Posts Tagged Brain plasticity

[VIDEO] How brain plasticity can change your life with Michael Merzenich at Mind & Its Potential 2014 – YouTube

Hear the latest on how the brain develops and how positive and negative brain plasticity remodels the brain across the lifespan. Learn how to evaluate your own brain and how to rejuvenate, remodel and reshape your brain at any age.

Professor Michael Merzenich, USA, world’s foremost expert on the science of brain training who featured in ABC TV hit series Redesign My Brain as Todd Sampson’s brain training mentor; author of Soft-Wired: How The New Science of Brain Plasticity Can Change Your Life

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[NEWS] Vitamin D Deficiency Linked to Loss in Brain Plasticity

Feb 21, 2019 | Original Press Release from the University of Queensland

Vitamin D Deficiency Linked to Loss in Brain Plasticity

Perineuronal nets (bright green) surround particular neurons (blue). Fluorescence labelling reveals just how detailed these structures are. Credit: Phoebe Mayne, UQ

University of Queensland research may explain why vitamin D is vital for brain health, and how deficiency leads to disorders including depression and schizophrenia.


via Vitamin D Deficiency Linked to Loss in Brain Plasticity | Technology Networks

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[WEB SITE] Vagus Nerve Stimulation Enhances Brain Plasticity

Sebastian Kaulitzki/Shutterstock

Vagus nerve illustrated in yellow.
Source: Sebastian Kaulitzki/Shutterstock

Vagus nerve stimulation (VNS) enhances targeted neuroplasticity, helping the brain build stronger neural connections after a stroke, according to pioneering research from the University of Texas at Dallas. Using an animal model, the researchers have demonstrated for the first time that pairing VNS with a physical therapy task accelerates the recovery of motor skills.

The researchers published their findings, “Vagus Nerve Stimulation Enhances Stable Plasticity and Generalization of Stroke Recovery,” in the journal Stroke. A human clinical trial of the same treatment, “Pivotal Study of VNS During Rehab After Stroke (VNS-REHAB),” is currently underway at 18 research sites across the US and in the UK. The goal of the study is to gauge the efficacy of paired vagus nerve stimulation in helping stroke patients recover motor skills more quickly.

What Is Vagus Nerve Stimulation?

Alila Medical Media/Shutterstock

Source: Alila Medical Media/Shutterstock

Vagus nerve stimulation is delivered via a small, surgically implanted device that uses electrical impulses of varying intensities and pulse-widths to activate the vagus nerve. Electrical stimulation of the vagus nerve using VNS is an FDA-approved treatment for drug-resistant epilepsy and treatment-resistant depression. A recent proof-of-concept human study also found that VNS is a viable treatment for inflammatory joint diseases such as rheumatoid arthritis.

The sudden loss of blood flow after a stroke causes neurons in any stroke-affected brain region to die, which cuts off connections to other nerve cells. The loss of motor skills in an arm or leg after a stroke is caused by a loss of connectivity between nerve cells in the limb with corresponding motor regions of the brain.

Using an animal model, the UT Dallas researchers found that brief bursts of VNS strengthen communication pathways by building stronger cell connections in the brain after a stroke. In fact, their results show that coupling VNS with targeted movement therapies dramatically boosts the benefit of rehabilitative training after a stroke. And, in animal studies, these improvements lasted for months after the completion of VNS targeted therapy.

As the authors of this study, led by Eric C. Meyers, explain: “This study provides the first evidence that VNS paired with rehabilitative training after stroke (1) doubles long-lasting recovery on a complex task involving forelimb supination, (2) doubles recovery on a simple motor task that was not paired with VNS, and (3) enhances structural plasticity in motor networks.”

Michael Kilgard, associate director of the Texas Biomedical Device Center and professor of neuroscience in the School of Behavioral and Brain Sciences at UT Dallas, was a senior co-author of this research. Kilgard is the principal investigator at the UTD Cortical Plasticity Laboratory. His teamalso includes Seth Hays, a postdoctoral researcher in the School of Behavioral and Brain Sciences at UT Dallas, who specializes in targeted plasticity therapy to alleviate motor dysfunction.

“Our experiment was designed to ask this new question: After a stroke, do you have to rehabilitate every single action?” Kilgard said in a statement. “If VNS helps you, is it only helping with the exact motion or function you paired with stimulation? What we found was that it also improves similar motor skills as well, and that those results were sustained months beyond the completion of VNS-paired therapy.”

The UT Dallas researchers are optimistic that their latest research on targeted vagus nerve stimulation is a pivotal step toward creating guidelines for standardized usage of VNS during post-stroke therapy in humans. “We have long hypothesized that VNS is making new connections in the brain, but nothing was known for sure,” Hays said in a statement. “This is the first evidence that we are driving changes in the brain in animals after brain injury. It’s a big step forward in understanding how the therapy works — this reorganization that we predicted would underlie the benefits of VNS.”

Another recent study from UT Dallas found that moderate intensity vagus nerve stimulation optimized the neuroplasticity-enhancing and memory-enhancing effects of VNS more effectively than low or high-intensity stimulation. Notably, the researchers pinpointed that the optimal pulse width and current intensity were marked by an “inverted-U” pattern in which too much or too little VNS was less effective than a ‘Goldilocks’ sweet spot of moderate intensity that was just right. These 2017 findings were published in the journal Brain Stimulation.

Paired Vagus Nerve Stimulation Offers New Hope for Stroke Rehabilitation

In 2017, the makers of a vagus nerve stimulation device launched a randomized, double-blind clinical trial of VNS rehab for patients after a cerebrovascular stroke. This study, currently underway, will include up to 120 subjects at 18 clinical locations across the US and in the UK. The estimated conclusion date of preliminary research for this clinical trial is June 30, 2019.

The Ohio State University is one of the institutions participating in the paired VNS clinical trial. Marcie Bockbrader of the Wexner Medical Center at OSU is their principal investigator for the trial.

In a recent press release, Bockbrader said: “This nerve stimulation is like turning on a switch, making the patient’s brain more receptive to therapy. The goal is to see if we can improve motor recovery in people who have what is, in effect, a brain pacemaker implanted in their body. The idea is to combine this brain pacing with normal rehab, and see if patients who’ve been through all of their other usual therapies after a stroke can get even better.”

Below is a YouTube video of Marcie Bockbrader and colleagues in their paired VNS therapy lab along with a patient describing his stroke rehab process:

For this clinical trial, each study participant receives three one-hour sessions of intensive physiotherapy per week for a total of six weeks. The goal is to improve task-specific motor arm function. Half of the group participating in this clinical trial had a vagus nerve stimulation device surgically implanted; the other half will serve as a control group.

During each rehabilitation therapy session, whenever a patient correctly performs a particular motor skill, the therapist pushes a button to trigger an optimal pulse width and current intensity of vagus nerve stimulation. The hypothesis is that if precise and accurate movements are positively reinforced by a brief burst of VNS during a trial-and-error learning process that these actions become “hardwired” into the brain more quickly.

“We are trying to see if this neurostimulator could be used to boost the effective therapy, creating a sort of ‘supercharged therapy.’ We want to determine if patients can recover more quickly through the use of this stimulation,” Bockbrader concluded.


Eric C. Meyers, Bleyda R. Solorzano, Justin James, Patrick D. Ganzer, Elaine S. Lai, Robert L. Rennaker, Michael P. Kilgard, Seth A. Hays. “Vagus Nerve Stimulation Enhances Stable Plasticity and Generalization of Stroke Recovery.” Stroke (First published online: January 25,  2018) DOI: 10.1161/STROKEAHA.117.019202

Kristofer W. Loerwald, Michael S. Borland, Robert L. Rennaker II, Seth A. Hays, Michael P. Kilgard. “The Interaction of Pulse Width and Current Intensity on the Extent of Cortical Plasticity Evoked by Vagus Nerve Stimulation.” Brain Stimulation (First published online: November 15, 2017) DOI: 10.1016/j.brs.2017.11.007

via Vagus Nerve Stimulation Enhances Brain Plasticity | Psychology Today

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[Editorial] Adult Neurogenesis: Beyond Rats and Mice – Neuroscience

Editorial on the Research Topic
Adult Neurogenesis: Beyond Rats and Mice

Most biological tissues routinely replace old cells with new ones. Unlike other tissues, the nervous system–being the most complex biological device found in nature–uniquely maintains most of its neurons throughout life and replaces relatively few. It preserves hotspots where it generates new neurons from resident stem cells during adulthood in a process known as adult neurogenesis, which varies among different species in its features, dynamics, and regulation. In spite of its widespread prevalence in the animal kingdom, the preponderance of studies conducted on a few laboratory rodent species such as rats and mice limits our understanding of the evolution, regulation, and function of adult neurogenesis. The anatomy, complexity and functions of the brain vary greatly in the animal kingdom: striking differences exist from simple bilaterians to humans, and, to a lesser extent, also among mammals. Therefore, both comparative and focused studies on different species will shed more light on the origin, development, and purpose of adult neurogenesis.

Adult neurogenesis was discovered and described by Joseph Altman and Das in rats (Altman and Das, 1965) and has been investigated in many species such as the zebrafish, frog, songbird, mole, mole-rat, vole, bat, fox, dog, dolphin, elephant, shrew, rabbit, monkey, and human. With the development of genetic manipulation techniques, researchers have focused largely on inbred laboratory rodents. While this provides a strong advantage of restricting genetic variation in the group, it also narrows our perspective on adult neurogenesis as a biological phenomenon (Bolker, 2017). Moreover, the rapid development of genetic tools has made Mus musculus the species of choice in studying adult neurogenesis. Yet, many unsolved issues and open questions cannot be resolved without the contribution of comparative studies spanning through widely different species. Such issues involve: how did adult neurogenesis evolve, whether our survival depend on adult neurogenesis, what is the link between adult neurogenesis and brain complexity, how do adult neurogenesis and animal behavior influence each other, how does adult neurogenesis contribute to brain plasticity, cognition and, possibly, repair, and how do experimental conditions affect adult neurogenesis.

Studying unconventional species will give us insights into the evolution and function of the brain, strengthening our understanding of the cellular basis of cognition and behavior, thus helping adult neurogenesis to find its place in the puzzle. With this Research Topic we, along with contributors from different areas, tried to answer the open questions and to encourage engaging discussions on the comparative and evolutionary aspects of adult neurogenesis. The diversity in adult neurogenesis indeed spans the de-novo formation of the entire adult brain in planaria (Brown and Pearson), neurogenesis in diverse brain areas in fish (Olivera-Pasilio et al.), reptiles (LaDage et al.Lutterschmidt et al.), and birds (Barkan et al.Kosubek-Langer et al.) to animals with restricted neurogenic niches such as invertebrates (Beltz and BentonSimões and Rhiner) and mammals (Taylor et al.Lévy et al.OosthuizenWiget et al.). The striking differences do not only concern the sites of occurrence and relative amounts (Brown and PearsonLévy et al.Olivera-Pasilio et al.Wiget et al.) but also in mechanistic aspects of stem cell biology. Intriguing examples are given by the adult-born neurons generated from the immune system and then traveling to the neurogenic niche via the circulatory system in the crayfish brain (Beltz and BentonSimões and Rhiner), or the heterogeneity of neoblasts, putative stem cells, in flatworms enabling the regeneration of the entire brain (Brown and Pearson). Yet, the main message from the comparative approach to adult neurogenesis is that the relative exclusive focus on laboratory rodents can result in a bias on how we think about this biological process. For instance, promising neuroprotective treatments developed in rodent models can fail in preclinical trials, and animal models with gyrencephalic brains might be necessary to study the behavior of neuroblasts in large white matter tracts (Taylor et al.). The bias is well-illustrated by the article of Faykoo-Martinez et al.: “species-specific adaptations in brain and behavior are paramount to survival and reproduction in diverse ecological niches and it is naive to think adult neurogenesis escaped these evolutionary pressures. A neuroethological approach to the study of adult neurogenesis is essential for a comprehensive understanding of the phenomenon.” Indeed, interactions of adult neurogenesis with neuroethological traits such as migration and mating behavior in snakes (Lutterschmidt et al.), territoriality in lizards (LaDage et al.), sociality and social interactions in mole-rats, birds, and sheep (Barkan et al.Lévy et al.Oosthuizen), or migratory lifestyle in birds (Barkan et al.) are presented here. The complexity of interactions is, to date, more an obstruction than a help in terms of publishability, but as Faykoo-Martinez et al. put it “most of us are guilty of making strong assertions about our data in order to have impact yet this ultimately creates bias in how work is performed, interpreted, and applied.” Such concerns are confirmed by the finding of remarkable reduction of adult neurogenesis in some large-brained, long-living mammals, including humans and dolphins (Sanai et al., 2011Sorrells et al., 2018), as reviewed and discussed in the article by Parolisi et al. More and more comparative data strongly support the view that adult neurogenesis is maintained in evolution only depending on strict relationships with its functional need(s). E.g., olfactory systems, mostly linked to paleocortical-hippocampal structures, were important in early mammalian evolution working as a reference system for spatial navigation for the location of food sources and mates, then replaced/integrated by the expansion of the isocortex as a “multimodal interface” for behavioral navigation based on vision and audition (Aboitiz and Montiel, 2015; see article by Parolisi et al.). The complex evolutionary aspects of adult neurogenesis role(s) and age-related reduction in mammals are addressed in the contribution by Hans-Peter Lipp. The main message of this opinion article is that no simple explanations can be called upon on such topic, a heavily actual conclusion even 30 years after neural stem cell discovery.

Animal models other than laboratory mice are by no means “out-of-reach” for advanced techniques, and the following examples could encourage and facilitate creative thinking in terms of research questions and how to approach them. Lindsey et al. present a thorough step-by-step protocol for visualizing cell proliferation in the whole zebrafish brain in 3 dimension. LaDage et al. used hormonal implants in lizards to study the interaction of testosterone and neurogenesis on territorial behavior. In fish and birds, Neurobiotin or lentivirus can be used to trace and characterize newly born neurons (Kosubek-Langer et al.Olivera-Pasilio et al.), and Brown and Pearson summarize the single-cell genomic data collected in planaria. Ideally, studies in laboratory rodents and non-conventional animal models can support and foster each other. For example, increased neurogenesis in laboratory mice confers stress resilience mediated by the temporal hippocampus (Anacker et al., 2018). Strikingly, wild rodents, naturally exposed to high stress levels, show more neurogenesis in the temporal hippocampus than the commonly used laboratory mouse C57BL/6 (Wiget et al.). Similarly, Reyes-Aguirre and Lamas identified the mechanism why the mouse retina cannot regenerate after damage, much in contrast to what has been reported in fish (Raymond et al., 2006). Finally, by using meta-analyses and a model to compare the neurodevelopmental sequences of different mammals, Charvet and Finlay try to put in a common time frame the envelopes of hippocampal neurogenesis, in order to interpret them in species with highly different lifespan.

In conclusion, with this Research Topic we strongly assert that adult neurogenesis research cannot rely exclusively on laboratory rodents, as each animal model can only cover certain aspects of the various flavors in which neuronal stem cells and their progeny in the postnatal brain can behave. The papers presented here emphasize the value of “… taking a step back and actually placing our results in a much larger, non-biomedical context, …[helping]… to reduce dogmatic thinking and create a framework for discovery” (Faykoo-Martinez et al.). After all, the failure of many clinical trials based on pre-clinical studies carried out on mice (Lindvall and Kokaia, 2010Donegà et al., 2013), do confirm the need for investments in comparative medicine (specifically on brain structural plasticity, see La Rosa and Bonfanti, 2018). A comparative view can indeed foster a more careful interpretation of the final impact of the biological process of neurogenesis in brain functioning and animal behavior.


Aboitiz, F., and Montiel, J. F (2015). Olfaction, navigation, and the origin of isocortex. Front. Neurosci. 9:402. doi: 10.3389/fnins.2015.00402

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Altman, J., and Das, G. D (1965). Post-natal origin of microneurones in the rat brain. Nature 207, 953–956. doi: 10.1038/207953a0

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Anacker, C., Luna, V. M., Stevens, G. S., Millette, A., Shores, R., Jimenez, J. C., et al. (2018). Hippocampal neurogenesis confers stress resilience by inhibiting the ventral dentate gyrus. Nature 559, 98–102. doi: 10.1038/s41586-018-0262-4

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Bolker, J. A. (2017). Animal models in translational research: rosetta stone or stumbling block? Bioessays 39, 1–8. doi: 10.1002/bies.201700089

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Donegà, M., Giusto, E., Cossetti, C., and Pluchino, S (2013). “Systemic neural stem cell-based therapeutic interventions for inflammatory CNS disorders,” in Neural Stem Cells: New Perspectives, ed. L. Bonfanti (Rijeka: INTECH), 287–347.

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La Rosa, C., and Bonfanti, L (2018). Brain plasticity in mammals: An example for the role of comparative medicine in the Neurosciences. Front. Vet. Sci.5:274. doi: 10.3389/fvets.2018.00274

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Lindvall, O., and Kokaia, Z (2010). Stem cells in human neurodegenerative disorders-time for clinical translation? J. Clin. Invest. 120, 29–40. doi: 10.1172/JCI40543

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Raymond, P. A., Barthel, L. K., Bernardos, R. L., and Perkowski, J (2006). Molecular characterization of retinal stem cells and their niches in adult zebrafish. BMC Dev. Biol. 6:36. doi: 10.1186/1471-213X-6-36

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Sanai, N., Nguyen, T., Ihrie, R. A., Mirzadeh, Z., Tsai, H.-H., Wong, M., et al. (2011). Corridors of migrating neurons in the human brain and their decline during infancy. Nature 478, 382–386. doi: 10.1038/nature10487

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Sorrells, S. F, Paredes, M. F., Cebrian-Silla, A., Sandoval, K., Qi, D., Kelley, K. W., et al. (2018). Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults. Nature 555, 377–381. doi: 10.1038/nature25975

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Keywords: comparative studies, evolution, brain plasticity, adult neurogenesis, brain repair, translation

via Frontiers | Editorial: Adult Neurogenesis: Beyond Rats and Mice | Neuroscience

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[Abstract] Simultaneous stimulation in bilateral leg motor areas with intermittent theta burst stimulation to improve functional performance after stroke: a feasibility pilot study



BACKGROUND: Intermittent theta burst stimulation (iTBS) was widely used in stroke rehabilitation and was more efficient than repetitive transcranial magnetic stimulation in terms of inducing larger motor evoked potential and producing longer effects. To our knowledge, the outcomes are not available combining rehabilitation and iTBS for improving motor function of lower extremities in patients with stroke.
AIM: To evaluate the feasibility and effectiveness of intermittent theta burst stimulation aiming to stimulate bilateral leg motor cortex and promote functional improvements.
DESIGN: A single blind, randomized controlled pilot study.
SETTING: Rehabilitation ward.
POPULATION: Twenty patients with chronic stroke finally enrolled for analyzed.
METHODS: Participants were randomized into two groups to receive 10 sessions of iTBS group and sham group over a 5-week period. The iTBS was delivered over the midline of skull to stimulate bilateral leg motor cortex. The outcome measures included balance, mobility, and leg motor functions were measured before and after interventions.
RESULTS: Within-group differences were significant in the Berg Balance Scale for both groups (Z=-2.442, P=0.015 in iTBS group; Z=-2.094, P=0.036 in sham group), in the Fugl-Meyer Assessment (Z=-2.264, P=0.024) and Overall Stability Index of Biodex Balance System of iTBS group (Z=-2.124, P=0.034). However, no significant between-group differences were found.
CONCLUSIONS: There was no powerful evidence to support the effectiveness of iTBS group better than sham control group. Some essential technical issues should be considered for future studies applying iTBS to stimulate bilateral leg motor cortex.
CLINICAL REHABILITATION IMPACT: iTBS combined with stroke rehabilitation are probably expected to be useful for promote brain plasticity and functional performance but some technical issues should be carefully considered.

via Simultaneous stimulation in bilateral leg motor areas with intermittent theta burst stimulation to improve functional performance after stroke: a feasibility pilot study – European Journal of Physical and Rehabilitation Medicine 2018 Aug 27 – Minerva Medica – Journals

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[WEB SITE] 5 Secrets to Building Up Your Neuroplasticity

5 Secrets to Building Up Your Neuroplasticity

Up until recently, we believed our brain plasticity was stagnant and fixed. Dr. Norman Doige, a psychiatrist from the University of Toronto, helped to reveal that this isn’t the case. Neuroplasticity is something fluid that you can build up, and that means… you can create new neural pathways for the rest of your life. 5 Secrets to Building Up Your Neuroplasticity

Why is this important?

Like any other muscle in your body, when it comes to your brain, you either use it or lose it. To keep your cognition strong and to help set yourself up for successful aging, it’s important to create growth experiences for yourself that build up your neuroplasticity.

That’s why I’ve gathered these five secrets to help you build up your neuroplasticity:

1.  Set meaningful goals

Too often I meet seniors who’ve lived a life of duty, where they dedicated their lives to the hustle bustle of work, family and responsibilities. This is a completely honorable commitment.

The main fallback is… your dream list of meaningful goals oftentimes gets trapped in a hope chest and by the time retirement hits, maybe you’ve not only lost sight of your dream list but you’ve also lost interest in creating meaningful challenges for yourself.

One of the ways to increase your neuroplasticity is to create new and exciting challenges for yourself, and the way to create new and exciting challenges for yourself is to set meaningful goals.

What’s the best way to set meaningful goals?

Find clarity through some serious self-reflection. This can really help you uncover some of the passions that you have deep inside you, which ultimately can help create some of your most vibrant new neural pathways in your brain.

2.  Adopt a growth mindset

Once you have your meaningful goals, a powerful way to chase them and to keep your brain activated is to adopt a growth mindset.

A growth mindset is based on Dr. Carol Dweck’s idea that you can “grow your brain’s capacity to learn and solve problems.” It’s a perspective that believes you’re not born either smart or not-so-smart, but instead you’re born with the ability to learn.

The hard part?

It takes work. A critical ingredient of adopting a growth mindset is to embrace challenge. When we’re faced with any pitfalls and “fails” in life, especially when we’re willing to try something new and exciting, it’s easy to give up and run away from any challenges or roadblocks.

If you can learn the skill of learning and train yourself to look forward to those hard and challenging moments, you’ll be that much more likely to accomplish any of your personal goals.

Some more tips on developing a growth mindset:

  • Focus on the process and not the outcome– if you can get in the habit of enjoying the journey, you’ll be less focused on the destination, which in turn will allow your brain to better engage in the act of learning
  • Seek constructive criticism and not opinions– it’s a tough thing to let go of approval from others, but if you can instead learn to seek constructive feedback from other people, you’ll likely be more drawn to the learning process
  • Create a new goal for every goal that you complete– this’ll keep you in the mindset of lifelong learning and can help you continue to engage your brain over and over again in the long-term

3.  Tackle your goals using micro-steps

A powerful way to accomplish any goal is to break it down into smaller chunks I like to call micro-steps. This does four promising things for you:

  • It keeps you less overwhelmed by the big picture goal
  • It makes your goal more achievable and realistic
  • You’ll know exactly what to tackle next
  • It builds up your momentum and nurtures a habit of working consistently toward your goal

The most important takeaway from using micro-steps is that you want to get in the habit of being consistent in tackling each one. In order to make lasting changes in your brain pattern, you need to be diligent about giving yourself a learning process. Continue to challenge yourself on a regular basis. If setting and achieving new meaningful goals can become habitual, that’s when the neuroplasticity magic can happen for you.

4.  Be self-aware and mindful

According to Roberts Wesleyan College, you make nearly 35,000 decisions a day, which means a ton of those decisions are made while your brain is on autopilot. If you can learn to engage the decision-making part of your brain, your prefrontal cortex, you can increase your neuroplasticity.

A way to do this is to practice mindfulness so that you’re more self-aware and more likely to make value-based(vs autopilot) decisions throughout the day.

Researchers Bas Verplanken and Rob Holland found that people make value-based choices only when those values are cognitively activated.

Some ideas on how to practice mindfulness:

  • Meditate, practice yoga or do breathing exercises
  • Connect with nature and be more aware of your physical surroundings
  • Keep a journal and write about things you’re grateful for
  • Exercise regularly
  • Spend less time on digital devices and social media
  • Watch less TV

5.  Align your social circle with growth experiences

Your circle of influence is everything when it comes to how your daily habits are impacted. You become who you most spend time with so be sure to align your social circle with your personal goals and good habits.

There are stats that highlight the power of association, like these:

  • If your friend is obese, you’re 57% more likely to gain weight
  • If your friend gets a divorce, your chance for divorce goes up by 75%

By surrounding yourself with like-minded people who care about the same meaningful things that you do, you’re much more likely to continue to conquer your goals and expand your growth experiences. This is what’ll keep your neuroplasticity built-up and strong.

Tip: Spend less time with people in your area of concern, which is the area that highlights negativity, gossip, the news, the stock market, drama, regrets, fear, etc.

So there you have it – five practical tactics that’ll help you build up your brain health and neuroplasticity.

Which secret will you tackle first? How will you continue to create new and meaningful growth experiences for yourself?

via 5 Secrets to Building Up Your Neuroplasticity –


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[WEB SITE] VR could trick stroke victims’ brains toward recovery.

Could virtual reality help stroke survivors regain motor function?

That’s a question Sook-Lei Liew is looking to answer.

Liew, an assistant professor at the University of Southern California and an affiliate of the Stevens Neuroimaging and Informatics Institute at the Keck School of Medicine, was inspired by research from Mel Slater and Jeremy Bailenson on embodiment in VR. If someone’s given a child’s body in VR, for example, they might start exhibiting more childlike behavior.

She wondered if giving stroke survivors with motor impairments a virtual avatar that moves properly could help promote brain plasticity (or the ability to change) and recovery. Maybe it would eventually lead to them to moving an impaired limb again.


USC researcher Sook-Lei Liew and her partners are testing to see whether virtual reality could help with stroke rehab. Nate Jense

“So, kind of like tricking the brain through visual input,” said Liew, who is also director of the Neural Plasticity and Neurorehabilitation Laboratory. “There’s a lot of emerging evidence from neuroscience and psychology that was showing that you can really identify [with the avatar], and it changes your behavior based on the avatar you’re given in VR.”

Virtual reality is a computer-generated simulation of a 3D environment. Using a VR headset with lenses that feed images to the eyes, a person can be virtually transported to another location, or interact with a setting in a seemingly realistic way. It’s commonly been used in gaming, but it’s being tested in other environments, too — like rehab.

Implementing VR in health care and patient treatment isn’t new. It’s been used to help people overcome phobias and anxiety disorders. But the application is starting to take off now that the technology is more developed and commercially available. Some medical schools are looking to train students with virtual simulations, and it’s even helping midwives learn how to deliver babies.

Liew’s research team has been working on a study for about two years called REINVENT, an acronym for Rehabilitation Environment using the Integration of Neuromuscular-based Virtual Enhancements for Neural Training. The researchers also collaborated with the USC Institute for Creative Technologies to develop the prototype.

The process works by using a brain-computer interface, which takes a signal from the brain and uses it to control another device: a computer, a robot or, in REINVENT’s case, an avatar in VR.

Next, researchers read electrical signatures of brain activity from the surface of the scalp using electroencephalography, or EEG, for short. The team also uses electromyography, which studies the electrical activity of the muscles. That can tell them whether somebody’s moving or if they’re trying to move.

Those signals are then fed into a program on a laptop. The program has thresholds so that when specific signals in the brain or muscle activity that correspond to an attempt to move are detected, they drive the movement of a virtual arm. The resulting visual feedback through a VR headset could help strengthen neural pathways from the damaged motor cortex to the impaired arm or limb.

While the researchers could theoretically extend this process to a patient’s lower limbs, Liew said it can be dangerous for someone with a motor impairment in the lower extremities to try to move with VR, so seated studies are much safer.

The research group recently finished testing the prototype using an Oculus DK2 with 22 healthy older adults, who provided a sample of what the brain and muscle signals look like when they move. They’re now starting to test with stroke patients in a controlled lab setting, aiming to work with 10 in the short term and hundreds in the long term, in both clinical and home environments.

The team also found that giving people neurofeedback of the virtual arm moving in a VR headset was more effective than simply showing it on a screen.

“Their brain activity in the motor regions that we’re trying to target is higher, and they’re able to control the brain-computer interface a little bit better and faster,” Liew said. “It makes the case that there is an added benefit from doing this in virtual reality, which is one of the first things we wanted to know.”

An unclear future

Because VR is still a relatively new technology, there are many unanswered questions on the best ways to use it in the medical profession.

“For the most part, nobody knows how to make great VR experiences, for business or consumer,” Gartner analyst Brian Blau said. “Over time, those issues will get resolved. But for the medical industry, they have the extra added bonus of having even more types of physical behaviors that they have to either mimic or want to measure.”

And while the possibilities for VR in health care are exciting, Liew is careful not to get ahead of herself.

“We think that VR is a promising medium, but we’re moving ahead cautiously,” she said. “A lot of the work that we’re trying to do is to test assumptions, because there’s a lot of excitement about VR, but there’s not that much that’s scientifically known.”

Only time — and plenty of research — will tell.

Tech Enabled: CNET chronicles tech’s role in providing new kinds of accessibility.

The Smartest Stuff: Innovators are thinking up new ways to make you, and the things around you, smarter.

via VR could trick stroke victims’ brains toward –

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[ARTICLE] The Optimal Speed for Cortical Activation of Passive Wrist Movements Performed by a Rehabilitation Robot: A Functional NIRS Study – Full Text

Objectives: To advance development of rehabilitation robots, the conditions to induce appropriate brain activation during rehabilitation performed by robots should be optimized, based on the concept of brain plasticity. In this study, we examined differences in cortical activation according to the speed of passive wrist movements performed by a rehabilitation robot.

Methods: Twenty three normal subjects participated in this study. Passive movements of the right wrist were performed by the wrist rehabilitation robot at three different speeds: 0.25 Hz; slow, 0.5 Hz; moderate and 0.75 Hz; fast. We used functional near-infrared spectroscopy to measure the brain activity accompanying the passive movements performed by a robot. The relative changes in oxy-hemoglobin (HbO) were measured in two regions of interest (ROI): the primary sensory-motor cortex (SM1) and premotor area (PMA).

Results: In the left SM1 the HbO value was significantly higher at 0.5 Hz, compared with movements performed at 0.25 Hz and 0.75 Hz (p < 0.05), while no significant differences were observed in the left PMA (p > 0.05). In the group analysis, the left SM1 was activated during passive movements at three speeds (uncorrected p < 0.05) and the greatest activation in the SM1 was observed at 0.5 Hz.

Conclusions: In conclusion, the contralateral SM1 showed the greatest activation by a moderate speed (0.5 Hz) rather than slow (0.25 Hz) and fast (0.75 Hz) speed. Our results suggest an ideal speed for execution of the wrist rehabilitation robot. Therefore, our results might provide useful data for more effective and empirically-based robot rehabilitation therapy.


A number of rehabilitation robots have been developed in the past two decades to aid functional recovery of impaired limbs in patients with brain injury (Volpe et al., 2000Hesse et al., 2005Kahn et al., 2006Lum et al., 2006Masiero et al., 2007Nef et al., 2007Coote et al., 2008Housman et al., 2009Chang et al., 2014). In the field of rehabilitation, high intensive, task-oriented and repetitive execution of movements is effective for functional recovery of impaired upper limbs following brain injury (Bütefisch et al., 1995Kwakkel et al., 2004Schaechter, 2004Levin et al., 2008Murphy and Corbett, 2009Oujamaa et al., 2009). Rehabilitation robots can easily and precisely provide these labor-intensive rehabilitative treatments, and the effect of rehabilitation robots on functional recovery in patients with brain injury has been demonstrated in many studies (Volpe et al., 2000Hesse et al., 2005Lum et al., 2006Masiero et al., 2007Coote et al., 2008Norouzi-Gheidari et al., 2012). Compared to conventional therapy (CT) provided by a therapist, the effectiveness of robot assisted therapy (RT) is questionable (Masiero et al., 2011Norouzi-Gheidari et al., 2012). There is no difference between RT and intensive CT of the same duration/intensity condition, and extra sessions of RT in addition to CT bring better motor recovery of the shoulder and elbow (not for hand and wrist) compared with CT (Norouzi-Gheidari et al., 2012). To make the best use of robot for upper limb rehabilitation, increased efficacy of robotic rehabilitation is necessary. However, research on the optimal conditions to maximize the rehabilitative effect during treatment with a rehabilitation robot has been limited (Reinkensmeyer et al., 2007).

Brain plasticity, the ability of our brain system to reorganize its structure and function, is the basic mechanism underlying functional recovery in patients with brain injury (Schaechter, 2004Murphy and Corbett, 2009). The underlying principle of rehabilitation in terms of brain plasticity is based on the modulation of cortical activation induced by the manipulation of external stimuli (Kaplan, 1988). Little is known about the cortical effects resulting from rehabilitation robot treatment (Li et al., 2013Chang et al., 2014Jang et al., 2015).

Functional neuroimaging techniques, including functional MRI (fMRI), Positron Emission Tomography (PET) and functional Near Infrared Spectroscopy (fNIRS) provide important information about the activation of the brain by external stimuli (Frahm et al., 1993Willer et al., 1993Miyai et al., 2001Fujii and Nakada, 2003Perrey, 2008Kim et al., 2011Leff et al., 2011Gagnon et al., 2012). Of these, fNIRS provides a non-invasive method for measurement of the hemodynamic responses associated with activation of the cerebral cortex based on the intrinsic optical absorption of blood (Arenth et al., 2007Irani et al., 2007Perrey, 2008Ye et al., 2009Leff et al., 2011). Compared with other functional neuroimaging techniques, fNIRS has a unique advantage of less sensitivity to motion artifact and metallic material. Therefore, fNIRS appears suitable for the study of brain response during treatment with rehabilitation robots (Perrey, 2008Mihara et al., 2010Leff et al., 2011Li et al., 2013Chang et al., 2014).

In this study, we hypothesized that there exists optimal conditions for robotic rehabilitation to enhance the rehabilitative effect. The speed of movement performed by rehabilitation robot could be a unique aspect of robot rehabilitation, because varied speed can be provided consistently only with the robot. To confirm our hypothesis, using fNIRS, we examined the optimal speed of passive wrist movements performed by a rehabilitation robot that induces cortical activation through proprioceptive input by passive movements (Radovanovic et al., 2002Francis et al., 2009Lee et al., 2012). As a part of upper limb, the wrist enhances the usefulness of the hand by allowing it to take different orientations with respect to the elbow (van der Lee, 2001). If there exists an optimal speed that offers the greatest cortical activation, it could be applicable for robotic rehabilitation and research for other optimal conditions such as duration.

Subjects and Methods


Healthy right-handed subjects (15 males, 8 females; mean age 26.5, range 21–30) with no history of neurological, psychiatric, or physical illness were recruited for this study. Handedness was evaluated using the Edinburg Handedness Inventory (Oldfield, 1971). All subjects were fully informed about the purpose of the research and provided written, informed consent prior to participation in this study. The study protocol was approved by the Institutional Review Board of the Daegu Gyeongbuk Institute of Science and Technology (DGIST). Data from two subjects were excluded because the subjects did not follow the required instructions during the data collection.



Regarding flexion and extension only, the human wrist can be simplified as a one degree of freedom (DOF) kinematic model with one revolute joint (Zatsiorsky, 2002). As mentioned above, the wrist rehabilitation robot was designed and manufactured as a simplified kinematic model of the wrist. The robot used for wrist rehabilitation has three parts: hand, wrist joint and forearm, and provides passive movement of flexion and extension (Figure 1). It has a gear driven mechanism using a single motor. The actuation system for the wrist part is composed of DC, a brushless motor with encoder (EC-i 40, Maxon motor), harmonic drive (CSF-11-50, Sam-ik THK, gear ratio 50:1), and force-torque sensor (Mini 45, ATI). In house developed software was used to control the robot. For the real-time control, Linux Fedora 11 and the Real Time Application Interface for Linux (RTAI) Ver 3.8 systems were mounted. Real-time sensing control was achieved using an encoder and Sensoray s626 board, in which time delay control (TDC) was used for precise position control. The robot showed a position error of 0.1°–1° during the experiment.

Enter Figure 1. (A) The wrist rehabilitation robot. Lateral view of the wrist rehabilitation robot, the hand part (dotted line), wrist part (solid line) and forearm part (dashed line). (B) A front view of robot and subjects with the trunk strap and near infrared spectroscopy (NIRS) optodes. (C) Wrist flexion of the robot. (D) Wrist extension of the robot.a caption

 When using the robot for wrist rehabilitation, the hand and forearm must be fixed to the robot in order to perform the passive wrist movement. First, the subjects placed their forearm on the armrest made of foam covered with a soft cloth. They were instructed to place their hand on the support bar under the hand part of the robot before fixing all fingers to the finger holder with velcro straps. The robot performs the passive wrist exercise using a rotary motion of a gear driven by a motor and realizes a full range of motion (ROM) from 80° (flexion) to 75° (extension) when the degree of neutral wrist position is 0°, with the wrist in a flat position, with velocity of the wrist motions up to 2 Hz.[…]


Continue —> Frontiers | The Optimal Speed for Cortical Activation of Passive Wrist Movements Performed by a Rehabilitation Robot: A Functional NIRS Study | Frontiers in Human Neuroscience

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[ARTICLE] Benign Effect of Extremely Low-Frequency Electromagnetic Field on Brain Plasticity Assessed by Nitric Oxide Metabolism during Poststroke Rehabilitation – Full Text


Nitric oxide (NO) is one of the most important signal molecules, involved in both physiological and pathological processes. As a neurotransmitter in the central nervous system, NO regulates cerebral blood flow, neurogenesis, and synaptic plasticity. The aim of our study was to investigate the effect of the extremely low-frequency electromagnetic field (ELF-EMF) on generation and metabolism of NO, as a neurotransmitter, in the rehabilitation of poststroke patients. Forty-eight patients were divided into two groups: ELF-EMF and non-ELF-EMF. Both groups underwent the same 4-week rehabilitation program. Additionally, the ELF-EMF group was exposed to an extremely low-frequency electromagnetic field of 40 Hz, 7 mT, for 15 min/day. Levels of 3-nitrotyrosine, nitrate/nitrite, and TNFα in plasma samples were measured, and NOS2 expression was determined in whole blood samples. Functional status was evaluated before and after a series of treatments, using the Activity Daily Living, Geriatric Depression Scale, and Mini-Mental State Examination. We observed that application of ELF-EMF significantly increased 3-nitrotyrosine and nitrate/nitrite levels, while expression of NOS2 was insignificantly decreased in both groups. The results also show that ELF-EMF treatments improved functional and mental status. We conclude that ELF-EMF therapy is capable of promoting recovery in poststroke patients.

1. Introduction

Cardiovascular diseases, including ischemic stroke (IS), are a serious problem of the modern age, killing 4 million people each year in Europe [1]. Stroke is caused by ischemia of brain tissue. Brain structure damage occurring during ischemia/reperfusion is due to the generation of significant amounts of reactive oxygen species and inflammatory mediators [2]. Damage to brain tissue as a result of a stroke cannot be undone. However, the most important part of poststroke therapy is immediate and long-term rehabilitation, considering the enormous plasticity of the brain [3]. Although extremely low-frequency electromagnetic field (ELF-EMF) therapy is not a standard treatment in the poststroke rehabilitation, some authors suggest its increased positive effect on patients [4]. ELF-EMF treatment is based on regeneration, osteogenesis, analgesics, and anti-inflammatory action. Its biological effect is related to processes of ion transport, cell proliferation, apoptosis, protein synthesis, and changes in the transmission of cellular signals [5]. The regenerative and cytoprotective effect of ELF-EMF is based on mechanism associated with nitric oxide induction, collateral blood flow, opioids, and heat shock proteins [6].

Nitric oxide (NO) is an unstable, colourless, water-soluble gas with a short half-life (3–6 sec). The compound has one unpaired electron, which makes it a highly reactive free radical. It is characterized by the multiplicity of action in the body, in both physiological and pathological conditions [7]. Synthesis of NO in the organism is catalysed by nitric oxide synthase (NOS), occurring in three isoforms: neuronal (nNOS), inducible (iNOS), and endothelial (eNOS), encoded by different genes whose expression is subject to varying regulation. The constituent isoforms of NOS are eNOS and nNOS, whose activity is associated with concentration of calcium ions and the level of calmodulin in a cell, as well as with hypoxia, physical activity, and the level of certain hormones, that is, oestrogens [8]. In contrast, because it is closely related with the calmodulin, iNOS does not require a high concentration of calcium ions but is regulated by various endogenous and exogenous proinflammatory factors [9].

The two-stage synthesis of NO consists of the oxidation of L-arginine to Nω-hydroxy-L-arginine and, under the influence of NOS and oxygen, formation of L-citrulline and release of NO. All isoforms of NOS require the same cofactors: nicotinamide adenine dinucleotide phosphate (NADPH), flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), tetrahydrobiopterin (BH4), iron protoporphyrin IX (heme), and O2 [7].

Nitric oxide is one of the most important signal molecules, involved in both physiological and pathological processes. One of the major functions of NO is as a potent vasodilation, increasing the blood flow and regulation of blood pressure, which has been used in clinical practice for many years. Deficiency of this compound is observed in various disorders of many systems: cardiovascular, gastrointestinal, respiratory, and genitourinary [10]. The beneficial effects of NO lie in its platelet inhibition, macrophage cytotoxicity (antibacterial, antiviral, and antiparasitic), and protection of the mucosal lining of the digestive system. On the other hand, excessive expression of iNOS can be disadvantageous, for example, during sepsis. The adverse action of NO is associated with the production of superoxide anions and subsequent generation of peroxynitrite and hydroxyl radicals, which are highly toxic [11].

In the central nervous system, NO as a neurotransmitter regulates cerebral blood flow, as well as neurogenesis and synaptic plasticity. Furthermore, neuronal death is caused by high concentrations of NO by caspase-dependent apoptosis process and promotion of inflammation. Elevated levels of nitric oxide promote necrosis by energy depletion. On the basis of these mechanisms, NO is involved in the etiology of many neurological diseases, such as major depression, schizophrenia, epilepsy, anxiety, and drug addiction [12].

Our study was designed to investigate the effect of ELF-EMF on the metabolism of NO, as a signal molecule in the central nervous system, in the rehabilitation of acute poststroke patients.[…]

Continue —>  Benign Effect of Extremely Low-Frequency Electromagnetic Field on Brain Plasticity Assessed by Nitric Oxide Metabolism during Poststroke Rehabilitation

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[WEB SITE] Neuroplasticity: The 10 Fundamentals Of Rewiring Your Brain

by Debbie Hampton

ON OCTOBER 28, 2015

Neuroplasticity has become a buzzword in psychology and scientific circles, as well as outside of them, promising that you can “re-wire” your brain to improve everything from health and mental wellbeing to quality of life. There’s a lot of conflicting, misleading, and erroneous information out there.

So, exactly how does it work?

Via: Thawornnurak and Ioan Panaite | Shutterstock

Via: Thawornnurak and Ioan Panaite | Shutterstock

What Is Neuroplasticity

Just in case you’ve managed to miss all the hype, neuroplasticity is an umbrella term referring to the ability of your brain to reorganize itself, both physically and functionally, throughout your life due to your environment, behavior, thinking, and emotions. The concept of neuroplasticity is not new and mentions of a malleable brain go all of the way back to the 1800s, but with the relatively recent capability to visually “see” into the brain allowed by functional magnetic resonance imaging (fMRI), science has confirmed this incredible morphing ability of the brain beyond a doubt.

The concept of a changing brain has replaced the formerly held belief that the adult brain was pretty much a physiologically static organ or hard-wired after critical developmental periods in childhood. While it’s true that your brain is much more plastic during the early years and capacity declines with age, plasticity happens all throughout your life.

For a thorough explanation of how plasticity physically happens in your brain, see blog: “Masterpiece Or Mess.”

Via: GaudiLab | Shutterstock

Via: GaudiLab | Shutterstock

How Neuroplasticity Shows Up In Your Life

Neuroplasticity makes your brain extremely resilient and is the process by which all permanent learning takes place in your brain, such as playing a musical instrument or mastering a different language. Neuroplasticity also enables people to recover from stroke, injury, and birth abnormalities, overcome autism, ADD and ADHD, learning disabilities and other brain deficits, pull out of depression and addictions, and reverse obsessive compulsive patterns. (Read more: “You’re Not Stuck With The Brain You’re Born With.”)

Neuroplasticity has far-reaching implications and possibilities for almost every aspect of human life and culture from education to medicine. It’s limits are not yet known. However, this same characteristic, which makes your brain amazingly resilient, also makes it vulnerable to outside and internal, usually unconscious, influences. In his book The Brain That Changes Itself: Stories of Personal Triumph from the Frontiers of Brain Science, Norman Doidge calls this the “plastic paradox.” (Read more: “Your Plastic Brain: The Good, The Bad, and The Ugly.”)

I know the power of neuroplasticity first hand, as I devised and performed my own home-grown, experience-dependant neuroplasticity based exercises for years to recover from a brain injury, the result of a suicide attempt. Additionally, through extensive cognitive behavioral therapy, meditation, and mindfulness practices, all of which encourage neuroplastic change, I overcame depression, anxiety, and totally revamped my mental health and life.

But it was because of neuroplastic change that I became entrenched in depressive, anxious, obsessive, and over-reactive patterns in the first place.

Via: Sergey Nivens | Shutterstock

Via: Sergey Nivens | Shutterstock

Ten Fundamentals Of Neuroplasticity 

Science has confirmed that you can access neuroplasticity for positive change in your own life in many ways, but it’s not quite as easy as some of the neuro-hype would have you believe. In the article, “Neuroplasticity: can you rewire your brain?,” Dr. Sarah McKay, neuroscientist, says:

“Plasticity dials back ‘ON’ in adulthood when specific conditions that enable or trigger plasticity are met. ‘What recent research has shown is that under the right circumstances, the power of brain plasticity can help adults minds grow. Although certain brain machinery tends to decline with age, there are steps people can take to tap into plasticity and reinvigorate that machinery,’ explains Merzenich. These circumstances include focused attention, determination, hard work and maintaining overall brain health.”

In his book, Soft-Wired: How the New Science of Brain Plasticity Can Change Your Life, Dr. Michael Merzenich (which Dr. McKay cites above), a leading pioneer in brain plasticity research and co-founder of Posit Science, lists ten core principles necessary for the remodeling of your brain to take place:

1. Change is mostly limited to  those situations in which the brain is in the mood for it. If you are alert, on the ball, engaged, motivated, ready for action, the brain releases the neurochemicals necessary to enable brain change. When disengaged, inattentive, distracted, or doing something without thinking that requires no real effort, your neuroplastic switches are “off.”

2. The harder you try, the more you’re motivated, the more alert you are, and the better (or worse)  the potential outcome, the bigger the brain change. If you’re intensely focused on the task and really trying to master something for an important reason, the change experienced will be greater.

3. What actually changes in the brain are the strengths of the connections of neurons that are engaged together, moment by moment, in time. The more something is practiced, the more connections are changed and made to include all elements of the experience (sensory info, movement, cognitive patterns). You can think of it like a “master controller” being formed for that particular behavior, which allows it to be performed with remarkable facility and reliability over time.

4. Learning-driven changes in connections increase cell-to cell cooperation, which is crucial for increasing reliability. Merzenich explains this by asking you to imagine the sound of a football stadium full of fans all clapping at random versus the same people clapping in unison. He explains, “The more powerfully coordinated your [nerve cell] teams are, the more powerful and more reliable their behavioral productions.”

5. The brain also strengthens its connections between teams of neurons representing separate moments of successive things that reliably occur in serial time. This allows your brain to predict what happens next and have a continuous “associative flow.” Without this ability, your stream of consciousness would be reduced to “a series of separate, stagnating puddles,” explains Merzenich.

6. Initial changes are temporary. Your brain first records the change, then determines whether it should make the change permanent or not. It only becomes permanent if your brain judges the experience to be fascinating or novel enough or if the behavioral outcome is important, good or bad.

7. The brain is changed by internal mental rehearsal in the same ways and involving precisely the same processes that control changes achieved through interactions with the external world. According to Merzenich, “You don’t have to move an inch to drive positive plastic change in your brain. Your internal representations of things recalled from memory work just fine for progressive brain plasticity-based learning.”

8. Memory guides and controls most learning. As you learn a new skill, your brain takes note of and remembers the good attempts, while discarding the not-so-good trys. Then, it recalls the last good pass, makes incremental adjustments, and progressively improves.

9. Every movement of learning provides a moment of opportunity for the brain to stabilize — and reduce the disruptive power of — potentially interfering backgrounds or “noise.” Each time your brain strengthens a connection to advance your mastery of a skill, it also weakens other connections of neurons that weren’t used at that precise moment. This negative plastic brain change erases some of the irrelevant or interfering activity in the brain.

10. Brain plasticity is a two-way street; it is just as easy to generate negative changes as it is positive ones. You have a “use it or lose it” brain. It’s almost as easy to drive changes that impair memory and physical and mental abilities as it is to improve these things. Merzenich says that older people are absolute masters at encouraging plastic brain change in the wrong direction.

Source: Neuroplasticity: The 10 Fundamentals Of Rewiring Your Brain –

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