Posts Tagged Neuroplasticity

[BLOG POST] How to Make New Brain Cells and Improve Brain Function

Scientists used to believe that the brain stopped making new brain cells past a certain age. But that believe changed in the late 1990’s as a result of several studies which were performed on mice at the Salk Institute.

After conducting maze tests, neuroscientist Fred H. Gage and his colleagues examined brain samples collected from mice. What they found challenged long standing believes held about neurogenesis, or the creation of new neurons.

To their astonishment, they discovered that the mice were creating new neurons. Their brains were regenerating themselves.

All of the mice showed evidence of neurogenesis but the brains of the athletic mice showed even more.

 These mice, the ones that scampered on running wheels, were producing two to three times as many new neurons as the mice that didn’t exercise.

The difference between the mice who performed well on the maze tests and those that floundered was exercise.

That’s great for the mice, but what about humans?

To find out if neurogensis occurred in adult humans, Gage and his colleagues obtained brain tissue from deceased cancer patients who had donated their bodies to research. While still living, these people were injected with the same type of compound used on Gage’s mice to detect new neuron growth. When Gage dyed their brain samples, he saw new neurons. Like in the mice study, they found evidence of neurogenesis – the growth of new brain cells.

From the mice study, it appears that those who exercise produce even more new brain cells than those who don’t. Several studies on humans seem to suggest the same thing.

Studies performed at both the University of Illinois at Urbana- Champaign and Columbia University in New York City have shown that exercise benefits brain function. The test subjects were given aerobic exercises such as walking for at least one hour three times a week. After 6 months they showed significant improvements in memory as measured by a word-recall test. Using fMRI scans they also showed increases in blood flow to the hippocampus (part of the brain associated with memory and learning). Scientists suspect that the blood pumping into that part of the brain was helping to produce fresh neurons.

Dr. Patricia A. Boyle and her colleagues of Rush Alzheimer’s Disease Center in Chicago found that the greater a person’s muscle strength, the lower their likelihood of being diagnosed with Alzheimer’s. The same was true for the loss of mental function that often precedes full-blown Alzheimer’s.

Neuroscientist Gage, by the way, exercises just about every day, as do most colleagues in his field. As Scott Small a neurologist at Columbia explains,

 I constantly get asked at cocktail parties what someone can do to protect their mental functioning. I tell them, ‘Put down that glass and go for a run.

So if you want to grow some new brain cells and improve your brain function, go get some exercise!

Source: How to Make New Brain Cells and Improve Brain Function | Online Brain Games Blog

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[WEB SITE] Traumatic Brain Injury Resource Guide – Neuroplasticity

Neuroplasticity

by Lisa Kreber, Ph.D. CBIS
Senior Neuroscientist, Centre for Neuro Skills

What is Neuroplasticity?
Neuronal Firing
How Neuroplasticity Works
Mechanisms of Plasticity
Synaptogenesis
Stem Cells
Modulation of Neurotransmission
Unmasking
Forms of Neuronal Plasticity
Neuronal Remodeling
Depression and Hippocampal Plasticity
Appreciating Plasticity
Ten Principles of Neuroplasticity
Learning, Injury and Recovery

Source: Traumatic Brain Injury Resource Guide – Neuroplasticity

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[ARTICLE] Spasticity, Motor Recovery, and Neural Plasticity after Stroke – Full Text

Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for post-stroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the key to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

Introduction

According to the CDC, approximately 800,000 people have a stroke every year in the United States. The continued care of seven million stroke survivors costs the nation approximately $38.6 billion annually. Spasticity and weakness (i.e., spastic paresis) are the primary motor impairments and impose significant challenges for patient care. Weakness is the primary contributor to impairment in chronic stroke (1). Spasticity is present in about 20–40% stroke survivors (2). Spasticity not only has downstream effects on the patient’s quality of life but also lays substantial burdens on the caregivers and society (2).

Clinically, poststroke spasticity is easily recognized as a phenomenon of velocity-dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex (3). Though underlying mechanisms of spasticity remain poorly understood, it is well accepted that there is hyperexcitability of the stretch reflex in spasticity (47). Accumulated evidence from animal (8) and human studies (918) supports supraspinal origins of stretch reflex hyperexcitability. In particular, reticulospinal (RS) hyperexcitability resulted from loss of balanced inhibitory, and excitatory descending RS projections after stroke is the most plausible mechanism for poststroke spasticity (19). On the other hand, animal studies have strongly supported the possible role of RS pathways in motor recovery (2036), while recent studies with stroke survivors have demonstrated that RS pathways may not always be beneficial (37, 38). The relation between spasticity and motor recovery and the role of plastic changes after stroke in this relation, particularly RS hyperexcitability, remain poorly understood among clinicians and researchers. Thus, management of spasticity and facilitation of motor recovery remain clinical challenges. This review is organized into the following sessions to understand this relation and its implication in clinical management.

• Poststroke spasticity and motor recovery are mediated by different mechanisms

• Motor recovery are mediated by cortical plastic reorganizations (spontaneous or via intervention)

• Reticulospinal hyperexcitability as a result of maladaptive plastic changes is the most plausible mechanism for spasticity

• Possible roles of RS hyperexcitability in motor recovery

• An example of spasticity reduction for facilitation of motor recovery

Continue —> Frontiers | Spasticity, Motor Recovery, and Neural Plasticity after Stroke | Stroke

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[Abstract] “Genetic Variation and Neuroplasticity: Role in Rehabilitation after Stroke”

Provisional Abstract:

Background and Purpose: Significant inter-individual variability in rehabilitation outcomes exits in many neurologic diagnoses. One factor that may impact response to rehabilitation interventions is genetic variation. Genetic variation refers to the presence of differences in the DNA sequence among a population. Genetic polymorphisms are variations that occur relatively commonly and, while not disease causing, can impact the function of biological systems. The purpose of this article is to describe genetic polymorphisms that may impact neuroplasticity, learning and recovery after stroke.

Summary of Key Points: Genetic polymorphisms for brain-derived neurotrophic factor (BDNF), dopamine, and apolipoprotein E have been shown to impact neuroplasticity and motor learning. Rehabilitation interventions that rely on the molecular and cellular pathways of these factors may be impacted by the presence of the polymorphism. For example, it has been hypothesized that individuals with the BDNF polymorphism may show a decreased response to neuroplasticity based interventions, decreased rate of learning, and overall less recovery after stroke. However, research to date has been limited and additional work is needed to fully understand the role of genetic variation in learning and recovery.

Recommendations for Clinical Practice: Genetic polymorphisms should be considered as possible predictors or covariates in studies that investigate neuroplasticity, motor learning, or motor recovery after stroke. Future predictive models of stroke recovery will likely include a combination of genetic factors and other traditional factors (e.g. age, corticospinal tract integrity) to determine an individual’s expected response to a specific rehabilitation intervention.

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Source: JUST ACCEPTED: “Genetic Variation and Neuroplasticity: Role in Rehabilitation after Stroke”

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[Abstract] Delivering Remote Rehabilitation at Home: An Integrated Physio-Neuro Approach to Effective and User Friendly Wearable Devices – SpringerLink

Abstract

There is a global shortage of manpower and technology in rehabilitation to attend to the five million new patients who are left disabled every year with stroke. Neuroplasticity is increasingly recognized to be a primary mechanism to achieve significant motor recovery. However, most rehabilitation devices either limit themselves to mechanical repetitive movement practice at a limb level or focus only on cognitive tasks. This may result in improvements in impairment but seldom translates into effective limb and hand use in daily activities. This paper presents an easy-to-use, wearable upper limb system, SynPhNe (pronounced like “symphony”), which trains brain and muscle as one system employing neuroplasticity principles. A summary of clinical results with stroke patients is presented. A new, wireless, home-use version of the solution architecture has been proposed, which can make it possible for patients to do guided therapy at home and thus have access to more therapy hours.

Source: Delivering Remote Rehabilitation at Home: An Integrated Physio-Neuro Approach to Effective and User Friendly Wearable Devices | SpringerLink

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[VIDEO] Why Can’t WE Reverse Nerve Damage ? – Reversing Nerve Damage: Central Nervous System Inhibits Cell Regeneration, But Stem Cell Treatment May Help

 

Our nervous system is involved in everything our body does, from maintaining our breath to controlling our muscles. Our nerves are vital to all we do; therefore, nerve pain and damage can heavily influence our quality of life. In Discovery News’ latest video, “Why Can’t We Reverse Nerve Damage?” host Lissette Padilla explains the central nervous system (CNS) has certain proteins that inhibit cell regeneration, because each cell in the nervous system has a unique function on the pathway, like a circuit, and can’t be replaced.

The nervous system can be divided into two sections, with the brain and spinal cord making up the CNS. Nerves are made up of sensory fibers and motor neurons, which comprise the peripheral nervous system. Nerve cells are made up of many parts, but they send signals through threads covered in a protective sheet of myelin. These threads are called axons.

Axons are the long part of the cell that reaches out to neighboring cells to send information down the line. Schwann cells, found only in the peripheral nervous system, are glial cells that produce protective myelin. Schwann cells could potentially clean up damaged nerves, which could make way for healing process to take place and new nerves to be formed.

The problem is these Schwann cells are missing from the CNS. The CNS is comprised of myelin-producing cells called oligodendrocytes. And these cells don’t clean up damaged nerve cells at all, hence the damage problem.

However, research is currently underway to examine the potential success of system cell treatment, where stem cells are injected directly at the injury site. It will still take a few years to see the results of such trials, but since the peripheral nervous system doesn’t have the same blocking proteins that the CNS has, the idea is Schwann cells could help heal the damage.

So it is possible to regrow nerves, albeit slowly. For instance, if you cut a nerve into your shoulder, it could take a year to regrow. By that time, the muscles in your arms could become atrophied. Researchers are working on helping the body heal faster.

Source: Reversing Nerve Damage: Central Nervous System Inhibits Cell Regeneration, But Stem Cell Treatment May Help

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[WEB SITE] Brain Derived Neurotrophic Factor (BDNF) and Exercise

Brain Derived Neurotrophic Factor (BDNF) has been referred to as a fertilizer for your brain. Find out how exercise can help you to get more of it.

Brain Derived Neurotrophic Factor (BDNF) has been referred to as a fertilizer for your brain. It is a substance that is found in your brain and helps to maintain the life of your brain cells, as well as grow new ones. You’ve probably heard all about ‘neuroplasticity’ and how we used to think our brains, once adult, were like a lump of concrete – unable to change and grow. Scientists now believe our brains are more like plastic – able to adapt, grow and change depending on what we do with them. BDNF is widely accepted as being a key player in this ‘plastic’ ability of the brain – its presence has been shown to make brain cells in petri dishes sprout new branches (necessary activity for a cell to make new connections!).

Low levels of BDNF have been associated with depression, anxiety, poor memory and brain degeneration as seen in conditions such as Alzheimer’s and dementia.

 

Why would you want more BDNF?

  • Improved learning and memory
  • May trigger the production of more serotonin (hello happy feelings!)
  • Helps with new skill acquisition
  • Improved mood (exercise increases BDNF as much or even more than taking antidepressants does)
  • Lower rates of Alzheimer’s disease and dementia in older age may be related to higher levels of BDNF.

Are you getting the picture? Better mood, better mental performance, healthier brain as you age…

How do you get more BDNF?

One word: STIMULATION.  Stimulation of your brain and all its cells can come in many forms. Of course, traditional brain exercise has been thought of as activities such as cross words and Sudoku (which are definitely good!) but here’s another aspect you can add to the list: exercise. As little as 30 minutes of jogging on three days a week has been shown to improve brain functioning, but even better gains have been suggested with more complex activity, which requires you to build or acquire a skill. An example of this is exercise that challenges your balance or thinking, like rock climbing or dancing.

The ultimate brain booster? A bit of aerobic exercise (at least ten minutes) to increase levels of BDNF and other neurotransmitters, as well as all those other wonderful benefits of aerobic exercise, followed by a skill-based exercise to get the new brain cells creating new networks with each other.

TIP: Want to maximize the increased learning capacity of your brain? Don’t try to learn something while exercising (stop taking your study notes to the spin bike!) – blood flow increases to the brain post-exercise, while BDNF levels are still increased, meaning immediately after exercise is the perfect time to take in new information. Put on that French language podcast on the way home from the gym…

 

EXERCISE RIGHT’S FIVE FAVOURITE WAYS TO MOVE FOR MORE BDNF

  • 1. Indoor rock-climbing – especially if you actively commute to the rock wall!
  • 2. Trail running – something with twists, turns and great views is awesome
  • 3. Dancing – where you’re learning new moves and also working your fitness
  • 4. Functional movement – wait until the after school rush has finished then go check out (and play on) your nearest playground – think monkey bars, crawling through tunnels and balancing on beams
  • 5. Team sports – they require you to be getting great aerobic gains by running around, whilst also working your brain in terms of strategy and quick thinking

References:

Aisen, P. S. (2014). Serum brain-derived neurotrophic factor and the risk for dementia. JAMA, 311(16), 1684-1685. doi: 10.1001/jama.2014.3120

Binder, Devin K., & Scharfman, Helen E. (2004). Brain-derived Neurotrophic Factor. Growth factors (Chur, Switzerland), 22(3), 123-131. doi: 10.1080/08977190410001723308

Hagerman, Eric, & Ratey, Dr John J. (2010). Spark! How Exercise Will Improve the Performance of Your Brain (Kindle Edition ed.).

Source: Brain Derived Neurotrophic Factor (BDNF) and Exercise

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[TED Talk] Carl Schoonover: How to look inside the brain.

There have been remarkable advances in understanding the brain, but how do you actually study the neurons inside it? Using gorgeous imagery, neuroscientist and TED Fellow Carl Schoonover shows the tools that let us see inside our brains.

 

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[WEB SITE] How Do Neuroplasticity and Neurogenesis Rewire Your Brain? – Psychology Today

Source: XStudio3D/Shutterstock

For over a decade, neuroscientists have been trying to figure out how neurogenesis (the birth of new neurons) and neuroplasticity (the malleability of neural circuits) work together to reshape how we think, remember, and behave.

This week, an eye-opening new study, “Adult-Born Neurons Modify Excitatory Synaptic Transmission to Existing Neurons” reported how newborn neurons (created via neurogenesis) weave themselves into a “new and improved” neural tapestry. The January 2017 findings were published in the journal eLife.

During this state-of-the-art study on mice, neuroscientists at the University of Alabama at Birmingham (UAB) found that the combination of neurogenesis and neuroplasticity caused less-fit older neurons to fade into oblivion and die off as the sprightly, young newborn neurons took over existing neural circuits by making more robust synaptic connections.

For their latest UAB study, Linda Overstreet-Wadiche and Jacques Wadiche—who are both associate professors in the University of Alabama at Birmingham Department of Neurobiology—focused on neurogenesis in the dentate gyrus region of the hippocampus.

The dentate gyrus is an epicenter of neurogenesis responsible for the formation of new episodic memories and the spontaneous exploration of novel environments, among other functions.

More specifically, the researchers focused on newly born granule cell neurons in the dentate gyrus that must become wired into a neural network by forming synapses via neuroplasticity in order to stay alive and participate in ongoing neural circuit function.

There are only two major brain regions that are currently believed to have the ability to continually give birth to new neurons via neurogenesis in adults; one is the hippocampus (long-term and spatial memory hub) the second is the cerebellum (coordination and muscle memory hub). Notably, granule cells have the highest rate of neurogenesis. Both the hippocampus and cerebellum are packed, chock-full with granule cells.

Interestingly, moderate to vigorous physical activity (MVPA) is one of the most effective ways to stimulate neurogenesis and the birth of new granule cells in the hippocampus and the cerebellum. (As a cornerstone of The Athlete’s Way platform, I’ve been writing about the link between MVPA and neurogenesis for over a decade. To read a wide range of Psychology Today blog posts on the topic click on this link.)

Drawing of Purkinje cells (A) and granule cells (B) from pigeon cerebellum by Santiago Ramón y Cajal, 1899. Source: Instituto Santiago Ramón y Cajal, Madrid, Spain

Granule cells were first identified by Santiago Ramón y Cajal, who made beautiful sketches in 1899 that illustrate how granule cells create synaptic connections with Purkinje cells in the cerebellum. His breathtaking and Nobel Prize-winning illustrations are currently on a museum tour across the United States (on loan from the Instituto Santiago Ramón y Cajal in Madrid, Spain) as part of “The Beautiful Brain” traveling art exhibit.

(As a side note, the olfactory bulb is the only other subcortical brain area known to have high rates of neurogenesis. Speculatively, this could be one reason that scent plays such an indelible and ever-changing role in our memory formation and ‘remembrance of things past.’)

Neurogenesis and Neuroplasticity Work Together to Rewire Neural Circuitry

One of the key aspects of neural plasticity is called Neural Darwinism, or “neural pruning,” which means that any neuron that isn’t ‘fired-and-wired’ together into a network is likely to be extinguished. The latest UAB research suggests that newborn neurons play a role in expediting this process by “winning out” in a survival of the fittest type of neuronal battle against their more elderly or worn out counterparts.

Long before there were neuroscientific studies on neuroplasticity and neurogenesis, Henry David Thoreau unwittingly described the process of how the paths that one’s mind travels can become hardwired (when you get stuck in a rut) by describing a well-worn path through the woods. In Walden, Thoreau writes,

“The surface of the earth is soft and impressible by the feet of men; and so with the paths which the mind travels. How worn and dusty, then, must be the highways of the world, how deep the ruts of tradition and conformity!”

From a psychological standpoint, the latest UAB discovery presents the exciting possibility that when adult-born neurons weave into existing neural networks that new memories are created and older memories may be modified.

Through neurogenesis and neuroplasticity, it may be possible to carve out a fresh and unworn path for your thoughts to travel upon. One could speculate that this process opens up the possibility to reinvent yourself and move away from the status quo or to overcome past traumatic events that evoke anxiety and stress. Hardwired fear-based memories often lead to avoidance behaviors that can hold you back from living your life to the fullest.

Future Research on Neurogenesis Could Lead to New PTSD Treatments

Granule cells in the dentate gyrus are part of a neural circuit that processes sensory and spatial input from other areas of the brain. By integrating sensory and spatial information, the dentate gyrus has the ability to generate unique and detailed memories of an experience.

Before this study, Overstreet-Wadiche and her UAB colleagues had a few basic questions about how the newly born granule cells in the dentate gyrus function. They asked themselves two specific questions:

  1. Since the number of neurons in the dentate gyrus increases by neurogenesis while the number of neurons in the cortex remains the same, does the brain create additional synapses from the cortical neurons to the new granule cells?
  2. Or do some cortical neurons transfer their connections from mature granule cells to the new granule cells?

Through a series of complex experiments with mice, Overstreet-Wadiche et al. found that some of the cortical neurons in the cerebral cortex transferred all of their former connections with older granule cells (that may have been worn out or past their prime) to the freshly born granule cells that were raring to go.

This revolutionary discovery opens the door to examine how the redistribution of synapses between old and new neurons helps the dentate gyrus stay up to date by forming new connections.

One of the key questions the researchers want to dive deeper into during upcoming experiments is: “How does this redistribution relate to the beneficial effects of exercise, which is a natural way to increase neurogenesis?”

In the future, it’s possible that cutting-edge research on neurogenesis and neuroplasticity could lead to finely-tuned neurobiological treatments for ailments such as post-traumatic stress disorder (PTSD) and dementia. In a statement to UAB, Overstreet-Wadiche said,

“Over the last 10 years there has been evidence supporting a redistribution of synapses between old and new neurons, possibly by a competitive process that the new cells tend to ‘win.’ Our findings are important because they directly demonstrate that, in order for new cells to win connections, the old cells lose connections.

So, the process of adult neurogenesis not only adds new cells to the network, it promotes plasticity of the existing network. It will be interesting to explore how neurogenesis-induced plasticity contributes to the function of this brain region.

Neurogenesis is typically associated with improved acquisition of new information, but some studies have also suggested that neurogenesis promotes ‘forgetting’ of existing memories.”

Aerobic Exercise Is the Most Effective Way to Stimulate Neurogenesis and Create Adult-Born Neurons

For the past 10 years, the actionable advice I’ve given in The Athlete’s Way has been rooted in the belief that through the daily process of working out anyone can stimulate neurogenesis and optimize his or her mindset and outlook on life via neuroplasticity.

“The Athlete’s Way” program is designed to reshape neural networks and optimize your mindset. Since the beginning, this program has been based on the discovery that aerobic activity produces brain-derived neurotrophic factor (BDNF) and stimulates the birth of new neurons through neurogenesis. I describe my philosophy in the Introduction to The Athlete’s Way,

“Shifting the focus from thinner thighs to stronger minds makes this exercise book unique. The Athlete’s Way does not focus just on sculpting six-pack abs or molding buns of steel. We are more interested in bulking up your neurons and reshaping your synapses to create an optimistic, resilient, and determined mindset. The goal is transformation from the inside out.

My mission is to get this message to you so that you can use neurobiology and behavioral models to help improve your life through exercise. I am a zealot about the power of sweat to transform people’s lives by transforming their minds. My conviction is strong and authentic because I have lived it.”

I created The Athlete’s Way along with the indispensable help of my late father, Richard Bergland, who was a visionary neuroscientist, neurosurgeon, and author of The Fabric of Mind (Viking).

A decade ago, when I published The Athlete’s Way: Sweat and the Biology of Bliss (St. Martin’s Press) I put neurogenesis and neuroplasticity in the spotlight. At the time, the discovery of neurogenesis was brand new, and still a radical notion in mainstream neuroscience.

In the early 21st century, most experts still believed that human beings were born with all the neurons they would have for their entire lifespan. If anything, it was believed that people could only lose neurons or “kill brain cells” as we got older.

Understandably, when I published The Athlete’s Way in 2007 there were lots of skeptics and naysayers who thought my ideas about reshaping mindset using a combination of neurogenesis and neuroplasticity through moderate to vigorous physical activity were ludicrous.

For the past 10 years, I’ve kept my antennae up and my finger on the pulse of all the latest research on neurogenesis and neuroplasticity hoping to find additional empirical evidence that gives more scientific credibility to my system of belief and The Athlete’s Way methodology.

Needless to say, I was over the moon and ecstatic this morning when I read about the new research by Linda Overstreet-Wadiche and Jacques Wadiche that pinpoints the specifics of how adult-born neurons modify existing neural circuits. This is fascinating stuff!

These are exciting times in neuroscience. Modern day neuroscientific techniques are poised to solve many more riddles regarding the complex mechanism by which neurogenesis and neuroplasticity work together as a dynamic duo to reshape our neural networks and functional connectivity between brain regions. Stay tuned for future empirical evidence and scientific research on neurogenesis and neuroplasticity in the months and years ahead.

In the meantime, if you’d like to read a free excerpt from The Athlete’s Way that provides some simple actionable advice and practical ways for you to stimulate neurogenesis and rewire your brain via neuroplasticity and moderate to vigorous physical activity—check out these pages from a section of my book titled: Neuroplasticity and Neurogenesis: Combining Neuroscience and Sport.”

References

Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, Linda Overstreet-Wadiche. Adult-born neurons modify excitatory synaptic transmission to existing neurons. eLife, 2017; 6 DOI: 10.7554/eLife.19886

Source: How Do Neuroplasticity and Neurogenesis Rewire Your Brain? | Psychology Today

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[BLOG POST] How aerobic exercise enhances neuroplasticity in the brain

New research published in the journal Experimental Brain Research suggests a single bout of moderate intensity aerobic exercise enhances neuroplasticity in the brain through its effects on the neurotransmitter GABA.

PsyPost interviewed the study’s corresponding authors, Winston D. Byblow and Ronan A. Mooney of the University of Auckland. Read their responses below:

PsyPost: Why were you interested in this topic?

Habitual exercise appears to be beneficial for health and well-being. It is becoming increasingly evident that acute and chronic participation in aerobic exercise exerts a number of positive effects on the brain such as improved memory and executive function. The underlying mechanisms of exercise-related changes in brain function are not completely understood.

What should the average person take away from your study?

A brief but intense period of aerobic exercise immediately reduces GABA, the main inhibitory neurotransmitter in the brain. GABA play an important role in regulating the brain’s capacity to undergo change or neuroplasticity. We observed reduced excitability of GABA-mediated networks in the motor cortex, which may explain findings from previous studies where enhanced neuroplasticity is observed after aerobic exercise.

Our findings may have implications for individuals after stroke, where GABA is a promising target for promoting neuroplasticity to promote recovery of motor function.

Are there any major caveats? What questions still need to be addressed?

A key limitation of our study was the small sample size of young healthy people. Future studies might examine similar mechanisms in older adults and in people after stroke. We used a stationary bicycle to permit moderate exercise intensity, tailored to the aerobic fitness levels of each participant. Further studies should explore the influence of other exercise modalities and intensities as this would help determine the boundaries for producing the effects which may enhance neuroplasticity. Admittedly, older or clinical populations may struggle with certain exercise intensities/modalities due to functional limitations.

In addition to Byblow and Mooney, the study “Acute aerobic exercise modulates primary motor cortex inhibition” was also co-authored by James P. Coxon, John Cirillo, Helen Glenny and Nicholas Gant.

Source: How aerobic exercise enhances neuroplasticity in the brain

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