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Cardiovascular fitness, cortical plasticity, and aging. - PubMed - NCBI

Cardiovascular fitness is thought to offset declines in cognitive performance, but little is known about the cortical mechanisms that underlie these changes in humans. Research using animal models shows that aerobic training increases cortical capillary supplies, the number of synaptic connections, and the development of new neurons. The end result is a brain that is more efficient, plastic, and adaptive, which translates into better performance in aging animals. Here, in two separate experiments, we demonstrate for the first time to our knowledge, in humans that increases in cardiovascular fitness results in increased functioning of key aspects of the attentional network of the brain during a cognitively challenging task. Specifically, highly fit (Study 1) or aerobically trained (Study 2) persons show greater task-related activity in regions of the prefrontal and parietal cortices that are involved in spatial selection and inhibitory functioning, when compared with low-fit (Study 1) or nonaerobic control (Study 2) participants. Additionally, in both studies there exist groupwise differences in activation of the anterior cingulate cortex, which is thought to monitor for conflict in the attentional system, and signal the need for adaptation in the attentional network. These data suggest that increased cardiovascular fitness can affect improvements in the plasticity of the aging human brain, and may serve to reduce both biological and cognitive senescence in humans.

Capitalizing on cortical plasticity: influence of physical activity on cognition and brain function. - PubMed - NCBI

In this review, we evaluate the hypothesis that physical activity and exercise might serve to protect, and also enhance, cognitive and brain function across the adult lifespan.

Running + challenges lead to neurogenisis

Voluntary physical exercise (wheel running, RUN) and environmental enrichment both stimulate adult hippocampal neurogenesis but do so by different mechanisms. RUN induces precursor cell proliferation, whereas ENR exerts a survival-promoting effect on newborn cells. In addition, continued RUN prevented the physiologically occurring age-related decline in precursor cell in the dentate gyrus but did not lead to a corresponding increase in net neurogenesis. We hypothesized that in the absence of appropriate cognitive stimuli the potential for neurogenesis could not be realized but that an increased potential by proliferating precursor cells due to RUN could actually lead to more adult neurogenesis if an appropriate survival-promoting stimulus follows the exercise. We thus asked whether a sequential combination of RUN and ENR (RUNENR) would show additive effects that are distinct from the application of either paradigm alone. We found that the effects of 10 days of RUN followed by 35 days of ENR were additive in that the combined stimulation yielded an approximately 30% greater increase in new neurons than either stimulus alone, which also increased neurogenesis.

Self-generated vision inputs suppressed

That's because the brain can tell if visual motion is self-generated, canceling out information that would otherwise make us feel -- and act -- as if the world was whirling around us. It's an astonishing bit of neural computation -- one that Maimon and his team are attempting to decode in fruit flies. And the results of their most recent investigations, published in Cell on January 5, provide fresh insights into how the brain processes visual information to control behavior. Each time you shift your gaze (and you do so several times a second), the brain sends a command to the eyes to move. But a copy of that command is issued internally to the brain's own visual system, as well. This allows the brain to predict that it is about to receive a flood of visual information resulting from the body's own movement -- and to compensate for it by suppressing or enhancing the activity of particular neurons.

Perceptually relevant remapping of human somatotopy in 24 hours. - PubMed - NCBI

Experience-dependent reorganisation of functional maps in the cerebral cortex is well described in the primary sensory cortices. However, there is relatively little evidence for such cortical reorganisation over the short-term. Using human somatosensory cortex as a model, we investigated the effects of a 24-hour gluing manipulation in which the right index and right middle fingers (digits 2 & 3) were adjoined with surgical glue. Somatotopic representations, assessed with two 7 tesla fMRI protocols, revealed rapid off-target reorganisation in the non-manipulated fingers following gluing, with the representation of the ring finger (digit 4) shifted towards the little finger (digit 5) and away from the middle finger (digit 3). These shifts were also evident in two behavioural tasks conducted in an independent cohort, showing reduced sensitivity for discriminating the temporal order of stimuli to the ring and little fingers, and increased substitution errors across this pair on a speeded reaction time task.

Runners' brains may be more connected, research shows | EurekAlert! Science News

University of Arizona researchers compared brain scans of young adult cross country runners to young adults who don't engage in regular physical activity. The runners, overall, showed greater functional connectivity -- or connections between distinct brain regions -- within several areas of the brain, including the frontal cortex, which is important for cognitive functions such as planning, decision-making and the ability to switch attention between tasks.

How hearing loss can change the way nerve cells are wired -- ScienceDaily

In mice whose ears were blocked, cells in the auditory nerve started to use their supplies of neurotransmitter more freely. They depleted their reserves of these chemicals rapidly each time a new auditory signal came in, and they decreased the amount of space within the cells that housed sac-like structures called vesicles -- biological storage tanks where neurotransmitter chemicals are kept. "When it's quiet, the demands on the auditory nerve cells are not as great," Xu-Friedman says. "So it makes sense that you would see these changes: You no longer need as much neurotransmitter, so why invest in a lot of storage? If you're not that active, you don't need a big gas tank. And you're not as afraid to use up what you have. This is one plausible explanation for what we observed." The changes in cellular structure and behavior were the opposite of what Xu-Friedman team's saw in a previous study that placed mice in a consistently noisy environment. In that project -- faced with an unusually high level of noise -- the mice's auditory nerve cells started to economize their resources, conserving supplies of neurotransmitter while increasing the storage capacity for the chemicals. "It looks like these effects are two sides of the same coin, and they might be the first hints of a general rule that nerve cells regulate their connections based on how active they are," Xu-Friedman says.

Substance present in ayahuasca brew stimulates generation of human neural cells: Harmine increases the number of neural progenitors, cells that give rise to neurons, study suggests -- ScienceDaily

In order to elucidate these effects, researchers from the D'Or Institute for Research and Education (IDOR) and the Institute of Biomedical Sciences at the Federal University of Rio de Janeiro (ICB-UFRJ) exposed human neural progenitors to this beta-carboline. After four days, harmine led to a 70% increase in proliferation of human neural progenitor cells. Researchers were also able to identify how the human neural cells respond to harmine. The described effect involves the inhibition of DYRK1A, which is located on chromosome 21 and is over activated in patients with Down syndrome and Alzheimer's Disease. "Our results demonstrate that harmine is able to generate new human neural cells, similarly to the effects of classical antidepressant drugs, which frequently are followed by diverse side effects. Moreover, the observation that harmine inhibits DYRK1A in neural cells allows us to speculate about future studies to test its potential therapeutic role over cognitive deficits observed in Down syndrome and neurodegenerative diseases," suggests Stevens Rehen, researcher from IDOR and ICB-UFRJ.

Portions of the brain fall asleep and wake back up all the time, Stanford researchers find | EurekAlert! Science News

The team used what amounts to sets of very sensitive pins that can record activity from a column of neurons in the brain. In the past, people had known that individual neurons go through phases of being more or less active, but with this probe they saw for the first time that all the neurons in a given column cycled together between firing very rapidly then firing at a much slower rate, similar to coordinated cycles in sleep. "During an on state the neurons all start firing rapidly," said Kwabena Boahen, a professor of bioengineering and electrical engineering at Stanford and a senior author on the paper. "Then all of a sudden they just switch to a low firing rate. This on and off switching is happening all the time, as if the neurons are flipping a coin to decide if they are going to be on or off." Those cycles, which occur on the order of seconds or fractions of seconds, weren't as visible when awake because the wave doesn't propagate much beyond that column, unlike in sleep when the wave spreads across almost the entire brain and is easy to detect.

Our 86 Billion Neurons: She Showed It | by Steven Mithen | The New York Review of Books

And then a surprise: the elephant brain had more neurons than the human brain, not just a few more but three times as many: 247 billion to our 86 billion. But 98 percent of these were located in the cerebellum at the back of the brain, leaving a mere 5.6 billion in the 2.8-kilogram cerebral cortex compared to the 16 billion in the 1.2-kilogram human cerebral cortex. What are all those neurons doing in the elephant cerebellum, ten times more than one would expect? Most likely controlling that other exceptional feature of the elephant, its 100-kilogram and highly sensory muscular trunk.

100 billion neurons, unsourced

She then returned to her alma mater to train young scientists in communication—with an allowance to pursue research if she were so inclined. She was inspired to do so by the pervasive myths about the brain she kept encountering, such as that we use only 10 percent of our capacity. Moreover, none of the distinguished neuroscientists she asked could tell her the source for the claim that there were 100 billion neurons in the brain, which they all believed.

Cooking is the essential human act

Our 86 billion neurons need so much energy that if we shared a way of life with other primates we couldn’t possibly survive: there would be insufficient hours in the day to feed our hungry brain. It needs 500 calories a day to function, which is 25 percent of what our entire body requires. That sounds like a lot, but a single cupful of glucose can fuel the brain for an entire day, with just over a teaspoon being required per hour. Nevertheless, the brains of almost all other vertebrates are responsible for a mere 10 percent of their overall metabolic needs. We evolved and learned a clever trick in our evolutionary past in order to find the time to feed our neuron-packed brains: we began to cook our food. By so doing, more energy could be extracted from the same quantity of plant stuffs or meat than from eating them raw.

Consciousness is tied to 'entropy', say researchers -

Key to this has been the study of synchronization – how the electrical activity of one set of neurons can oscillate in phase with that of another set. Synchronization in turn implies that those sets of neurons are physically tied to one another, just as oscillating physical systems, such as pendulums, become synchronized when they are connected together. The latest work stems from the observation that consciousness, or at least the proper functioning of brains, is associated not with high or even low degrees of synchronicity between neurons but by middling amounts. Jose Luis Perez Velazquez, a biochemist at the University of Toronto, and colleagues hypothesized that what is maximized during consciousness is not connectivity itself but the number of different ways that a certain degree of connectivity can be achieved.

Running triggers brain repair and extends life in mouse model - Medical News Today

The researchers allowed some of the mice the opportunity to run by installing a wheel into their cages. Surprisingly, the mice given the opportunity to run lived more than 12 months (a relatively normal lifespan for a mouse). On top of their extended lives, the running mice also put on more weight and achieved a better sense of balance, compared with their less active siblings. "We saw that the existing neurons became better insulated and more stable. This means that the unhealthy neurons worked better and the previously damaged circuits in the brain became stronger and more functional." Dr. Matías Alvarez-Saavedra, lead author However, these changes were reversed if the opportunity to exercise was taken away. Once the running wheel was removed, the symptoms returned, and their lives were once more cut short.

What Learning Looks Like: Researcher Teaches Fake Words To Watch Learning Happen | KPBS

Abel has crafted more than 700 of these sentence sets so she can chart the progression in brain activity as children hear them. In this way, she can actually see learning happening. It starts with a big dip on the line graph during the first sentence, "The boys fought over the shap." That dip means Duncan is confused — his neurons aren't sure what he’s just encountered. The second and third sentences add context. "They played catch with the shap. I like to throw the shap." The dip gets shallower and shallower until it becomes a peak on the line graph. "So the third time they hear the nonsense word, it looks like their brain is processing it like it's a real word," Abel said. "The brain is responding to it the exact same way that the brain responds to a known word."

Waves on waves

They found that they could closely replicate the shape of the beta waves in the model by delivering two kinds of excitatory synaptic stimulation to distinct layers in the cortical columns of cells: one that was weak and broad in duration to the lower layers, contacting spiny dendrites on the pyramidal neurons close to the cell body; and another that was stronger and briefer, lasting 50 milliseconds (i.e., one beta period), to the upper layers, contacting dendrites farther away from the cell body. The strong distal drive created the valley in the waveform that determined the beta frequency.

A neural link between affective understanding and interpersonal attraction

At the neural level, changes in interpersonal attraction were predicted by activity in the reward system of the observer’s brain. Importantly, these effects were specific to individual observer–target pairs and could not be explained by a target’s general attractiveness or expressivity. Furthermore, using multivoxel pattern analysis (MVPA), we found that neural activity in the reward system of the observer’s brain varied as a function of how well the target’s affective behavior matched the observer’s neural representation of the underlying affective state: The greater the match, the larger the brain’s intrinsic reward signal. Taken together, these findings provide evidence that reward-related neural activity during social encounters signals how well an individual’s “neural vocabulary” is suited to infer another person’s affective state, and that this intrinsic reward might be a source of changes in interpersonal attraction.

Neuronal structures associated with memory sprout in response to novel molecules: Drug candidates protect neurons against damage from substance implicated in Alzheimer's disease -- ScienceDaily

"Problems with learning and memory in many neurodegenerative and neurodevelopment disorders, such as Alzheimer's disease and certain forms of autism or mental retardation involve either loss or misregulation of dendritic spines," said Jerry Yang, a professor of chemistry and biochemistry who led the work. "The compounds we have developed may offer the possibility to compensate, or ideally preserve, neuronal communication in people suffering from problems with memory."

Exercise strengthens your nerves too

Unsurprisingly, the elite masters athletes’ legs were much stronger than the legs of the other volunteers, by an average of about 25 percent. The athletes had about 14 percent more total muscle mass than the control group. More interesting to the researchers, the athletes also had almost 30 percent more motor units in their leg muscle tissue, and these units were functioning better than those of people in the sedentary group. In the control group, many of the electrical messages from the motor neuron to the muscle showed signs of “jitter and jiggle,” which are actual scientific terms for signals that stutter and degrade before reaching the muscle fiber. Such weak signaling often indicates a motor neuron that is approaching death. In essence, the sedentary elderly people had fewer motor units in their muscles, and more of the units that remained seemed to be feeling their age than in the athletes’ legs.

Running boosts neurogenesis (in rats)

Those rats that had jogged on wheels showed robust levels of neurogenesis. Their hippocampal tissue teemed with new neurons, far more than in the brains of the sedentary animals. The greater the distance that a runner had covered during the experiment, the more new cells its brain now contained. There were far fewer new neurons in the brains of the animals that had completed high-intensity interval training. They showed somewhat higher amounts than in the sedentary animals but far less than in the distance runners. And the weight-training rats, although they were much stronger at the end of the experiment than they had been at the start, showed no discernible augmentation of neurogenesis. Their hippocampal tissue looked just like that of the animals that had not exercised at all.

Lots of good links on mindfulness and brains

Mindfulness should no longer be considered a “nice-to-have” for executives. It’s a “must-have”:  a way to keep our brains healthy, to support self-regulation and effective decision-making capabilities, and to protect ourselves from toxic stress. It can be integrated into one’s religious or spiritual life, or practiced as a form of secular mental training.  When we take a seat, take a breath, and commit to being mindful, particularly when we gather with others who are doing the same, we have the potential to be changed.

Neurons change across basil ganglia with habit formation

Interestingly, the group observed that changes in go and stop activity occurred across the entire region of the basal ganglia they were studying as opposed to specific subsets of brain cells. O'Hare said this may relate to the observation that an addiction to one thing can make a person more likely to engage in other unhealthy habits or addictions as well.

Why are habits so hard to break? Getting hooked changes the brain

Experiments by Duke neurobiology graduate student Justin O'Hare found that the stop and go pathways were both more active in the sugar-habit mice. O'Hare said he didn't expect to see the stop signal equally ramped up in the habit brains, because it has been traditionally viewed as the factor that helps prevent a behavior. The team also discovered a change in the timing of activation in the two pathways. In mice that had formed a habit, the go pathway turned on before the stop pathway. In non-habit brains, the stop signal preceded the go. These changes in the brain circuitry were so long-lasting and obvious that it was possible for the group to predict which mice had formed a habit just by looking at isolated pieces of their brains in a petri dish.

Brain levels of vitamin B12 decrease with age and are prematurely low in people with autism and schizophrenia -- ScienceDaily

An active form of B12 called methylcobalamin, or methyl B12, supports normal brain development by its control through a process known as epigenetic regulation of gene expression. Remarkably, the brain level of methyl B12 was found to be more than 10 times lower in healthy elderly people than in healthy younger people. A lower than normal level of methyl B12 in the brain could adversely affect neurodevelopment in younger years and could disrupt learning and memory later in life. Both autism and schizophrenia are associated with oxidative stress, which also plays an important role in aging, and oxidative stress may underlie the decreased brain B12 levels observed in this study. The findings suggest the need for further research to determine if the use of supplemental methyl B12 and antioxidants like glutathione could help prevent oxidative stress and be useful in treating these conditions.

Your body is your brain

"We have now uncovered an unforeseen role of motor neurons in the elaboration of the final program for motor behaviour," says principal investigator Abdel El Manira at Karolinska Institutet's Department of Neuroscience. "Our unexpected findings demonstrate that motor neurons control locomotor circuit function retrogradely via gap junctions, so that motor neurons will directly influence transmitter release and the recruitment of upstream excitatory interneurons."

Changes in brain connectivity protect against developing bipolar disorder -- ScienceDaily

"The ability of the siblings to rewire their brain networks means they have adaptive neuroplasticity that may help them avoid the disease even though they still carry the genetic scar of bipolar disorder when they process emotional information," said Sophia Frangou, MD, PhD, Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai and lead author of the study. Dr. Frangou's ongoing research uses neuroimaging to study how differences in brain wiring can either increase or decrease the likelihood of developing mental health problems.