Get Moving! Walking Helps!

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walking

Get Moving!  Walking Helps!

 

An article published recently by the American Academy of Neurology stresses the benefits of walking for people with PARKINSON’S DISEASE.  Actually, the advice is equally appropriate for people who do not have PARKINSON’S DISEASE!   A small study conducted at the University of Iowa and the Veterans Affairs Medical Center in Iowa City suggested that a brisk walk was a simple, easy way to alleviate some of the symptoms of PARKINSON’S DISEASE.

 

The study observed 60 subjects who walked for 45 minutes three times a week over a period of six months while wearing heart rate monitors.  The biggest changes were clinically significant improvements in motor symptoms and mood and the scores to tests measuring attention and control responses were also considerably improved.  Walkers also reported that they felt less tired and more physically fit overall.

 

Lead author of this study, Dr. Ergun Y. Uc suggests  “People with mild-moderate Parkinson’s who do not have dementia and are able to walk independently without a cane or walker can safely follow he recommended exercise guidelines for health adults, which includes 150 minutes per week of moderate intensity aerobic activity, and experience benefits.”  People without PARKINSON’S DISEASE….take note!!!

E. Y. Uc, K. C. Doerschug, V. Magnotta, J. D. Dawson, T. R. Thomsen, J. N. Kline, M. Rizzo, S. R. Newman, S. Mehta, T. J. Grabowski, J. Bruss, D. R. Blanchette, S. W. Anderson, M. W. Voss, A. F. Kramer, W. G. Darling. Phase I/II randomized trial of aerobic exercise in Parkinson disease in a community settingNeurology, 2014; DOI: 10.1212/WNL.0000000000000644

 

 

Two Studies of the Dynamics of Dopamine in PARKINSON’S DISEASE

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Two Studies of the Dynamics of Dopamine in PARKINSON’S DISEASE

 

Two new studies have been published recently that examine how the neurotransmitter dopamine affects the neurons involved in PARKINSON’S DISEASE. The first study, from the Medical University of Vienna compared brain tissue from deceased human to that of deceased non-Parkinsonian controls to find out why the brain cells of people with PARKINSON’S do not process dopamine effectively.  This study was lead by Oleh Hornykiewicz, M.D. who was one of the early pioneers studying the role of neurotransmitters in the brain.  He was the first to demonstrate the lack of dopamine as a cause of PARKINSON’S DISEASE and also in developing L-dopa for dopamine replacement therapy.

 

The second study comes from the Rollins School of Public Health at Emory University, in Atlanta. Gary W. Miller, Ph.D. is the principal investigator for a large team of researchers involved in this study.  Dr. Miller’s team found a unique way that may help increase the function of dopamine and thereby help people with PARKINSON’S DISEASE.

 

To appreciate the scope of these studies, a basic understanding of neuroscience may help.  Neurons communicate by means of the exchange of neurotransmitters such as dopamine, norepinephrine or serotonin (just to name a few) between their synapses.  These neurotransmitters are constantly being created and then are pumped into storage vesicles to be used in the synapse as needed. A synapse can contain many different neurotransmitter vesicles and can fire them off extremely rapidly.

 

In Dr. Hornykiewicz’s study, they were able to image the dopamine storing vesicles and found that the pumps that load dopamine into those vesicles were not functioning efficiently. Dopamine is constantly being reformed or created at the contact points of the neurons, but if it is not loaded into the vesicles for storage, it can damage the surrounding neurons and actually destroy them.  Dr. Christian Piff, one of the contributing researchers explains “This pump deficiency and the associated reduction in dopamine storage capacity of the Parkinson’s vesicles cold lead to dopamine collection in the nerve cells, developing its toxic effect and destroying nerve cells.”

 

Dr. Miller’s team used a novel mouse model to examine the dynamics of vesicular activities, how the neurotransmitters are loaded into the vesicle, their capacity and their release into the synapse of the neuron.  These mice had a modification that increased the transporter’s ability to pump dopamine into the vesicle.  They found that if the transporter pumping the dopamine into the vesicle was increased to double, then the storage capacity of the vesicle and its release into the synapse was also increased.  The mice in this model showed improvement in their locomotor activity and improvement in anxiety and depressive-like behaviors.  The increase in dopamine release from the vesicle into the synapse also provided protection from toxic effects and reduced cell loss in the substantia nigra.  Dr. White says “Results of this study suggests that enhanced vesicular filling can be enhanced over time and may be a viable therapeutic approach for a variety of central nervous system disorders that involve the storage and release of dopamine, serotonin, or norepinephrine.”

 

 

1.  C. Pifl, A. Rajput, H. Reither, J. Blesa, C. Cavada, J. A. Obeso, A. H. Rajput, O. Hornykiewicz. Is Parkinson’s Disease a Vesicular Dopamine Storage Disorder? Evidence from a Study in Isolated Synaptic Vesicles of Human and Nonhuman Primate Striatum. Journal of Neuroscience, 2014; 34 (24): 8210 DOI: 10.1523/JNEUROSCI.5456-13.2014

 

2.  K. M. Lohr, A. I. Bernstein, K. A. Stout, A. R. Dunn, C. R. Lazo, S. P. Alter, M. Wang, Y. Li, X. Fan, E. J. Hess, H. Yi, L. M. Vecchio, D. S. Goldstein, T. S. Guillot, A. Salahpour, G. W. Miller. Increased vesicular monoamine transporter enhances dopamine release and opposes Parkinson disease-related neurodegeneration in vivo. Proceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1402134111

 

 

Review by Marcia McCall

 

New Technique for Dopamine Cell Replacement in PARKINSON’S DISEASE

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New Technique for Dopamine Cell Replacement in PARKINSON’S DISEASE

 

Love those Italians…. they excel in fashion design and make the best designer shoes!  Now they have taken design to the cellular level and are creating designer drugs for designer receptors on those cells.  They call it DREADD (designer receptor exclusively activated by designer drug.  But this is really serious science.

 

Cell transplantation in PARKINSON’S DISEASE, while in theory, sounds very plausible, in practice has yielded mixed results with the development of serious dyskinesias or even tumors being a major problem. Because it is a particular type of neuronal cell that is affected in PARKINSON’S DISEASE, cell therapy with dopamine producing cells could yield a potential therapeutic treatment.  If dopamine producing cells could be developed, transplanted and become effective and efficient producers of dopamine, the troublesome motor symptoms that plague people with PARKINSON’S could be banished.

 

Embryonic stem cells or induced pluripotent stem cells have been developed from both mouse and human cells and have been somewhat effective in alleviating motor symptoms when transplanted into animal models of PARKINSON’S DISEASE.  But if the differentiation from stem cell to dopamine producing cell is not well controlled, tumors can develop.  Cells developed from human fibroblasts can be induced to become neurons, but are more difficult to produce, with more opportunity for potential error.  Much stem cell technology exists only in petri dishes, and the degree to which these reprogrammed cells would be functional or stable when transplanted into living models is not yet known. For modified cells to be transplanted and become effective a system needs to be developed that will allow the transplanted cells to be monitored and modulated to serve the physiological environment into which they are introduced.

 

Previous studies have shown that only dopamine neurons from the mid brain region were successful in reversing motor function in lesioned rats.  This team developed an induced dopaminergic neuron (iDA) from fibroblast, so the challenge was to see if it could be as effective as mid brain dopamine neurons.  The grafted iDA neurons did improve the motor function of the animals, but not as well as native embryonic DA neurons.  Stereological cell counting showed that there were as many surviving iDA cells as there were native DA cells and this lead to the idea that iDA neurons were less functional intrinsically. The team believes that an improved method for generating better quality induced pluripotent stem cells from the fibroblasts will result in more uniformly expressing iDA neurons.

 

To measure the integration of the iDA neurons into the host environment, they used the DREADD technology.  This technology allows the addition of a uniquely designed receptor that permits a specific interaction with a pharmacological drug to manipulate the activity of the re-programmed neuron.  It thus enforces a sort of “remote control” over the transplanted neuron to enhance its effects in living animals. This method may offer a better approach to cell replacement therapy by combining an external, pharmacological agent with the transplanted re-programmed neurons to respond to the physiological needs and requirements of the recipient.

This research study was done by a large team of researchers under the direction of Vania Broccoli, Ph.D. who is a developmental neurologist at the Hospital San Rafaele in Milan, Italy.  It will be published in the Journal of Clinical Investigation on July 1, 2013.

 

Broccoli, V. et al; Remote control of induced dopaminergic neurons in parkinsonian rats; J Clin Invest. 2014;124(7):3215-3229. doi:10.1172/JCI74664

 

 

Review by Marcia McCall

Picture Credits

http://www.stemcell.ucsb.edu/compliance/

Improvement Seen in First Clinical Trial of Magnetic Stimulation for PARKINSON’S DISEASE

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Improvement Seen in First Clinical Trial of Magnetic Stimulation for PARKINSON’S DISEASE

 

A double blind, randomized trial tested two targets of magnetic stimulation as well as a sham stimulation on 60 subjects that had moderate PARKINSON’S DISEASE.  They received their usual Parkinson’s medications in addition to the stimulation. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive treatment that researchers hope will augment pharmaceutical treatments for PARKINSON’S DISEASE.  This trial has safety and efficacy as its primary outcome measures as well as improving clinical results when the subjects were off their drugs. While other studies have reported mixed results from transcranial magnetic stimulation, this trial used a larger, unique coil with the ability to generate a larger field of stimulation that penetrated deeper into the brain.

 

Principal investigator of this trial was Mario FIchera, M.D. from the Institute of Experimental Neurology at the Scientific Institute Hospital San Raffaele in Milan, Italy who presented his findings at the 24th Meeting of the European Neurological Society on June 1, 2014. He stated that compared to the group receiving sham stimulation, both groups that received targeted stimulation improved significantly, with no serious adverse events.  In addition to reported improvements as measured by the Unified Parkinson’s Disease Rating Scale (UPDRS) part III, subjects reported they experienced a better quality of life, but he cautioned that a further trial should be done to “validate the efficacy seen in this trial and to gauge the duration of the effects.”

 

Transcranial Magnetic Stimulation is a relatively new technique that changes neuronal function by using an electromagnetic field generated by a coil.  Electricity passes in opposite directions through the shape of the coil and where the current crosses it generates an electrical field, whose intensity can be modified by regulating the amount of electrical current.  Pulses can be applied singly or repetitively and at varying intensities.  The strength and frequency of the pulses can determine excitability or inhibition of the target neurons. The coil is placed against the scalp and the magnetic field passes through the skull to change the electrical field of the underlying neurons.  In this study TMS was applied in repetitive pulses, timed milliseconds apart.  TMS treatment is usually done several times a week for several weeks.

 

In this study, all groups of subjects received treatment three times a week for four weeks. One group received treatment on the motor cortex region, contralateral to their affected side, and also to the prefrontal cortex.  Group two received treatment to the motor cortex region, but sham treatment on the prefrontal cortex.  Group three received sham treatments on both treatment sites. Both groups that received actual treatment showed reductions in the motor symptoms and tremors compared to the sham group.

 

Dr. Josep Valis-Solis, a neurologist and neurophysiologist at the Hospital Clinic in Barcelona, Spain said “I think that we have to promote a bit this kind of treatment that is noninvasive and nonpharmacological, so some hope that we are escaping from toxicity from drugs.”  It is still early and there needs to be more investigation into the types and differences of effects from different coils.  Cost and availability of the equipment and training and availability of personnel to administer treatment is another issue that needs to be studied together with the rate of retreatment necessary to maintain a positive effect over an as yet unknown, period of time.

 

Magnetic Stimulation Improves Parkinson’s Symptoms, Medscape Jun 17, 2014

 

 

Review by Marcia McCall.

Picture Credits

http://www.magventure.com/en-gb/products/stimulators/magprocompact.aspx

New PARKINSON’S Gene Discovery Could Lead to New Treatment

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New PARKINSON’S Gene Discovery Could Lead to New Treatment

 

The new molecular sciences continue to delve deeper into the mysteries of the cellular actions and interactions to unlock the keys to PARKINSON’S DISEASE.  A team of genetic researchers at the University of California at Los Angeles headed by Dr. Ming Guo has found one more clue, a gene that mediates the interactions of two mutated genes and helps cells maintain their health to prevent neurodegeneration.

 

The genes PINK1and Parkin play important roles in protecting the energy producing mitochondria of cells.  When these genes are mutated, they do not operate correctly and allow for accumulations of unhealthy cells with damaged mitochondria that leads to the early on-set of PARKINSON’S DISEASE.  Working in fruit flies and mouse models of disease, Guo and her team found that a gene called MUL-1 mediated the interaction of PINK-1 and Parkin and contributed to the health of the mitochondria. When MUL-1 was removed from the interaction with PINK-1 and Parkin in the neurons in the mouse model, they found it caused deterioration of the mitochondria, but when an extra amount of MUL-1 was added, the mitochondrial damage was repaired.

 

The discovery of this new genetic interaction is exciting, showing a new mechanism for improving the function of mitochondria and maintaining the health of the cell, but also because it may lead to the development of a drug that could enhance its presence and prevent neurodegeneration.  Such a new drug would be of immense benefit to people with PARKINSON’S DISEASE.

 

Further studies will test these findings in more complex biological organisms and will help to find more cellular interactions related to MUL-1.  Testing for drugs that will enhance MUL-1  and become a basis for treatment is another a priority.  The team will also be looking for mutations of the MUL-1 gene and to understand its heritability to see if it exists in all PARKINSON’S patients or if it is found only in the inherited forms of PARKINSON’S.

 

J. Yun, R. Puri, H. Yang, M. A. Lizzio, C. Wu, Z.-H. Sheng, M. Guo. MUL1 acts in parallel to the PINK1/parkin pathway in regulating mitofusin and compensates for loss of PINK1/parkineLife, 2014; 3 (0): e01958 DOI:10.7554/eLife.01958

 

Review by Marcia McCall

Picture Credits

http://cssb2.biology.gatech.edu/kinomelhm/kinases/PINK1_Hsap.html

Hopeful New Drug Therapy Being Developed at University of Alabama

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Hopeful New Drug Therapy Being Developed at University of Alabama

 

Alpha-synuclein is one of the most prevalent proteins found in human brains.  It is also the one that when it fails to conform to its normal configuration, or mis-folds, contributes to the neurodegeneration seen in PARKINSON’S DISEASE.  Researchers at the University of Alabama led by Andrew West, Ph.D. think they may have found a key to prevent alpha-synuclein from misfolding and aggregating.

 

The gene LRRK2 has been linked to PARKINSON’S DISEASE and West’s lab demonstrated that the known mutations of this gene all increase its activity.  Other studies have shown that it is related to alpha-synuclein in several ways.  This study has shown that blocking the expression of LRRK2 in mouse models that are genetically very similar to human models, blocked the over-expression of alpha-synuclein.  Blocking alpha-synuclein may prevent the death of dopamine producing cells in the substantia nigra, thus offering a potential treatment to prevent or slow the progress of PARKINSON’S DISEASE.  The search for a drug to inhibit the expression of LRRK2 is now underway.

 

LRRK2 is known to be significantly involved in the genetic forms of PARKINSONS, in populations of Ashkenazy Jews from Eastern Europe and from Mediterranean ethnic populations such as the Berbers of North Africa, but is not as highly involved in non inherited forms of the disease.   Still, West’s team thinks LRRK2 has more than one method of action as seen in the genetic forms.  It may interact with alpha-synuclein in other ways.

 

He asks, “What would happen if you simply remove all LRRK2 activity?  Modern approaches allow us to approximate what a perfect drug would do in rats and mice.  We think LRRK2 is plugging into PARKINSON’S DISEASE in more than one way.  It is making the disease more likely to happen and making it progress faster when it does happen.  So we think knocking out LRRK2 will do the opposite–slow the disease or make it much less likely to develop.”

 

Simply slowing the progress of the disease would be a major break through.  It could extend the length of time that levodopa effectively alleviates the symptoms and could even reduce or eliminate some of the side effects that can sometimes be worse than the disease.

 

Southern Research Institute is pharmaceutical research company partnering with Dr. West’s lab to develop a drug to inhibit LRRK2.  They hope to be able to test it in humans early next year.

 

J. P. L. Daher, L. A. Volpicelli-Daley, J. P. Blackburn, M. S. Moehle, A. B. West.Abrogation of  -synuclein-mediated dopaminergic neurodegeneration in LRRK2-deficient ratsProceedings of the National Academy of Sciences, 2014; DOI: 10.1073/pnas.1403215111

 

Review by Marcia McCall

 

Picture Credit

http://cssb2.biology.gatech.edu/kinomelhm/kinases/LRRK2_Hsap.html

Early Diagnosis of PARKINSON’S DISEASE by a New MRI Process

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fmri scan

 

Early Diagnosis of PARKINSON’S DISEASE by a New MRI Process

 

Early detection of PARKINSON’S DISEASE, before the symptoms become obvious, will lead to early interventions to slow the disease process and improve the lives of people at risk for this disease.  While there still is no cure for this disease, it has not been possible to even make a positive diagnosis until after symptoms have already appeared.  By then, some estimates indicate that over 75% of the dopamine producing neurons in the patients’ brains have been destroyed.  Medications do offer symptomatic relief of some of the symptoms, but early treatment could limit the damage to dopamine producing neurons and dramatically improve the quality of life for people with PARKINSON’S DISEASE.

 

A research team at Oxford University in the United Kingdom has used a new simple MRI scanning technique that has predicted PARKINSON’S DISEASE with very high accuracy.  Standard MRI techniques are not sufficient to detect early changes in the brain that would signal development of the disease.  Dr. Clare Mackay found an approach that allowed the team to study the connectivity strength of brain networks in the basal ganglia.  Using his technique for resting state functional MRI (fMRI) the researchers compared the connectivity levels of 19 subjects with early stage PARKINSON’S DISEASE and 19 healthy control subjects.  With 100% accuracy, they found a much lower level of connectivity in the brains of the subjects with PARKINSON’S DISEASE; it also picked up a small percentage of healthy people. So they repeated the study on a second group of subjects and the results were almost the same, sufficient to validate the results of the first study.

 

The technique is non-invasive; subjects are simply required to lie still in the scanner. Researchers hope that this new technique will become part of clinical practice and have the ability to allow physicians to predict which of their patients is at risk of developing PARKINSON’S DISEASE before any symptoms arise.  The study was done with subjects known to be in the early stages, so more research will be done to refine the technique to be sensitive enough to predict risk for non-symptomatic subjects.  Early detection combined with other new research discoveries may hold the key to better and earlier treatment, making life with PARKINSON’S DISEASE much easier.

 

Clare Mackay et al. Functional connectivity in the basal ganglia network differentiates PD patients from controlsNeurology, June 2014 DOI:10.1212/WNL.0000000000000592

 

Review by Marcia McCall

Picture Credits

http://www.vanderbilt.edu/exploration/text/index.php?action=view_section&id=1481&story_id=365&images=

Scientists Make Diseased Cells Synthesize Their Own Drug

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Scientists Make Diseased Cells Synthesize Their Own Drug

By Eric Sauter

In a new study that could ultimately lead to many new medicines, scientists from the Florida campus of The Scripps Research Institute (TSRI) have adapted a chemical approach to turn diseased cells into unique manufacturing sites for molecules that can treat a form of muscular dystrophy.

“We’re using a cell as a reaction vessel and a disease-causing defect as a catalyst to synthesize a treatment in a diseased cell,” said TSRI Professor Matthew Disney“Because the treatment is synthesized only in diseased cells, the compounds could provide highly specific therapeutics that only act when a disease is present. This means we can potentially treat a host of conditions in a very selective and precise manner in totally unprecedented ways.”

The promising research was published recently in the international chemistry journal Angewandte Chemie.

Targeting RNA Repeats

In general, small, low molecular weight compounds can pass the blood-brain barrier, while larger, higher weight compounds tend to be more potent. In the new study, however, small molecules became powerful inhibitors when they bound to targets in cells expressing an RNA defect, such as those found in myotonic dystrophy.

Myotonic dystrophy type 2, a relatively mild and uncommon form of the progressive muscle weakening disease, is caused by a type of RNA defect known as a “tetranucleotide repeat,” in which a series of four nucleotides is repeated more times than normal in an individual’s genetic code. In this case, a cytosine-cytosine-uracil-guanine (CCUG) repeat binds to the protein MBNL1, rendering it inactive and resulting in RNA splicing abnormalities that, in turn, results in the disease.

In the study, a pair of small molecule “modules” the scientists developed binds to adjacent parts of the defect in a living cell, bringing these groups close together. Under these conditions, the adjacent parts reach out to one another and, as Disney describes it, permanently hold hands. Once that connection is made, the small molecule binds tightly to the defect, potently reversing disease defects on a molecular level.

“When these compounds assemble in the cell, they are 1,000 times more potent than the small molecule itself and 100 times more potent than our most active lead compound,” said Research Associate Suzanne Rzuczek, the first author of the study. “This is the first time this has been validated in live cells.”

Click Chemistry Construction

The basic process used by Disney and his colleagues is known as “click chemistry”—a process invented by Nobel laureate K. Barry Sharpless, a chemist at TSRI, to quickly produce substances by attaching small units or modules together in much the same way this occurs naturally.

“In my opinion, this is one unique and a nearly ideal application of the process Sharpless and his colleagues first developed,” Disney said.

Given the predictability of the process and the nearly endless combinations, translating such an approach to cellular systems could be enormously productive, Disney said. RNAs make ideal targets because they are modular, just like the compounds for which they provide a molecular template.

Not only that, he added, but many similar RNAs cause a host of incurable diseases such as ALS (Lou Gehrig’s Disease), Huntington’s disease and more than 20 others for which there are no known cures, making this approach a potential route to develop lead therapeutics to this large class of debilitating diseases.

In addition to Rzuczek and Disney, the other author of the study, “A Toxic RNA Catalyzes the In Cellulo Synthesis of Its Own Inhibitor,” is HaJeung Park of TSRI. For more information on the study, seehttp://onlinelibrary.wiley.com/doi/10.1002/anie.201406465/abstract

The work was supported by the Muscular Dystrophy Foundation, the Myotonic Dystrophy Foundation and the State of Florida.

Article Link: http://www.scripps.edu/newsandviews/e_20140908/disney.html

Do Microbes Rule Your Brain?

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Do Microbes Rule Your Brain on Food Choices?

People no longer have to blame their food cravings — and giving in to them — on poor self-control.

Now scientists are arguing that microbes living in the gut are responsible for manipulating eating behavior by causing cravings for food they favor for fitness or that suppress their competition. Alternatively, microbiota in the gut may send out signals via the vagus nerve to the brain to induce dysphoria and goad people into eating what the microbe needs whether it’s good for the host or not, a diverse group of researchers are suggesting.

“Bacteria within the gut are manipulative,” Carlo Maley, PhD, director, Center for Evolution and Cancer, University of California at San Francisco, states in a press release. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals and others not.”

In their overview of eating behavior and the microbiome published online August 7, 2014 in BioEssays, Joe Alcock, MD, University of New Mexico, Albuquerque, and colleagues argue that certain microbes are highly dependent on the nutrient composition of the diet.

For example, Prevotella grows best on carbohydrates while dietary fiber provides a competitive advantage to Bifidobacteria. “Even microbes with a generalist strategy tend to do better on some combinations of nutrients than others,” the authors write, “and competition will determine which microbes survive.”

Microbes can manipulate host behavior in a variety of ways, but one way may be by “hijacking” the host’s nervous system. As the authors point out, evidence shows that microbes can have dramatic effects on behavior through the microbiome-gut-brain axis.

“The vagus nerve is a central actor in this communication axis, connecting the 100 million neurons in the enteric nervous system in the gut to the base of the brain at the medulla,” they explain. And, they add, enteric nerves have receptors that react to the presence of particular bacteria as well as to bacterial metabolites. Research has also shown that blockade or transection of the vagus nerve causes drastic weight loss while stimulation of its activity through norepinephrine appears to drive excessive eating behavior in satiated rats.

Other pathways through which microbes may influence host eating behavior is through secretion of hormones involved in mood and behavior, including dopamine and serotonin. Microbes may also manipulate eating behavior by altering receptor expression. Changes in taste receptor expression and activity have been reported following gastric bypass surgery, a procedure that changes gut microbiota and alters satiety and food preference, as the authors point out.

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad and releasing chemical rewards to make us feel good,” coauthor Athena Aktipis, PhD, Arizona State University, Phoenix, states in a press release.

“Together, these results suggest that microbes have opportunities to manipulate vagus nerve traffic in order to control host eating. Exerting self-control over eating choices may be partly a matter of suppressing microbial signals that originate in the gut.”

Happily, researcher add, the use of prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes can rapidly alter the microbiome within 24 hours of administration.

The study was funded by the National Institutes of Health, the American Cancer Society, the Bonnie D. Addario Lung Cancer Foundation, and the Institute for Advanced study in Berlin, Germany. The authors have disclosed no relevant financial relationships.

BioEssays. Published online August 7, 2014. Abstract

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