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terça-feira, 27 de outubro de 2015

The Tantalizing Links between Gut Microbes and the Brain

 

 

Neuroscientists are probing the idea that intestinal microbiota might influence brain development and behavior

Nearly a year has passed since Rebecca Knickmeyer first met the participants in her latest study on brain development. Knickmeyer, a neuroscientist at the University of North Carolina School of Medicine in Chapel Hill, expects to see how 30 newborns have grown into crawling, inquisitive one-year-olds, using a battery of behavioural and temperament tests. In one test, a child's mother might disappear from the testing suite and then reappear with a stranger. Another ratchets up the weirdness with some Halloween masks. Then, if all goes well, the kids should nap peacefully as a noisy magnetic resonance imaging machine scans their brains.

“We try to be prepared for everything,” Knickmeyer says. “We know exactly what to do if kids make a break for the door.”

Knickmeyer is excited to see something else from the children—their faecal microbiota, the array of bacteria, viruses and other microbes that inhabit their guts. Her project (affectionately known as 'the poop study') is part of a small but growing effort by neuroscientists to see whether the microbes that colonize the gut in infancy can alter brain development.

The project comes at a crucial juncture. A growing body of data, mostly from animals raised in sterile, germ-free conditions, shows that microbes in the gut influence behaviour and can alter brain physiology and neurochemistry.

In humans, the data are more limited. Researchers have drawn links between gastrointestinal pathology and psychiatric neurological conditions such as anxiety, depression, autism, schizophrenia and neurodegenerative disorders—but they are just links.

“In general, the problem of causality in microbiome studies is substantial,” says Rob Knight, a microbiologist at the University of California, San Diego. “It's very difficult to tell if microbial differences you see associated with diseases are causes or consequences.” There are many outstanding questions. Clues about the mechanisms by which gut bacteria might interact with the brain are starting to emerge, but no one knows how important these processes are in human development and health.

That has not prevented some companies in the supplements industry from claiming that probiotics—bacteria that purportedly aid with digestive issues—can support emotional well-being. Pharmaceutical firms, hungry for new leads in treating neurological disorders, are beginning to invest in research related to gut microbes and the molecules that they produce.

Scientists and funders are looking for clarity. Over the past two years, the US National Institute of Mental Health (NIMH) in Bethesda, Maryland, has funded seven pilot studies with up to US$1 million each to examine what it calls the 'microbiome–gut–brain axis' (Knickmeyer's research is one of these studies). This year, the US Office of Naval Research in Arlington, Virginia, agreed to pump around US$14.5 million over the next 6–7 years into work examining the gut's role in cognitive function and stress responses. And the European Union has put €9 million (US$10.1 million) towards a five-year project called MyNewGut, two main objectives of which target brain development and disorders.

The latest efforts aim to move beyond basic observations and correlations—but preliminary results hint at complex answers. Researchers are starting to uncover a vast, varied system in which gut microbes influence the brain through hormones, immune molecules and the specialized metabolites that they produce.

“There's probably more speculation than hard data now,” Knickmeyer says. “So there's a lot of open questions about the gold standard for methods you should be applying. It's very exploratory.”

Gut reactions
Microbes and the brain have rarely been thought to interact except in instances when pathogens penetrate the blood–brain barrier—the cellular fortress protecting the brain against infection and inflammation. When they do, they can have strong effects: the virus that causes rabies elicits aggression, agitation and even a fear of water. But for decades, the vast majority of the body's natural array of microbes was largely uncharacterized, and the idea that it could influence neurobiology was hardly considered mainstream. That is slowly changing.

Studies on community outbreaks were one key to illuminating the possible connections. In 2000, a flood in the Canadian town of Walkerton contaminated the town's drinking water with pathogens such as Escherichia coli and Campylobacter jejuni. About 2,300 people suffered from severe gastrointestinal infection, and many of them developed chronic irritable bowel syndrome (IBS) as a direct result.

During an eight-year study of Walkerton residents, led by gastroenterologist Stephen Collins at McMaster University in Hamilton, Canada, researchers noticed that psychological issues such as depression and anxiety seemed to be a risk factor for persistent IBS. Premysl Bercik, another McMaster gastroenterologist, says that this interplay triggered intriguing questions. Could psychiatric symptoms be driven by lingering inflammation, or perhaps by a microbiome thrown out of whack by infection?

The McMaster group began to look for answers in mice. In a 2011 study, the team transplanted gut microbiota between different strains of mice and showed that behavioural traits specific to one strain transmitted along with the microbiota. Bercik says, for example, that “relatively shy” mice would exhibit more exploratory behaviour when carrying the microbiota of more-adventurous mice. “I think it is surprising. The microbiota is really driving the behavioural phenotype of host. There's a marked difference,” Bercik says. Unpublished research suggests that taking faecal bacteria from humans with both IBS and anxiety and transplanting it into mice induces anxiety-like behaviour, whereas transplanting bacteria from healthy control humans does not.

Such results can be met with scepticism. As the field has developed, Knight says, microbiologists have had to learn from behavioural scientists that how animals are handled and caged can affect things such as social hierarchy, stress and even the microbiome.

And these experiments and others like them start with a fairly unnatural model: germ-free—or 'gnotobiotic'—mice. These animals are delivered by Caesarean section to prevent them from picking up microbes that reside in their mothers' birth canals. They are then raised inside sterile isolators, on autoclaved food and filtered air. The animals are thus detached from many of the communal microbes that their species has evolved with for aeons.

In 2011, immunologist Sven Pettersson and neuroscientist Rochellys Diaz Heijtz, both at the Karolinska Institute in Stockholm, showed that in lab tests, germ-free mice demonstrated less-anxious behaviour than mice colonized with natural indigenous microbes. (Less anxiety is not always a good thing, evolutionarily speaking, for a small mammal with many predators.)

When the Karolinska team examined the animals' brains, they found that one region in germ-free mice, the striatum, had higher turnover of key neurochemicals that are associated with anxious behaviour, including the neurotransmitter serotonin. The study also showed that introducing adult germ-free mice to conventional, non-sterile environments failed to normalize their behaviour, but the offspring of such 'conventionalized' mice showed some return to normal behaviour, suggesting that there is a critical window during which microbes have their strongest effects.

By this time, many researchers were intrigued by the mounting evidence, but results stemmed mostly from fields other than neuroscience. “The groups working on this are primarily gut folks, with a few psychology-focused people collaborating,” says Melanie Gareau, a physiologist at the University of California, Davis. “So the findings tended to describe peripheral and behavioural changes rather than changes to the central nervous system.”

But Pettersson and Diaz Heijtz's research galvanized the field, suggesting that researchers could get past observational phenomenology and into the mechanisms affecting the brain. Nancy Desmond, a programme officer involved in grant review at the NIMH, says that the paper sparked interest at the funding agency soon after its publication and, in 2013, the NIMH formed a study section devoted to neuroscience research that aims to unravel functional mechanisms and develop drugs or non-invasive treatments for psychological disorders.

Judith Eisen, a neuroscientist at the University of Oregon in Eugene, earned a grant to study germ-free zebrafish, whose transparent embryos allow researchers to easily visualize developing brains. “Of course, 'germ-free' is a completely unnatural situation,” Eisen says. “But it provides the opportunity to learn which microbial functions are important for development of any specific organ or cell type.”

Chemical exploration
Meanwhile, researchers were starting to uncover ways that bacteria in the gut might be able to get signals through to the brain. Pettersson and others revealed that in adult mice, microbial metabolites influence the basic physiology of the blood–brain barrier. Gut microbes break down complex carbohydrates into short-chain fatty acids with an array of effects: the fatty acid butyrate, for example, fortifies the blood–brain barrier by tightening connections between cells (see 'The gut–brain axis').

Recent studies also demonstrate that gut microbes directly alter neurotransmitter levels, which may enable them to communicate with neurons. For example, Elaine Hsiao, a biologist now at the University of California, Los Angeles, published research this year examining how certain metabolites from gut microbes promote serotonin production in the cells lining the colon—an intriguing finding given that some antidepressant drugs work by promoting serotonin at the junctions between neurons. These cells account for 60% of peripheral serotonin in mice and more than 90% in humans.

Like the Karolinska group, Hsiao found that germ-free mice have significantly less serotonin floating around in their blood, and she also showed that levels could be restored by introducing to their guts spore-forming bacteria (dominated by Clostridium, which break down short-chain fatty acids). Conversely, mice with natural microbiota, when given antibiotics, had reduced serotonin production. “At least with those manipulations, it's quite clear there's a cause–effect relationship,” Hsiao says.

But it remains unclear whether these altered serotonin levels in the gut trigger a cascade of molecular events, which in turn affect brain activity—and whether similar events take place in humans, too. “It will be important to replicate previous findings, and translate these findings into human conditions to really make it to the textbooks,” Hsiao says.

For John Cryan, a neuroscientist at University College Cork in Ireland, there is little question that they will. His lab has demonstrated that germ-free mice grow more neurons in a specific brain region as adults than do conventional mice. He has been promoting the gut–brain axis to neuroscientists, psychiatric-drug researchers and the public. “If you look at the hard neuroscience that has emerged in the last year alone, all the fundamental processes that neuroscientists spend their lives working on are now all shown to be regulated by microbes,” he says, pointing to research on the regulation of the blood–brain barrier, neurogenesis in mice and the activation of microglia, the immune-like cells that reside in the brain and spinal cord.

At the 2015 Society for Neuroscience meeting in Chicago, Illinois, this month, Cryan and his colleagues plan to present research showing that myelination—the formation of fatty sheathing that insulates nerve fibres—can also be influenced by gut microbes, at least in a specific part of the brain. Unrelated work has shown that germ-free mice are protected from an experimentally induced condition similar to multiple sclerosis, which is characterized by demyelination of nerve fibres. At least one company, Symbiotix Biotherapies in Boston, Massachusetts, is already investigating whether a metabolite produced by certain types of gut bacterium might one day be used to stem the damage in humans with multiple sclerosis.

A move to therapy
Tracy Bale, a neuroscientist at the University of Pennsylvania in Philadelphia, suspects that simple human interventions may already be warranted. Bale heard about Cryan's work on the radio programme Radiolab three years ago. At the time, she was researching the placenta, but wondered how microbes might fit into a model of how maternal stress affects offspring.

In research published this year, Bale subjected pregnant mice to stressful stimuli. She found that it noticeably reduced the levels of Lactobacilli present in the mice's vaginas, which are the main source of the microbes that colonize the guts of offspring. These microbial shifts carried over to pups born vaginally, and Bale detected signs that microbiota might affect neurodevelopment, especially in males.

In work that her group plans to present at the Society for Neuroscience meeting, Bale has shown that by feeding vaginal microbiota from stressed mice to Caesarean-born infant mice, they can recapitulate the neurodevelopmental effects of having a stressed mother. Bale and her colleagues are now wrapping up research investigating whether they can treat mice from stressed mums with the vaginal microbiota of non-stressed mice.

The work, Bale says, has “immediate translational effects”. She points to a project headed by Maria Dominguez-Bello, a microbiologist at the New York University School of Medicine, in which babies born by means of Caesarean section are swabbed on the mouth and skin with gauze taken from their mothers' vaginas. Her team wants to see whether these offspring end up with microbiota similar to babies born vaginally. “It's not standard of care,” Bale says, “but I will bet you, one day, it will be.”

Many are still sceptical about the link between microbes and behaviour and whether it will prove important in human health — but scientists seem more inclined to entertain the idea now than they have in past. In 2007, for example, Francis Collins, now director of the US National Institutes of Health, suggested that the Human Microbiome Project, a large-scale study of the microbes that colonize humans, might help to unravel mental-health disorders. “It did surprise a few people who assumed we were talking about things that are more intestinal than cerebral,” Collins says. “It was a little bit of leap, but it's been tentatively backed up.”

Funding agencies are supporting the emerging field, which spans immunology, microbiology and neuroscience, among other disciplines. The NIMH has offered seed funding for work on model systems and in humans to probe whether the area is worth more-substantial investment, a move that has already brought more researchers into the fold. The MyNewGut project in Europe has an even more optimistic view of the value of such research, specifically seeking concrete dietary recommendations that might alleviate brain-related disorders.

Today, Knickmeyer's project on infants represents what she calls “a messy take-all-comers kind of sample”. Among the brain regions that Knickmeyer is scanning, the amygdala and prefrontal cortex hold her highest interest; both have been affected by microbiota manipulations in rodent models. But putting these data together with the dozens of other infant measures that she is taking will be a challenge. “The big question is how you deal with all the confounding factors.” The children's diets, home lives and other environmental exposures can all affect their microbiota and their neurological development, and must be teased apart.

Knickmeyer speculates that tinkering with microbes in the human gut to treat mental-health disorders could fail for other reasons. Take, for instance, how microbes might interact with the human genome. Even if scientists were to find the therapeutic version of a “gold Cadillac of microbiota”, she points out, “maybe your body rejects that and goes back to baseline because your own genes promote certain types of bacteria.” There is much more to unravel, she says. “I'm always surprised. It's very open. It's a little like a Wild West out there.”

This article is reproduced with permission and was first published on October 14, 2015.

 

http://www.scientificamerican.com/article/the-tantalizing-links-between-gut-microbes-and-the-brain/?WT.mc_id=SA_HLTH_20151027

quinta-feira, 8 de outubro de 2015

Staying healthy: Experiment finds key to natural detoxifier’s reactivity

 

 

A chalk drawing showing the key bonds in the cytochrome intermediate compound. The shorter iron-sulfur bond enables the more reactive double-bonded oxygen atom to extend farther out on the other side and participate in an activation reaction.

Credit: Michael T. Green, Elizabeth L. Onderko/ Penn State University

Researchers working at the Department of Energy's SLAC National Accelerator Laboratory have discovered that a mere 9-trillionths-of-a-meter reduction in the length of a chemical bond dramatically boosts the reactivity of a family of molecules that helps keep humans and many other organisms healthy.

This result, reported recently in Nature Chemistry, is expected to help scientists design and manufacture new and more effective medicines.

The molecules, called cytochrome P450s, are known as "nature's detoxifiers," said Courtney Krest Roach, a beamline scientist at SLAC's Stanford Synchrotron Radiation Lightsource (SSRL) -- a DOE Office of Science User Facility -- and first author of the paper.

Since cytochrome P450 was discovered more than 50 years ago, more than 11,000 variants have been identified in every kingdom of life, including animals, plants, fungi and bacteria. Some 57 different P450s are found in humans, typically in the liver, where they help break down poisons and unwanted molecules. They are also essential in the body's manufacture of certain hormones, and chemists hope to be able to use them in the future to catalyze the creation of complex molecules for use in medicine and industry.

"Our bodies use P450s to perform one step in the metabolism of some 75 percent of pharmaceuticals," Roach said. "And the P450s' extreme selectivity can enable much more direct and efficient synthesis of a number of high-value hydrocarbons and organic molecules."

Molecular Structure is Key

Each cytochrome P450 is optimized to catalyze an initial "activation" step in a specific chemical reaction. They all share the same basic atomic structure: A central iron atom is surrounded by four nitrogen atoms, with a sulfur-based structure sticking out from one side of the ring. Activation creates an intermediate compound that has an oxygen atom double-bonded to the iron atom; it sticks out from the other side of the ring.

Because the P450s' intermediate compounds were short-lived, chemists who were trying to learn how they worked tried studying a slightly simpler molecule, called CPO, which had a more stable intermediate. But they found it was much less reactive than the P450s ­- in some cases only one-fortieth as reactive. Researchers needed to know why, because a more reactive P450 can break stronger bonds, metabolize new medicines or make different final products.

The new experiments at SSRL were led by Penn State University Professor Michael Green, who was Roach's PhD advisor. The research team used the absorption of X-rays by the intermediate forms of CPO and P450s to make ultraprecise measurements of their atomic structures. The results showed that the big difference in reactivity was caused by a miniscule, 9-trillionths-of-a-meter difference in the lengths of their iron-sulfur bonds.

Small Changes, Big Impact

Slight changes in hydrogen bonding near the central iron atom shortened the length of the P450s' iron-sulfur bond by 4 percent. This changed the distribution of nearby electrons in a way that weakened and lengthened the iron-oxygen double bond on the opposite side of the ring. This, in turn, made it easier for the oxygen atom to carry out its part in the activation process, thus increasing P450s' reactivity.

"SSRL is the only place that we could do these experiments with the necessary quality," Roach said.

In their "News & Views" commentary on this research published in the same issue of Nature Chemistry, University of Illinois professors Ilia Denisove and Stephen Silgar said this result is a significant breakthrough that will provide the basis for researchers to design and make new catalysts and adapt P450-based systems for use in biotechnology.


Story Source:

The above post is reprinted from materials provided by SLAC National Accelerator Laboratory. Note: Materials may be edited for content and length.


Journal Reference:

  1. Courtney M. Krest, Alexey Silakov, Jonathan Rittle, Timothy H. Yosca, Elizabeth L. Onderko, Julio C. Calixto, Michael T. Green. Significantly shorter Fe–S bond in cytochrome P450-I is consistent with greater reactivity relative to chloroperoxidase. Nature Chemistry, 2015; 7 (9): 696 DOI: 10.1038/nchem.2306

 

http://www.sciencedaily.com/releases/2015/10/151007145246.htm

quarta-feira, 7 de outubro de 2015

The Science Behind Consciously Controlling Your Immune System: The Mind-Body Connection

 

 

 

The results of a study conducted with the use of Wim Hof method suggest that a person can learn to consciously control his immune responses.

Wim Hof is a Dutch world record holder who is famous worldwide for his ability to resist cold. For this incredible invulnerability to cold, he was commonly nicknamed “the Iceman”.

Scientists led by Matthijs Kox of the Radboud University Medical Center in Nijmegen, the Netherlands, studied his method, which is somehow similar to the Tibetan Tummo technique (yoga of inner heat) and involves third-eye meditation, breathing exercises and cold exposure, and used it to train 12 volunteers to fend off inflammation.

In the framework of the study, 24 volunteers, including 12 people trained in the Wim Hof method and 12 who did not undergo any training, were subjected tothe inflammation test, during which they were injected with a strain of bacteria that provokes flu-like symptoms.

As a result, volunteers who underwent training with Hof method reported fewer and less intense flu-like symptoms than those who did not. At the same time, trained volunteers produced smaller amounts of proteins related to inflammation, and higher levels of interleukin-10, an inflammation-fighting protein.

“Hitherto, both the autonomic nervous system and innate immune system were regarded as systems that cannot be voluntarily influenced. The present study demonstrates that, through practicing techniques learned in a short-term training program, the sympathetic nervous system and immune system can indeed be voluntarily influenced,” writes the scientific journal PNAS, where the study was published.

“Orthodox neurobiologists and orthodox immunologists have been skeptical. They think the study of the interactions between the nervous and immune systems is a ‘field in the shadows’. This study is a nice way to show that link,” said Guiseppe Matarese, an immunologist of the University of Salerno in Italy who was not involved in the study.

Yet, it is not the only scientific study to show that the mind can control the immune system. In particular, Australian scientists came to the conclusion thatconsciousness is able to influence the intensity of the allergic reaction.

As a part of an experiment, several healthy volunteers had their arms injected with histamine, a substance that plays a major role in many allergic reactions. The experiment was structured so that they thought that the drug was injected in a rubber doll, while a real injection was made in their other arm.

After the experiment, the intensity of the allergic response on both arms of the volunteers was evaluated and compared to the one of the control group who had no rubber doll illusion. As a result, the researchers found that the volunteers who thought that the injection had been given to the doll manifested a much stronger effect of histamine on the arm that had been replaced by the fake one.

“Such a finding is particularly relevant to the immune system because a primary role of the immune system is to discriminate self from non-self,” said Prof Lorimer Moseley, who led the study. “These findings strengthen the argument that the brain exerts some kind of control over specific body parts according to how strongly we own them”.

Both studies show that the immune system can be influenced by the consciousness in many ways, which could mean that our thoughts, beliefs and mood can affect the physical state of our body. Knowing that, you can learn to control your thinking and thus your immune system and health. Focus on the bright side of life, visualize yourself being happy and healthy, meditate every day, and soon you will see positive changes not only in your health but in your whole life!

 

ABOUT THE AUTHOR

Anna LeMind is the owner and lead editor of the website Learning-mind.com, and a staff writer for The Mind Unleashed.

 

http://themindunleashed.org/2014/07/science-behind-consciously-controlling-your-immune-system-mind-body-connection.html

sábado, 22 de agosto de 2015

Fat and sugar cause bacterial changes that may relate to loss of cognitive function

 

 

High fat, high sugar, we all know that sometimes the foods we crave most are the worst for us. Yeah, I get that. But new findings on the subject in an Oregon State University study suggest high fat-or high sugar can cause changes in the bacteria in the gut that affect our brain function.

Typically, bacteria release compounds that act as neurotransmitters which stimulate sensory nerves and the immune system, and affect a wide range of biological functions. In test diets high in fat or sugar, bacterial communication with the brain was impaired. And the body's ability to adapt and adjust to changing situations or, "cognitive flexibility," was reduced.

The research was done using laboratory mice, fed various diets and put through a battery of challenges to monitor changes in mental and physical function and the impact on various types of bacteria. In just four weeks, test scores on the challenges started dropping in both the high fat and high sugar mice compared to the "normal" diet group.

Most dramatic was the reduction in cognitive flexibility. The team says their work indicates it's not just the food that could be influencing our brain, but the interaction between the food and microbial changes.

A study at Oregon State University indicates that both a high-fat and a high-sugar diet, compared to a normal diet, cause changes in gut bacteria that appear related to a significant loss of "cognitive flexibility," or the power to adapt and adjust to changing situations. This effect was most serious on the high-sugar diet, which also showed an impairment of early learning for both long-term and short-term memory.

Credit: NSF/Karson Productions

 

sábado, 25 de julho de 2015

Clues to human molecular interactions

 

 

The tetrameric TOPLESS complex with the EAR motif peptides bound at its repressor-peptide binding grooves. The repressor peptides are shown as a ball presentation.

Credit: Karsten Melcher, Ph.D., Van Andel Research Institute

Scientists at Van Andel Research Institute (VARI) have revealed an important molecular mechanism in plants that has significant similarities to certain signaling mechanisms in humans, which are closely linked to early embryonic development and to diseases such as cancer.

In plants as in animals and humans, intricate molecular networks regulate key biological functions, such as development and stress responses. The system can be likened to a massive switchboard--when the wrong switches are flipped, genes can be inappropriately turned on or off, leading to the onset of diseases.

Now, VARI scientists have unraveled how an important plant protein, known as TOPLESS, interacts with other molecules responsible for turning genes off. The findings in plants provide a general model across species for this type of gene silencing, which is linked to several vital biological functions in humans. The discovery was published today in Science Advances.

"This is really a fundamental discovery--our structure shows the corepressor TOPLESS interacting with key repressor motifs, which constitutes a major component of gene silencing in plants," said Van Andel Research Institute's Karsten Melcher, Ph.D., one of the study's corresponding authors. "Understanding this interaction in plants gives us unique insight into similar pathways in humans that involve these proteins, which are notoriously tough to investigate."

Using a method called X-ray crystallography, the team determined the three- dimensional structure of TOPLESS, both on its own and when linked with other molecules responsible for turning genes off, thereby regulating gene expression. Although these interacting molecules were chosen from different signaling pathways in plants, they all linked up with TOPLESS in the same manner

"This structure will allow us to take a more targeted approach to investigating TOPLESS's counterparts in humans and significantly expands our knowledge base," said VARI's H. Eric Xu, Ph.D., who also is a corresponding author. "We're extremely excited to continue this work to better understand these proteins and how they interact with other molecules in health and disease states."

The new paper is the third in a trio of publications that unveil key components of fundamental molecular processes. Although the new study provides further insight into human molecular pathways, the work also directly describes how components of the molecular switchboard in plants interact to regulate responses to a multitude of stressors, including temperature fluctuations. The new findings follow an earlier Nature paper, which was included in the top ten list of scientific breakthroughs of 2009 by Science magazine, and an earlier Science paper, both of which describe how plants respond to drought and temperature stress. Taken together, the papers not only have implications for developing hardier plants but also for determining molecular structures for components of entire pathways.

Authors include Jiyuan Ke, Honglei Ma, and Xin Gu of VARI and VARI-Shanghai Institute of Materia Medica; Jiayang Li of the Chinese Academy of Sciences; Joseph S. Brunzelle of Northwestern University; and Adam Thelen, now at Michigan State University.

Additional background information on TOPLESS and gene regulation:

Gene expression is regulated by both activators and repressors. Although gene repression is thought to be equally important as gene activation for this regulation, relatively little is known about the mechanisms of gene repressors and co-repressors.

TOPLESS functions as a co-repressor and interacts with repressors containing ethylene-responsive element binding factor-associated amphiphilic repression (EAR) motifs. EAR motifs are the most common form of transcriptional repression motifs found in plants and are thought to facilitate stable epigenetic regulation of gene expression via recruitment of chromatin modifiers.

TOPLESS plays important roles in plant development; its name stems from the fact that mutations in TOPLESS can give rise to seedlings in which the shoot is transformed into a second root, hence "topless" seedlings.

In humans, similar proteins also are altered in many types of tumors, and control embryonic development and the development of neurons.


Story Source:

The above post is reprinted from materials provided by Van Andel Research Institute. Note: Materials may be edited for content and length.


Journal Reference:

  1. Jiyuan Ke, Honglei Ma, Xin Gu, Adam Thelen, Joseph S. Brunzelle, Jiayang Li, H. Eric Xu, and Karsten Melcher. Structural basis for recognition of diverse transcriptional repressors by the TOPLESS family of corepressors. Science Advances, 2015 DOI: 10.1126/sciadv.1500107

 

terça-feira, 2 de dezembro de 2014

Unravelling the complexity of proteins

 

 

December 1, 2014

International Union of Crystallography

Knowledge of the three-dimensional structures of proteins is essential for understanding biological processes. Structures help to explain molecular and biochemical functions, visualize details of macromolecular interactions, facilitate understanding of underlying biochemical mechanisms and define biological concepts. A new article seeks to address the fundamental question of whether the three-dimensional structures of all proteins and all functional annotations can be determined using X-ray crystallography.


Knowledge of the three-dimensional structures of proteins is essential for understanding biological processes.

Structures help to explain molecular and biochemical functions, visualize details of macromolecular interactions, facilitate understanding of underlying biochemical mechanisms and define biological concepts.

The human genome and follow-up sequencing projects have revolutionized biology and medicine; structural genomic programmes have developed and applied structure-determination pipelines to a wide range of protein targets, facilitating the visualization of macromolecular interactions and the understanding of their molecular and biochemical functions.

A paper recently published by Mizianty et al. seeks to address the fundamental question of whether the three-dimensional structures of all proteins and all functional annotations can be determined using X-ray crystallography.

The researchers set out to perform the first large scale analysis of its kind covering all known complete proteomes (the sets of proteins thought to be expressed by an organism whose genome has been completely sequenced, as defined by the UniProt Consortium in 2012) and all functional and localization annotations available in the Gene Ontology for the corresponding proteins.

The Canadian and US team show that current X-ray crystallographic knowhow combined with homology modeling can provide structures for 25% of modelling families (protein clusters for which structural models can be obtained through homology modelling), with at least one structural model produced for each Gene Ontology functional annotation. The coverage varies between super-kingdoms, with 19% for eukaryotes, 35% for bacteria and 49% for archaea, and with those of viruses following the coverage values of their hosts. It is shown that the crystallization propensities of proteomes from the taxonomic super kingdoms are distinct. The use of knowledge-based target selection is shown to substantially increase the ability to produce X-ray structures.

Talking to the IUCr Mizianty commented "We believe our method has helped to advance our understanding of the coverage by X-ray structures of proteins and complete proteomes on a global scale."


Story Source:

The above story is based on materials provided by International Union of Crystallography. Note: Materials may be edited for content and length.


Journal Reference:

  1. Marcin J. Mizianty, Xiao Fan, Jing Yan, Eric Chalmers, Christopher Woloschuk, Andrzej Joachimiak, Lukasz Kurgan. Covering complete proteomes with X-ray structures: a current snapshot. Acta Crystallographica Section D Biological Crystallography, 2014; 70 (11): 2781 DOI: 10.1107/S1399004714019427

 

quarta-feira, 29 de outubro de 2014

Identifying the biological clock that governs female fertility

 


Some women can have successful pregnancies at the age of 50, whereas other are unable to get pregnant when they are 30. Researchers are not yet able to fully explain such differences. One factor is that the onset of menopause is influenced by the point at which the uterus runs out of eggs to release.

A recent study at the University of Gothenburg sheds light on the mystery of the biological clock that governs fertility.

Just as newborn infants require nurturance in order to survive, eggs in the uterus need nourishment and support from the granulosa cells of the primary follicle. According to the latest discovery by Professor Kui Liu's research team, a signaling pathway in these cells plays a key role in enabling immature eggs to survive.

Pathways that determine the fate of an egg

The mTOR signaling pathway in the granulosa cells is necessary for activating expression of the kit ligand growth factor, which subsequently binds to the c-kit receptors of eggs and determines their fate.

According to Professor Liu, who is affiliated with the Department of Chemistry and Molecular Biology at the University of Gothenburg, "This mechanism permits the granulosa cells to decide when eggs will begin to grow and when they will die. In that sense, they serve as a kind of biological clock that monitors the onset of menopause."

Researchers believe that the discovery will point the way to interventions that stimulate the growth of eggs that have been unable to mature. Their hope is that increased knowledge about the molecular mechanisms that govern development in human eggs can be applied to clinical treatment of female infertility in the years to come. Professor Liu's team is plunging ahead with that goal in mind.


Story Source:

The above story is based on materials provided by University of Gothenburg. The original article was written by Carina Eliasson. Note: Materials may be edited for content and length.


Journal Reference:

  1. Hua Zhang, Sanjiv Risal, Nagaraju Gorre, Kiran Busayavalasa, Xin Li, Yan Shen, Benedikt Bosbach, Mats Brännström, Kui Liu. Somatic Cells Initiate Primordial Follicle Activation and Govern the Development of Dormant Oocytes in Mice. Current Biology, 2014; DOI: 10.1016/j.cub.2014.09.023

 

segunda-feira, 20 de outubro de 2014

Cellular self-destruct program has deep roots throughout evolution

 


In what seems like a counter-intuitive move against survival, within animals, some cells are fated to die from the triggering of an elaborate cell death program, known as apoptosis. Now, Sakamaki et. al., have honed in on understanding the evolution of caspase-8, a key cell death initiator molecule that was first identified in humans.

By performing the most extensive evolutionary analysis of the Casp8 protein to date, they found that Casp8 activity arose very early (more than 500 MYA), and is universally conserved throughout evolution, demonstrating its functional significance throughout the animal kingdom.

"It is of great significance that the programmed cell death system is established in more simpler animals," said professor Sakamaki.

In addition, they were able to substitute Casp8 proteins from non-mammalian examples and trigger the same cell death pathways when placed into cultured mammalian cell experiments using a killing assay, demonstrating its universal functionality in evolution. They also demonstrate that key protein interactions between Casp8 and another called FADD are also observed across the animal kingdom.

Thus, the cell death toolkit is of core importance to animal evolution, with cell death occurring to eliminate unnecessary, non-functional, unhealthy, or dangerous cells from the body. "In mammals, the cells producing a death ligand and expressing death receptor (and FADD/casp8) are different, suggesting that cell-cell communication is required for this vital phenomenon," said Sakamaki.

 


Story Source:

The above story is based on materials provided by Molecular Biology and Evolution (Oxford University Press). Note: Materials may be edited for content and length.


Journal Reference:

  1. K. Sakamaki, K. Shimizu, H. Iwata, K. Imai, Y. Satou, N. Funayama, M. Nozaki, M. Yajima, O. Nishimura, M. Higuchi, K. Chiba, M. Yoshimoto, H. Kimura, A. Y. Gracey, T. Shimizu, K. Tomii, O. Gotoh, K. Akasaka, T. Sawasaki, D. J. Miller. The Apoptotic Initiator Caspase-8: Its Functional Ubiquity and Genetic Diversity during Animal Evolution. Molecular Biology and Evolution, 2014; DOI: 10.1093/molbev/msu260

domingo, 6 de julho de 2014

Biological signal processing: Body cells -- instrumentalists in a symphony orchestra


Like an isolated note in a symphony orchestra, an isolated signal in the cell is of subordinate importance.

Every organism has one aim: to survive. Its body cells all work in concert to keep it alive. They do so through finely tuned means of communication. Together with cooperation partners from Berlin and Cambridge, scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have now successfully revealed for the first time the laws by which cells translate signals from their surroundings into internal signals. Like an isolated note in a symphony orchestra, an isolated signal in the cell is of subordinate importance. "What is important is the relative variation of intensity and frequency at which the signals are transmitted from the cell membrane into the cell," says Dr. Alexander Skupin, who led the studies at LCSB. The research group published their results now in the scientific journal Science Signaling.

The instruments in an orchestra produce signals -- musical notes -- by causing the air to vibrate. Inside a cell, calcium ions carry signals. When a piece of information from the environment -- say a biological messenger -- meets the outer envelope of the cell, calcium ions are released inside the cell. There, they control various adaptation processes. "At first sight, there is no simple pattern to the ion impulses," Skupin explains; "yet they still culminate in a meaningful response inside the cell, like the activation of a specific gene, for instance."

In order to determine the laws underlying this phenomenon, the researchers studied human kidney cells and rat liver cells using a combination of imaging technologies and mathematical methods. They discovered that the intensity and frequency of calcium impulses undergo extreme variation -- both cell-internally and cell-to-cell. Accordingly, the information they convey cannot be interpreted by analyzing isolated signals alone. "It's like in an orchestra, where studying an isolated note on its own allows no inference of the melody," Skupin continues the musical analogy. "You have to hear how the frequency and volume of all instruments vary and produce the melody. Then you gain an impression of the musical piece."

Now, for the first time, the researchers have managed to gain such an impression of the whole by listening in on the cells' communications. They discovered that the plethora of calcium impulses vary relatively to one another in a specific relationship: A stimulus from outside does not lead to an absolute increase in calcium impulses, but instead to a change in the frequency at which they occur -- in the concert hall, the notes of the instruments rise and fall in symphony. "This pattern is the actual signal that leads to a response in the cells," Skupin says. "With our analyses, we have rendered it interpretable."

"The results are of great importance for analyzing diseases," says Director of LCSB Prof. Dr. Rudi Balling. "We know that, in Parkinson's disease, the calcium balance in the nerve cells is disrupted, and suspect that errant communications between the cells could play a role in the onset of neurodegenerative diseases. With the discovery of the fundamental laws of these communications, as Alexander Skupin, his team and our cooperation partners have now achieved, we are set to take a major step forward in the analysis of Parkinson's disease."


Story Source:

The above story is based on materials provided by University of Luxembourg. Note: Materials may be edited for content and length.


Journal Reference:

  1. K. Thurley, S. C. Tovey, G. Moenke, V. L. Prince, A. Meena, A. P. Thomas, A. Skupin, C. W. Taylor, M. Falcke. Reliable Encoding of Stimulus Intensities Within Random Sequences of Intracellular Ca2 Spikes. Science Signaling, 2014; 7 (331): ra59 DOI: 10.1126/scisignal.2005237

sexta-feira, 4 de julho de 2014

New discovery in living cell signaling

 

"Ras is a family of membrane-anchored proteins whose activation is a critical step in cellular signaling, but almost everything we know about how Ras signals are activated has been derived from bulk assays, in solution or in live cells, in which information about the role of the membrane environment and anything about variation among individual molecules is lost," says Jay Groves, a chemist with Berkeley Lab's Physical Biosciences Division and UC Berkeley's Chemistry Department. "Using a supported-membrane array platform, we were able to perform single molecule studies of Ras activation in a membrane environment and discover a surprising new mechanism though which Ras signaling is activated by Son of Sevenless (SOS) proteins."

Groves, who is also a Howard Hughes Medical Institute (HHMI) investigator, is the corresponding author of a paper in Science that reports this discovery. The paper is titled "Ras activation by SOS: Allosteric regulation by altered fluctuation dynamics." The lead authors were Lars Iversen and Hsiung-Lin Tu, both members of Groves' research group at the time of the study.

The cellular signaling networks of living cells start with receptor proteins residing on a cell's surface that detect and interact with the environment. Signals from these receptors are transmitted to chemical networks within the cell that process the incoming information, make decisions, and direct subsequent cellular activities.

"Although cellular signaling networks perform logical operations like a computer microprocessor, they do not operate in the same way," Groves says. "The individual computational steps in a standard computer are deterministic; the outcome is determined by the inputs. For the chemical reactions that compose a cellular signaling network, however, the molecular level outcomes are defined by probabilities only. This means that the same input can lead to different outcomes."

For cellular signaling networks involving large numbers of protein molecules, the outcome can be directly determined by the process of averaging. Even though the behavior of an individual protein is intrinsically variable, the average behavior from a large group of identical proteins is precisely determined by molecular level probabilities. Ras activation in a living cell, however, involves a relatively small number of SOS molecules, making it impossible to average the variable behavior of the individual molecules. This variation is referred to as stochastic "noise" and has been widely viewed by scientists as an error a cell must overcome.

"Our study showed that, in fact, an important aspect of the SOS signal that activates Ras is encoded in the noise," says Groves. "The protein's dynamic fluctuations between different states of activity transmit information, which means we have found a regulatory coupling in a protein signaling reaction that is entirely based on dynamics, without any trace of the signal being seen in the average behavior."

The Ras Enigma

Ras proteins are essential components of signaling networks that control cellular proliferation, differentiation and survival. Mutations in Ras genes were the first specific genetic alterations linked to human cancers and it is now estimated that nearly a third of all human cancers can be traced to something going wrong with Ras activation. Defective Ras signaling has also been cited as a contributing factor to other diseases, including diabetes and immunological and inflammatory disorders. Despite this long history of recognized association with cancers and other diseases, Ras proteins have been dubbed "un-druggable," largely because their activation mechanism has been poorly understood.

A roadblock to understanding Ras signaling is that the membranes to which Ras proteins are anchored play a major role in their activation through SOS exchange factors. SOS activity in turn was believed to be allosterically regulated through protein and membrane interactions, but this was deduced from cell biological studies rather than direct observations. For a better understanding of how Ras activation by SOS is regulated, scientists need to observe individual SOS molecules interacting with Ras in a membrane environment. However, membrane environments have traditionally presented a stiff experimental challenge.

Groves and his research group overcame this challenge with the development of supported membrane arrays constructed out of lipid layers embedded with fixed patterns of metal nanostructures and assembled onto a silica substrate. The metal structures allow for the controlled spacing of proteins and other cellular molecules placed on the membranes. This makes it possible for the membranes to serve as a platform for assays that can be used to observe in real-time the activity of single molecules.

"In this case, our supported membrane allowed us to corral individual SOS molecules into nanofabricated patches that trapped all the membrane-associated Ras molecules they activated," Groves says. "This in turn allowed us to monitor the individual contribution of every molecule in the ensemble and reveal how the dynamic transitions of individual molecules encoded information that is lost in the average."

What the collaboration discovered is that SOS regulation is based on the dynamics of distinct stochastic fluctuations between different activity states that last approximately 100 seconds but do not show up in ensemble averages. These long-lived fluctuations provide the mechanism of allosteric SOS regulation and Ras activation.

"The allosteric regulation of SOS deduced from cell biological and bulk biochemical studies is conspicuously absent in direct single molecule studies," Groves says. "This means that something that was inferred to exist proved to be missing when we did an experiment that explicitly measured it. The dynamic fluctuations we observed within the system correlated with the expected allosteric regulation, and subsequent theoretical modeling confirmed that such stochastic fluctuations can give rise to known bulk effects."

Understanding the role of stochastic dynamic fluctuations as signaling transduction mechanisms for Ras proteins, could point the way to new and effective therapies for Ras-driven cancers and other cellular disorders. In their Science paper, the collaborators also express their belief that the dynamic fluctuations mechanism they discovered is not unique to Ras proteins but could be applicable to a broad range of other cellular signaling proteins.

"The reason this mechanism has not been reported before is that no previous experiment could have revealed it," Groves says. "All previous experiments on this system -- and most others for that matter -- were based on average behavior. Only single molecule measurements that can look at all the molecules in the system are capable of revealing this type of effect, which we think may prove to be very important in the function of living cell signaling systems."

Other co-authors of the Science paper were Wan-Chen Lin, Rebecca Petit, Scott Hansen, Peter Thill and Christopher Rhodes with UC Berkeley; Jeff Iwig and Jodi Gureasko, HHMI; Sune Christensen and Dimitrios Stamou, University of Copenhagen; Steven Abel, University of Tennessee; Hung-Jen Wu, Texas A&M; Cheng-Han Yu, National University of Singapore; Arup Chakraborty, MIT; and John Kuriyan, who also holds joint appointments with Berkeley Lab, UC Berkeley and HHMI. This study was primarily supported by the National Institutes of Health, and leveraged collaborations with the Mechanobiology Institute in Singapore as part of the Berkeley Educational Alliance for Research in Singapore, and the Singapore CREATE program.

sábado, 21 de junho de 2014

Equations reveal rebellious rhythms at the heart of nature


Illustration of neurons (stock image). "Because oscillations occur in myriads of systems in nature and engineering, these results have broad applicability," said Professor Aneta Stefanovska, of a recent study that uses equations to reveal the hidden complexities of the human body.

Physicists are using equations to reveal the hidden complexities of the human body.

From the beating of our hearts to the proper functioning of our brains, many systems in nature depend on collections of 'oscillators'; perfectly-coordinated, rhythmic systems working together in flux, like the cardiac muscle cells in the heart.

Unless they act together, not much happens. But when they do, powerful changes occur. Cooperation between neurons results in brain waves and cognition, synchronized contractions of cardiac cells cause the whole heart to contract and pump the blood around the body. Lasers would not function without all the atomic oscillators acting in unison. Soldiers even have to break step when they reach a bridge in case oscillations caused by their marching feet cause the bridge to collapse.

But sometimes those oscillations go wrong.

Writing in the journal Nature Communications , scientists at Lancaster University report the possibility of "glassy states" and a "super-relaxation" phenomenon, which might appear in the networks of tiny oscillators within the brain, heart and other oscillating entities.

To uncover these phenomena, they took a new approach to the solution of a set of equations proposed by the Japanese scientist Yoshiki Kuramoto in the 1970s. His theory showed it was possible in principle to predict the properties of a system as a whole from a knowledge of how oscillators interacted with each other on an individual basis.

Therefore, by looking at how the microscopic cardiac muscle cells interact we should be able to deduce whether the heart as a whole organ will contract properly and pump the blood round. Similarly, by looking at how the microscopic neurons in the brain interact, we might be able to understand the origins of whole-brain phenomena like thoughts, or dreams, or amnesia, or epileptic fits.

Physicists Dmytro Iatsenko , Professor Peter McClintock, and Professor Aneta Stefanovska, have reported a far more general solution of the Kuramoto equations than anyone has achieved previously, with some quite unexpected results.

One surprise is that the oscillators can form "glassy" states, where they adjust the tempos of their rhythms but otherwise remain uncoordinated with each other, thus giving birth to some kind of "synchronous disorder" rather like the disordered molecular structure of window glass. Furthermore and even more astonishingly, under certain circumstances the oscillators can behave in a totally independent manner despite being tightly coupled together, the phenomenon the authors call "super-relaxation."

These results raise intriguing questions. For example, what does it mean if the neurons of your brain get into a glassy state?

Dmytro Iatsenko, the PhD student who solved the equations, admitted the results posed more questions than they answered.

"It is not fully clear yet what it might mean if, for example, this happened in the human body, but if the neurons in the brain could get into a "glassy state" there might be some strong connection with states of the mind, or possibly with disease."

Lead scientist Professor Aneta Stefanovska said: "With populations of oscillators, the exact moment when something happens is far more important than the strength of the individual event. This new work reveals exotic changes that can happen to large-scale oscillations as a result of alterations in the relationships between the microscopic oscillators. Because oscillations occur in myriads of systems in nature and engineering, these results have broad applicability."

Professor Peter McClintock said: "The outcome of the work opens doors to many new investigations, and will bring enhanced understanding to several seemingly quite different areas of science."

sábado, 24 de maio de 2014

Cells: RaDAR guides proteins into the nucleus

 

May 22 / 2014

Ludwig Institute for Cancer Research

A novel pathway by which proteins are actively and specifically shuttled into the nucleus of a cell has been discovered by scientists. The finding captures a precise molecular barcode that flags proteins for such import and describes the biochemical interaction that drives this critically important process. The discovery could help illuminate the molecular dysfunction that underpins a broad array of ailments, ranging from autoimmune diseases to cancers.


A Ludwig Cancer Research study has identified a novel pathway by which proteins are actively and specifically shuttled into the nucleus of a cell. Published online today in Cell, the finding captures a precise molecular barcode that flags proteins for such import and describes the biochemical interaction that drives this critically important process. The discovery could help illuminate the molecular dysfunction that underpins a broad array of ailments, ranging from autoimmune diseases to cancers.

Although small proteins can diffuse passively through pores built into the nuclear membrane, most nuclear proteins have to be actively driven into the nucleus through specialized pores to ensure that the cell functions normally. Proteins targeted to specific compartments in cells often carry a sequence of amino acids that, like a barcode, tells components of the cell's transport machinery where they should be located in order to perform their biochemical duties.

"Until now, only one nuclear import pathway for active transport has been extensively characterized," says Xin Lu, Ludwig director at the University of Oxford whose laboratory led the study. "It targets proteins that encode what's known as the nuclear localization signal (NLS). Yet about half of the proteins that get into the nucleus do not bear an NLS, and how they get there has long puzzled researchers. Now we have discovered an alternative signal by which proteins devoid of NLS are tagged for nuclear import." The finding will help scientists better understand the roles many hitherto poorly characterized proteins play in cellular life, and identify many others that work within the nucleus on such tasks as gene regulation and expression.

The researchers were led to their discovery while investigating how an important tumor suppressor protein known as ASPP, which Lu's laboratory has been studying for many years, gets into the nucleus. Their experiments revealed that a widely shared element of protein structure found in ASPP, known as the ankyrin repeat (AR), plays a central role in the protein's nuclear localization.

Lu's team shows in the study that the import signal that flags proteins for the new pathway consists of two consecutive ARs that share one feature: each has a hydrophobic amino acid (one with chemical properties that repel water) that is located 13 amino acids into the repeat. This structural signature, they find, is bound by a small protein named RanGDP. Lu and her colleagues have named this new pathway the RaDAR (RanGDP-Ankyrin Repeat) nuclear import pathway. They have so far identified more than 46 proteins encoded by the human genome that carry this barcode for nuclear delivery.

In decoding this new nuclear import signal, Lu and her team also uncover a possible molecular mechanism underlying human familial melanomas, which are often linked to mutations in a protein known as p16. "We show that the p16 mutation most frequently associated with such cancers," Lu explains, "confers the RaDAR barcode to the protein, resulting in its aberrant accumulation in the nucleus." The RaDAR signature is also associated with a number of regulators of cell proliferation and gene regulation, including the NF-kB family of proteins, which shuttle between the cytoplasm and nucleus, and have been implicated in several human cancers, and autoimmune and inflammatory diseases.

Lu's team is now investigating the spectrum of proteins that use the RaDAR pathway and exploring methods by which the ankyrin repeat that bears that barcode might be exploited to develop entirely novel diagnostics and therapies. That includes incorporating the new nuclear import barcode into synthetic molecules named DARPins to target biologics and other kinds of drugs specifically to the nucleus.


Story Source:

The above story is based on materials provided by Ludwig Institute for Cancer Research. Note: Materials may be edited for content and length.


Journal Reference:

  1. Min Lu, Jaroslav Zak, Shuo Chen, Luis Sanchez-Pulido, David T. Severson, Jane Endicott, Chris P. Ponting, Christopher J. Schofield, Xin Lu. A Code for RanGDP Binding in Ankyrin Repeats Defines a Nuclear Import Pathway. Cell, 2014; 157 (5): 1130 DOI: 10.1016/j.cell.2014.05.006

terça-feira, 15 de abril de 2014

La velocidad de rendimiento cognitivo entra en declive a partir de los 24 años

 

 

El cerebro al desnudo

A los 24 años no solo dejamos de ser adolescentes, sino que según un nuevo estudio de la Universidad Simon Fraser (Canadá), una persona alcanza su punto máximo en términos de desarrollo motor y cognitivo a esta edad. A partir de aquí, comienza a experimentar un declive.

El estudio, publicado en la revista Plos One, trataba de averiguar en qué momento de la vida comenzamos a sufrir una bajada en todo lo relacionado con nuestras habilidades motoras y su relación con el rendimiento cognitivo. Para ello, los investigadores analizaron los registros de rendimiento online de 3.305 jugadores de Starcraft 2 (Blizzard) con edades comprendidas entre los 16 y los 44 años de edad.

Los registros de rendimiento de los jugadores online constituyen una base de datos muy valiosa, ya que representan miles de horas representativas de las estrategias cognitivas en tiempo real. Así, los investigadores pudieron analizar profundamente de qué forma respondieron los jugadores a sus oponentes y qué tiempo emplearon para reaccionar.

El examen del volumen total de datos arrojó que “después de los 24 años, los jugadores muestran una desaceleración en sus reacciones; esta disminución del rendimiento cognitivo estaba presente incluso en los jugadores con más habilidad”, afirma Joe Thompson, autor principal del estudio.

De cualquier forma, los resultados también sugieren que aunque nos volvamos más lentos de respuesta con la edad, la experiencia adquirida con los años nos ayuda a desenvolvernos con más eficiencia y por tanto compensar esta pérdida de velocidad provocada por la edad.

 

La velocidad de rendimiento cognitivo entra en declive a partir de los 24 años 2014-04-15 07-47-07