device used it for at least 4 h/d, every day for 4 weeks. Upper-limb function was assessed at baseline and weeks 2, 4, and 8 using the Action Research Arm Test (ARAT), which has 4 subdomains (Grasp, Grip, Pinch, and Gross).

Results. Severity across the 3 groups was comparable at baseline. Only the paired stimulation group showed significant improvement in total ARAT (median baseline: 7.5; week 8: 11.5; P = .019) and the Grasp subscore (median baseline: 1; week 8: 4; P = .004).

Conclusion. A wearable device delivering paired clicks and shocks over 4 weeks can produce a small but significant improvement in upper-limb function in stroke survivors.

via A Novel Wearable Device for Motor Recovery of Hand Function in Chronic Stroke Survivors – Supriyo Choudhury, Ravi Singh, A. Shobhana, Dwaipayan Sen, Sidharth Shankar Anand, Shantanu Shubham, Suparna Gangopadhyay, Mark R. Baker, Hrishikesh Kumar, Stuart N. Baker,

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[WEB SITE] Why Your Brain Needs Exercise

Why Your Brain Needs Exercise

Credit: Bryan Christie Design

Why Your Brain Needs Exercise

The evolutionary history of humans explains why physical activity is important for brain health


  • It is by now well established that exercise has positive effects on the brain, especially as we age.
  • Less clear has been why physical activity affects the brain in the first place.
  • Key events in the evolutionary history of humans may have forged the link between exercise and brain function.
  • Cognitively challenging exercise may benefit the brain more than physical activity that makes fewer cognitive demands.


In the 1990s researchers announced a series of discoveries that would upend a bedrock tenet of neuroscience. For decades the mature brain was understood to be incapable of growing new neurons. Once an individual reached adulthood, the thinking went, the brain began losing neurons rather than gaining them. But evidence was building that the adult brain could, in fact, generate new neurons. In one particularly striking experiment with mice, scientists found that simply running on a wheel led to the birth of new neurons in the hippocampus, a brain structure that is associated with memory. Since then, other studies have established that exercise also has positive effects on the brains of humans, especially as we age, and that it may even help reduce the risk of Alzheimer’s disease and other neurodegenerative conditions. But the research raised a key question: Why does exercise affect the brain at all?

Physical activity improves the function of many organ systems in the body, but the effects are usually linked to better athletic performance. For example, when you walk or run, your muscles demand more oxygen, and over time your cardiovascular system responds by increasing the size of the heart and building new blood vessels. The cardiovascular changes are primarily a response to the physical challenges of exercise, which can enhance endurance. But what challenge elicits a response from the brain?

Answering this question requires that we rethink our views of exercise. People often consider walking and running to be activities that the body is able to perform on autopilot. But research carried out over the past decade by us and others would indicate that this folk wisdom is wrong. Instead exercise seems to be as much a cognitive activity as a physical one. In fact, this link between physical activity and brain health may trace back millions of years to the origin of hallmark traits of humankind. If we can better understand why and how exercise engages the brain, perhaps we can leverage the relevant physiological pathways to design novel exercise routines that will boost people’s cognition as they age—work that we have begun to undertake.


To explore why exercise benefits the brain, we need to first consider which aspects of brain structure and cognition seem most responsive to it. When researchers at the Salk Institute for Biological Studies in La Jolla, Calif., led by Fred Gage and Henriette Van Praag, showed in the 1990s that running increased the birth of new hippocampal neurons in mice, they noted that this process appeared to be tied to the production of a protein called brain-derived neurotrophic factor (BDNF). BDNF is produced throughout the body and in the brain, and it promotes both the growth and the survival of nascent neurons. The Salk group and others went on to demonstrate that exercise-induced neurogenesis is associated with improved performance on memory-related tasks in rodents. The results of these studies were striking because atrophy of the hippocampus is widely linked to memory difficulties during healthy human aging and occurs to a greater extent in individuals with neurodegenerative diseases such as Alzheimer’s. The findings in rodents provided an initial glimpse of how exercise could counter this decline.

Following up on this work in animals, researchers carried out a series of investigations that determined that in humans, just like in rodents, aerobic exercise leads to the production of BDNF and augments the structure—that is, the size and connectivity—of key areas of the brain, including the hippocampus. In a randomized trial conducted at the University of Illinois at Urbana-Champaign by Kirk Erickson and Arthur Kramer, 12 months of aerobic exercise led to an increase in BDNF levels, an increase in the size of the hippocampus and improvements in memory in older adults.

Other investigators have found associations between exercise and the hippocampus in a variety of observational studies. In our own study of more than 7,000 middle-aged to older adults in the U.K., published in 2019 in Brain Imaging and Behavior, we demonstrated that people who spent more time engaged in moderate to vigorous physical activity had larger hippocampal volumes. Although it is not yet possible to say whether these effects in humans are related to neurogenesis or other forms of brain plasticity, such as increasing connections among existing neurons, together the results clearly indicate that exercise can benefit the brain’s hippocampus and its cognitive functions.

Researchers have also documented clear links between aerobic exercise and benefits to other parts of the brain, including expansion of the prefrontal cortex, which sits just behind the forehead. Such augmentation of this region has been tied to sharper executive cognitive functions, which involve aspects of planning, decision-making and multitasking—abilities that, like memory, tend to decline with healthy aging and are further degraded in the presence of Alzheimer’s. Scientists suspect that increased connections between existing neurons, rather than the birth of new neurons, are responsible for the beneficial effects of exercise on the prefrontal cortex and other brain regions outside the hippocampus.


With mounting evidence that aerobic exercise can boost brain health, especially in older adults, the next step was to figure out exactly what cognitive challenges physical activity poses that trigger this adaptive response. We began to think that examining the evolutionary relation between the brain and the body might be a good place to start. Hominins (the group that includes modern humans and our close extinct relatives) split from the lineage leading to our closest living relatives, chimpanzees and bonobos, between six million and seven million years ago. In that time, hominins evolved a number of anatomical and behavioral adaptations that distinguish us from other primates. We think two of these evolutionary changes in particular bound exercise to brain function in ways that people can make use of today.

Graphic shows how increased production of the protein BDNF may promote neuron growth and survival in the adult brain.

Credit: Tami Tolpa


For more, visit —->  Why Your Brain Needs Exercise – Scientific American

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[WEB SITE] Play Therapeutic Games with EDNA to Aid Stroke Rehab

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A new touch-screen therapy tool could accelerate the recovery of patients who have experienced a stroke and change the way rehabilitation is delivered in hospitals and homes, RMIT University researchers suggest in a media release.

Designed for people with acquired brain injuries, EDNA is a digital rehabilitation software that delivers therapy through a series of fun and challenging therapeutic games via a touchscreen device.

Findings from a randomized clinical trial showed stroke patients who incorporated EDNA into their treatment programs experienced an improvement two to three times greater than those who received only conventional therapy, according to the release, from RMIT University.

The digital form of rehabilitation was intended to maintain patient engagement, improving compliance and recovery, says RMIT University lead researcher, Associate Professor Jonathan Duckworth.

“We designed EDNA so that patients could be doing therapy without it feeling like therapy,” he adds.

EDNA features a range of therapeutic games that involve tangible and graspable tools with augmented feedback, promoting brain plasticity to regain motor, cognitive and functional ability.

Performance data is then collected in the cloud, allowing therapists to remotely review the integrated data, monitor recovery and deliver tailored treatment programs.

While the results couldn’t yet be used to predict longer-term recovery, the findings were promising and showed the value of including EDNA as part of a therapy toolkit, Duckworth states.

“EDNA is the first upper-limb brain injury rehabilitation system to integrate clinic and home therapy to monitor recovery, so there’s great potential to transform the industry and improve outcomes for patients.”

The recent clinical trial, published in the Journal of NeuroEngineering and Rehabilitation, involved a specialized table-top touch screen.

A new study is now underway at Sydney’s Prince of Wales hospital using a portable version that allows for increased treatment frequency with independent therapy at home.

Principal investigator and neuropsychologist from the University of Sydney, Dr Jeff Rogers, shares in the release that the innovative technology had delivered benefits for stroke patients that had exceeded expectations.

“We’ve worked closely with patients in testing and designing EDNA to ensure it will actually be used and we’re really happy with the results,” he says.

Study co-author, Professor Peter Wilson from the Australian Catholic University, comments that a home-based therapeutic solution had the potential to reduce the number of weekly hospital visits and aligned with recent trends towards patient-centered rehabilitation.

“Patients can struggle to maintain therapy activities between sessions, so having a portable device to take home and use on their own could increase therapy uptake and speed up recovery,” he says.

[Source(s): RMIT University, MedicalXPRess]


via Play Therapeutic Games with EDNA to Aid Stroke Rehab – Rehab Managment

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[VIDEO] Harnessing the Power of Neuroplasticity: The Nuts and Bolts of Better Brains – YouTube

What if your brain at 77 were as plastic as it was at 7? What if you could learn Mandarin with the ease of a toddler or play Rachmaninoff without breaking a sweat? A growing understanding of neuroplasticity suggests these fantasies could one day become reality. Neuroplasticity may also be the key to solving diseases like Alzheimer’s, depression, and autism. In this program, leading neuroscientists discuss their most recent findings and both the tantalizing possibilities and pitfalls for our future cognitive selves.

PARTICIPANTS: Alvaro Pascual-Leone, Nim Tottenham, Carla Shatz



This program is part of the BIG IDEAS SERIES, made possible with support from the JOHN TEMPLETON FOUNDATION.

TOPICS: – Opening film 00:07 – What is neuroplasticity? 03:53 – Participant introductions 04:21 – Structure of the brain 05:21 – Is the brain fundamentally unwired at the start? 07:02 – Why does the process of human brain development seem inefficient? 08:30 – Balancing stability and plasticity 10:43 – Critical periods of brain development 13:01 – Extended human childhood development compared to other animals 14:54 – Stability and. plasticity in the visual system 17:37 – Reopening the visual system 25:13 – Pros and cons of brain plasticity vs. stability 27:28 – Plasticity in the autistic brain 29:55 – What is Transcranial magnetic stimulation (TMS) 31:25 – Phases of emotional development 33:10 – Schizophrenia and plasticity 37:40 – Recovery from brain injury 40:24 – Modern rehabilitation techniques 47:21 – Holy grail of Neuroscience 50:12 – Enhancing memory performance as we age 53:37 – Regulating emotions 57:19

PROGRAM CREDITS: – Produced by Nils Kongshaug – Associate Produced by Christine Driscoll – Opening film written / produced by Vin Liota – Music provided by APM – Additional images and footage provided by: Getty Images, Shutterstock, Videoblocks

This program was recorded live at the 2018 World Science Festival and has been edited and condensed for YouTube.

via Harnessing the Power of Neuroplasticity: The Nuts and Bolts of Better Brains – YouTube

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[WEB SITE] When it Comes to Stroke Recovery, Who You See Matters

(a) Top view of the experiment. A tablet monitor was placed over the participant’s right forearms on the desk in front of them. (b) Diagrammatic view of the experiment from the left. There is a space to open the hand, which made it easier to imagine the opening-clench hand movement. (Photo courtesy of Toshihisa Tanaka, TUAT)

For stroke patients, observing their own hand movements in a video-assisted therapy – as opposed to someone else’s hand – could enhance brain activity and speed up rehabilitation, according to researchers.

The scientists, from Tokyo University of Agriculture and Technology (TUAT), published their findings in IEEE Transactions on Neural Systems and Rehabilitation Engineering.

Brain plasticity, where a healthy region of the brain fulfills the function of a damaged region of the brain, is a key factor in the recovery of motor functions caused by stroke. Studies have shown that sensory stimulation of the neural pathways that control the sense of touch can promote brain plasticity, essentially rewiring the brain to regain movement and senses.

To promote brain plasticity, stroke patients may incorporate a technique called motor imagery in their therapy. Motor imagery allows a participant to mentally simulate a given action by imagining themselves going through the motions of performing that activity. This therapy may be enhanced by a brain-computer interface technology, which detects and records the patients’ motor intention while they observe the action of their own hand or the hand of another person, a media release from Tokyo University of Agriculture and Technology explains.

“We set out to determine whether it makes a difference if the participant is observing their own hand or that of another person while they’re imagining themselves performing the task,” says co-author Toshihisa Tanaka, a professor in the Department of Electrical and Electrical Engineering at TUAT in Japan and a researcher at the RIKEN Center for Brain Science and the RIKEN Center for Advanced Intelligent Project.

The researchers monitored brain activity of 15 healthy right-handed male participants under three different scenarios. In the first scenario, participants were asked to imagine their hand moving in synchrony with hand movements being displayed in a video clip showing their own hand performing the task, together with corresponding voice cues.

In the second scenario, they were asked to imagine their hand moving in synchrony with hand movements being displayed on a video clip showing another person’s hand performing the task, together with voice cues. In the third scenario, the participants were asked to open and close their hands in response to voice cues only.

Using electroencephalography (EEG), brain activity of the participants was observed as they performed each task.

The team found meaningful differences in EEG measurements when participants were observing their own hand movement and that of another person. The findings suggest that, in order for motor imagery-based therapy to be most effective, video footage of a patient’s own hand should be used.

“Visual tasks where a patient observes their own hand movement can be incorporated into brain-computer interface technology used for stroke rehabilitation that estimates a patient’s motor intention from variations in brain activity, as it can give the patient both visual and sense of movement feedback,” Tanaka explains.

[Source(s): Tokyo University of Agriculture and Technology, EurekAlert]

via When it Comes to Stroke Recovery, Who You See Matters – Rehab Managment

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