Gut Bacteria Linked to Age Related Conditions
A new study shows for the first time that gut bacteria from old mice induce age-related chronic inflammation when transplanted into young mice. Called “inflammaging,” this low-grade chronic inflammation is linked to life-limiting conditions such as stroke, dementia and cardiovasuclar disease. The research, published today in open-access journal Frontiers in Immunology, brings the hope of a potentially simple strategy to contribute to healthy ageing, as the composition of bacteria in the gut is, at least in part, controlled by diet.
“Since inflammaging is thought to contribute to many diseases associated with ageing, and we now find that the gut microbiota plays a role in this process, strategies that alter the gut microbiota composition in the elderly could reduce inflammaging and promote healthy ageing,” explains Dr Floris Fransen, who performed the research at the University Medical Center Groningen, The Netherlands. “Strategies that are known to alter gut microbiota composition include changes in diet, probiotics, and prebiotics.”
Previous research shows that the elderly tend to have a different composition of gut bacteria than younger people.
Immune responses also tend to be compromised in the elderly, resulting in inflammaging.
Knowing this, Fransen and his team set out to investigate a potential link.
The scientists transferred gut microbiota from old and young conventional mice to young germ-free mice, and analysed immune responses in their spleen, lymph nodes and tissues in the small intestine. They also analysed whole-genome gene expression in the small intestine.
All results showed an immune response to bacteria transferred from the old mice but not from the young mice.
The results suggest that an imbalance of the bacterial composition in the gut may be the cause of inflammaging in the elderly. Imbalances, or “dysbiosis” of gut bacteria results in “bad” bacteria being more dominant than “good” bacteria. An overgrowth of bad bacteria can make the lining of the gut become more permeable, allowing toxins to enter the bloodstream where they can travel around the body with various negative effects.
Dysbiosis can have serious health implications: several disorders, such as inflammatory bowel disease, obesity, diabetes, cancer, anxiety and autism are already linked to the condition.
“Our gut is inhabited by a huge number of bacteria” explains Fransen. “Moreover, there are many different kinds of bacterial species, and the bacterial species that are present can vary a lot from person to person.”
Maintaining a healthy gut microbiota is clearly important to a healthy body and healthy ageing, but why the gut microbiota is different in the elderly is not fully understood. Many people are aware of the effect a course of antibiotics can have on the digestive system for example, but as Fransen explains, it may not be down to just one thing: “It is likely a combination of factors such as reduced physical activity, changes in diet, but also as part of a natural process.”
Most, if not all, age-related diseases can be linked back to inflammaging. Despite the fact that this particular study was conducted on mice, it is clear that maintaining a healthy gut microbiota is key to a healthy lifestyle. However, more research is needed to confirm that the human body mirrors the mice in this study.
“Both in humans and mice there is a correlation between altered gut microbiota composition and inflammaging, but the link between the two remains to be proven in humans” concludes Fransen.
The article is part of the Frontiers Research Topic Immunomodulatory Functions of Nutritional Ingredients in Health and Disease.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Frontiers
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Frontiers “Gut Bacteria Linked to Age Related Conditions.” NeuroscienceNews. NeuroscienceNews, 5 November 2017.
<http://neurosciencenews.com/microbiome-aging-inflammation-7878/>.
<http://neurosciencenews.com/microbiome-aging-inflammation-7878/>.
Abstract
Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice
Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study, gut microbiota from young or old conventional mice was transferred to young germ-free (GF) mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized GF mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here, we show by transferring aged microbiota to young GF mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the GF mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young GF mice.
“Aged Gut Microbiota Contributes to Systemical Inflammaging after Transfer to Germ-Free Mice” by Floris Fransen, Adriaan A. van Beek, Theo Borghuis, Sahar El Aidy, Floor Hugenholtz, Christa van der Gaast – de Jongh, Huub F. J. Savelkoul, Marien I. De Jonge, Mark V. Boekschoten, Hauke Smidt, Marijke M. Faas, and Paul de Vos in Frontiers in Immunology. Published online November 2 2017 doi:10.3389/fimmu.2017.01385
Bursts of Beta Waves, Not Sustained Rhythms, Filter Sensory Processing in Brain
What does this mean? When we are busy focusing or doing some focused task, we cannot feel some other sensation including pain. So I experimented on childbirth pain issue by focusing on the baby coming out of the birth canal and when my focus is off, I can feel more pain.
Connie
Bursts of Beta Waves, Not Sustained Rhythms, Filter Sensory Processing in Brain
Summary: In both human and animal subject, bursts of beta wave activity in the brain help to filter distraction in order to process different sensations, a new study reports.
Source: Brown University.
To better understand the brain and to develop potential therapies, neuroscientists have been investigating how “beta” frequency brainwaves help the brain filter distractions to process sensations. A new Brown University study stands to substantially refine what they thought was going on: What really matters is not a sustained elevation in beta wave power, but instead the rate of specific bursts of beta wave activity, ideally with perfect timing.
The new insight, reported in the journal eLife, arose from the scientists looking beneath the covers of the typical practice of averaging beta brain wave data. With a closer examination, trial-by-trial for each subject, they saw that what really reflected attention and impacted perception were discrete, powerful bursts of beta waves at frequencies around 20 hertz.
“When people were trying to block distraction in a brain area, the probability of seeing these beta events went up,” said senior author Stephanie R. Jones, an associate professor of neuroscience at Brown. “The brain seemed to be flexibly modulating the expression of these beta events for optimal perception.”
The findings, made with consistency in humans and mice, can not only refine ongoing research into how beta waves arise and work in the brain, Jones said, but also provide guidance to clinicians as they develop therapies that seek to modulate beta waves.
Testing touch
The research team, led by graduate student Hyeyoung Shin, acquired the data through a series of experiments in which they measured beta waves in the somatosensory neocortex of humans and mice in the second leading up to inducing (or not inducing) varying amounts of a tactile sensation. Humans wore a cap of magnetoencephalography sensors, while mice had implanted electrodes. For people, the sensation was a tap on a finger tip or the foot. For mice, it was a wiggle of a whisker.
Subjects were merely required to report the sensations they felt — people pushed a button, while mice were trained to lick a sensor in exchange for a reward. The researchers tracked the association of beta power with whether subjects accurately detected, or didn’t detect, stimuli. What they found, as expected, is that the more beta activity there was in the corresponding region of cortex, the less likely subjects were to report feeling a sensation. Elevated beta activity is known to help suppress distractions.
A particularly good example, Shin said, was that in experiments where people were first instructed to focus on their foot, there was more beta power in the hand region of the neocortex. Correspondingly, more beta in the hand region resulted in less detection of a sensation in the hand.
“We think that beta acts a filter mechanism,” Shin said.
Beta bursts
Consistently throughout various iterations of the experiments across both the human and mouse subjects, increases in beta activity did not manifest as a continuously elevated rhythm. Instead, when beta appeared, it quickly spiked in short, distinct bursts of power. Only if a subject’s beta was averaged over many trials would it look like a smooth plateau of high-power activity.
After discovering this pattern, the researchers performed analyses to determine what features of the bursts best predicted whether subjects would report, or miss, a touch sensation. After all, it could be the number of bursts, their power, or maybe how long they lasted.
What Shin and the team found is that number of bursts and their timing both mattered independently. If there were two or more bursts any time in the second before a sensation, it was significantly more likely to go undetected. Alternatively, if just one burst hit within 200 milliseconds of the sensation, the stimulus would also be more likely to be overlooked.
“The ideal case was having large numbers and being close in timing to the stimulus,” Shin said.
A better idea of beta
While the study helps to characterize the nature of beta in the somatosensory neocortex, it doesn’t explain how it affects sensations, Jones acknowledged. But that’s why it is important that the results were in lockstep in both mice and in people. Confirming that mice model the human experience means researchers can rely on mice in experiments that delve more deeply into how beta bursts arise and what their consequence are in neurons and circuits. Shin is already doing experiments to dissect how distinct neural subpopulations contribute to beta bursts and somatosensory detection, respectively. Co-author and postdoctoral researcher Robert Law is applying computational neural models that link the human and animal recordings for further discovery.
In the clinical realm, Jones said, an improved understanding of how beta works could translate directly into improving therapies such as transcranial magnetic stimulation or transcranial alternating current to treat neurological disorders, such as chronic pain, or depression. Rather than using those technologies to generate a consistent elevation in beta in a brain region, Jones said, it might be more effective to use them to induce (or suppress) shorter, more powerful bursts and to time those to be as close in time to a target brain activity as possible.
“Typically with non-invasive brain stimulation you are trying to entrain a rhythm,” Jones said. “What our results suggest is that’s not what the brain is doing. The brain is doing this intermittent pattern of activity.”
The findings could also help scientists better understand other beta-associated disorders, such as Parkinson’s disease or obsessive compulsive disorder, and influence brain computer interfaces that rely on beta activity.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
The paper’s other authors are Shawn Tsutsui and Christopher Moore.
Funding for the research came from the National Institutes of Health, the U.S. Department of Veterans Affairs, the National Science Foundation, the Brown Institute for Brain Science and the Fulbright Association.
Source: David Orenstein – Brown University
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Shin et. al./Brown University.
Original Research:Abstract for “The rate of transient beta frequency events predicts behavior across tasks and species” by Hyeyoung Shin, Robert Law, Shawn Tsutsui, Christopher I Moore, and Stephanie R Jones in eLife. Published online November 6 2017 doi:10.7554/eLife.29086
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Brown University “Bursts of Beta Waves, Not Sustained Rhythms, Filter Sensory Processing in Brain.” NeuroscienceNews. NeuroscienceNews, 8 November 2017.
<http://neurosciencenews.com/beta-waves-sensory-processing-7896/>.
<http://neurosciencenews.com/beta-waves-sensory-processing-7896/>.
Abstract
The rate of transient beta frequency events predicts behavior across tasks and species
Beta oscillations (15-29Hz) are among the most prominent signatures of brain activity. Beta power is predictive of healthy and abnormal behaviors, including perception, attention and motor action. In non-averaged signals, beta can emerge as transient high-power ‘events’. As such, functionally relevant differences in averaged power across time and trials can reflect changes in event number, power, duration, and / or frequency span. We show that functionally relevant differences in averaged beta power in primary somatosensory neocortex reflect a difference in the number of high-power beta events per trial, i.e. event rate.
Further, beta events occurring close to the stimulus were more likely to impair perception. These results are consistent across detection and attention tasks in human magnetoencephalography, and in local field potentials from mice performing a detection task. These results imply that an increased propensity of beta events predicts the failure to effectively transmit information through specific neocortical representations.
“The rate of transient beta frequency events predicts behavior across tasks and species” by Hyeyoung Shin, Robert Law, Shawn Tsutsui, Christopher I Moore, and Stephanie R Jones in eLife. Published online November 6 2017 doi:10.7554/eLife.29086
Beta Waves Function
Low amplitude beta waves with multiple and varying frequencies are often associated with active, busy or anxious thinking and active concentration.
Over the motor cortex beta waves are associated with the muscle contractions that happen in isotonic movements and are suppressed prior to and during movement changes.
Bursts of beta activity are associated with a strengthening of sensory feedback in static motor control and reduced when there is movement change.
Beta activity is increased when movement has to be resisted or voluntarily suppressed.
The artificial induction of increased beta waves over the motor cortex by a form of electrical stimulation called Transcranial alternating-current stimulation consistent with its link to isotonic contraction produces a slowing of motor movements.
Relationship with GABA
Diffuse beta waves present alongside other frequencies in spontaneous EEG recorded from a 28-month-old child with Dup15q syndrome.
Beta waves are often considered indicative of inhibitory cortical transmission mediated by gamma aminobutyric acid (GABA), the principal inhibitory neurotransmitter of the mammalian nervous system. Benzodiazepines, drugs that modulate GABAA receptors, induce beta waves in EEG recordings from humans [8] and rats.[9] Spontaneous beta waves are also observed diffusely in scalp EEG recordings from children with duplication 15q11.2-q13.1 syndrome (Dup15q) who have duplications of GABAA receptor subunit genes GABRA5, GABRB3, and GABRG3.[10] For this reason, it is possible that, in certain clinical contexts, beta waves could be a general biomarker of GABAA receptor gene overexpression or otherwise aberrant GABAergic transmission.
Rangaswamy M, Porjesz B, Chorlian DB, Wang K, Jones KA, Bauer LO, Rohrbaugh J, O’Connor SJ, Kuperman S, Reich T, Begleiter (2002). “Beta power in the EEG of alcoholics”. BIOLOGICAL PSYCHOLOGY. 52 (8): 831–842. doi:10.1016/s0006-3223(02)01362-8. PMID 12372655.
Jump up ^ Buzsáki, György (2006). Rhythms of the Brain. New York: Oxford University Press. p. 4.
Jump up ^ Baumeister J, Barthel T, Geiss KR, Weiss M (2008). “Influence of phosphatidylserine on cognitive performance and cortical activity after induced stress”. NUTRITIONAL NEUROSCIENCE. 11 (3): 103–110. doi:10.1179/147683008X301478. PMID 18616866.
Jump up ^ Baker, SN (2007). “Oscillatory interactions between sensorimotor cortex and the periphery”. Current Opinion in Neurobiology. 17 (6): 649–55. doi:10.1016/j.conb.2008.01.007. PMC 2428102 Freely accessible. PMID 18339546.
Jump up ^ Lalo, E; Gilbertson, T; Doyle, L; Di Lazzaro, V; Cioni, B; Brown, P (2007). “Phasic increases in cortical beta activity are associated with alterations in sensory processing in the human”. Experimental brain research. Experimentelle Hirnforschung. Experimentation cerebrale. 177 (1): 137–45. doi:10.1007/s00221-006-0655-8. PMID 16972074.
Jump up ^ Zhang, Y; Chen, Y; Bressler, SL; Ding, M (2008). “Response preparation and inhibition: the role of the cortical sensorimotor beta rhythm”. Neuroscience. 156 (1): 238–46. doi:10.1016/j.neuroscience.2008.06.061. PMC 2684699 Freely accessible. PMID 18674598.
Jump up ^ Pogosyan, A; Gaynor, LD; Eusebio, A; Brown, P (2009). “Boosting cortical activity at Beta-band frequencies slows movement in humans”. Current Biology. 19 (19): 1637–41. doi:10.1016/j.cub.2009.07.074. PMC 2791174 Freely accessible. PMID 19800236.
Jump up ^ Feshchenko, V; Veselis, R; Reinsel, R (1997). “Comparison of the EEG effects of midazolam, thiopental, and propofol: the role of underlying oscillatory systems”. Neuropsychobiology. PMID 9246224.
Jump up ^ Van Lier, Hester; Drinkenburg, Wilhelmus; Van Eeten, Yvonne; Coenen, Anton (2004). “Effects of diazepam and zolpidem on EEG beta frequencies are behavior-specific in rats”. Neuropharmacology. Retrieved 4 January 2017.
Jump up ^ Frohlich, Joel; Senturk, Damla; Saravanapandian, Vidya; Golshani, Peyman; Reiter, Lawrence; Sankar, Raman; Thibert, Ronald; DiStefano, Charlotte; Huberty, Scott; Cook, Edwin; Jeste, Shafali (December 2016). “A Quantitative Electrophysiological Biomarker of Duplication 15q11.2-q13.1 Syndrome” (PDF). PLOS One. Retrieved 4 January 2017.
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| One Virus and Two Types of Bacteria as Major Causes of Alzheimer’s |
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One Virus and Two Types of Bacteria as Major Causes of Alzheimer’s
A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria – are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.
This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.
Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.
Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.
“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.
Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said “The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”
The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.
ABOUT THIS ALZHEIMER’S DISEASE RESEARCH
Source: University of Manchester
Image Credit: The image is adapted from the University of Manchester press release.
Original Research: Full open access editorial for “Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152
Abstract
Microbes and Alzheimer’s Disease
We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain, notably herpes simplex virus type 1 (HSV1), Chlamydia pneumoniae, and several types of spirochaete, in the etiology of AD. Fungal infection of AD brain [5, 6] has also been described, as well as abnormal microbiota in AD patient blood. The first observations of HSV1 in AD brain were reported almost three decades ago]. The ever-increasing number of these studies (now about 100 on HSV1 alone) warrants re-evaluation of the infection and AD concept.
AD is associated with neuronal loss and progressive synaptic dysfunction, accompanied by the deposition of amyloid-β (Aβ) peptide, a cleavage product of the amyloid-β protein precursor (AβPP), and abnormal forms of tau protein, markers that have been used as diagnostic criteria for the disease. These constitute the hallmarks of AD, but whether they are causes of AD or consequences is unknown. We suggest that these are indicators of an infectious etiology. In the case of AD, it is often not realized that microbes can cause chronic as well as acute diseases; that some microbes can remain latent in the body with the potential for reactivation, the effects of which might occur years after initial infection; and that people can be infected but not necessarily affected, such that ‘controls’, even if infected, are asymptomatic
“Microbes and Alzheimer’s Disease” by Itzhaki, Ruth F.; Lathe, Richard; Balin, Brian J.; Ball, Melvyn J.; Bearer, Elaine L.; Bullido, Maria J.; Carter, Chris; Clerici, Mario; Cosby, S. Louise; Field, Hugh; Fulop, Tamas; Grassi, Claudio; Griffin, W. Sue T.; Haas, Jürgen; Hudson, Alan P.; Kamer, Angela R.; Kell, Douglas B.; Licastro, Federico; Letenneur, Luc; Lövheim, Hugo; Mancuso, Roberta; Miklossy, Judith; Lagunas, Carola Otth; Palamara, Anna Teresa; Perry, George; Preston, Christopher; Pretorius, Etheresia; Strandberg, Timo; Tabet, Naji; Taylor-Robinson, Simon D.; and Whittum-Hudson, Judith A. in Journal of Alzheimer’s Disease. Published online March 8 2016 doi:10.3233/JAD-160152
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Aging and resveratrol in berries and grapes
Old Human Cells Rejuvenated – resveratrol in dark choco, berries and grapes
A team led by Professor Lorna Harries, Professor of Molecular Genetics at the University of Exeter, has discovered a new way to rejuvenate inactive senescent cells. Within hours of treatment the older cells started to divide, and had longer telomeres – the ‘caps’ on the chromosomes which shorten as we age.
The researchers applied compounds called resveratrol analogues, chemicals based on a substance naturally found in red wine, dark chocolate, red grapes and blueberries, to cells in culture.
This discovery, funded by the Dunhill Medical Trust, builds on earlier findings from the Exeter group that showed that a class of genes called splicing factors are progressively switched off as we age. The University of Exeter research team, working with Professor Richard Faragher and Dr Elizabeth Ostler from the University of Brighton, found that splicing factors can be switched back on with chemicals, making senescent cells not only look physically younger, but start to behave more like young cells and start dividing.
The researchers applied compounds called resveratrol analogues, chemicals based on a substance naturally found in red wine, dark chocolate, red grapes and blueberries, to cells in culture.
The chemicals caused splicing factors, which are progressively switched off as we age to be switched back on. Within hours, the cells looked younger and started to rejuvenate, behaving like young cells and dividing.
The research, Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence, is published in the journal, BMC Cell Biology.
The discovery has the potential to lead to therapies which could help people age better, without experiencing some of the degenerative effects of getting old. Most people by the age of 85 have experienced some kind of chronic illness, and as people get older they are more prone to stroke, heart disease and cancer.
Professor Harries said: “This is a first step in trying to make people live normal lifespans, but with health for their entire life. Our data suggests that using chemicals to switch back on the major class of genes that are switched off as we age might provide a means to restore function to old cells.”
Dr Eva Latorre, Research Associate at the University of Exeter, who carried out the experiments, was surprised by the extent and rapidity of the changes in the cells.
“When I saw some of the cells in the culture dish rejuvenating I couldn’t believe it. These old cells were looking like young cells. It was like magic,” she said. “I repeated the experiments several times and in each case the cells rejuvenated. I am very excited by the implications and potential for this research.”
As we age, our tissues accumulate senescent cells which are alive but do not grow or function as they should. These old cells lose the ability to correctly regulate the output of their genes. This is one reason why tissues and organs become susceptible to disease as we age. When activated, genes make a message that gives the instructions for the cell to behave in a certain way. Most genes can make more than one message, which determines how the cell acts.
Splicing factors are crucial in ensuring that genes can perform their full range of functions. One gene can send out several messages to the body to perform a function – such as the decision whether or not to grow new blood vessels – and the splicing factors make the decision about which message to make.
As people age, the splicing factors tend to work less efficiently or not at all, restricting the ability of cells to respond to challenges in their environment. Senescent cells, which can be found in most organs from older people, also have fewer splicing factors.
Professor Harries added:
“This demonstrates that when you treat old cells with molecules that restore the levels of the splicing factors, the cells regain some features of youth. They are able to grow, and their telomeres – the caps on the ends of the chromosomes that shorten as we age – are now longer, as they are in young cells. Far more research is needed now to establish the true potential for these sort of approaches to address the degenerative effects of ageing. ”
Professor Richard Faragher of the University of Brighton, will today argue for more research into the degenerative effects of ageing in a debate into whether science should be used to extend people’s lifespans.
“At a time when our capacity to translate new knowledge about the mechanisms of ageing into medicines and lifestyle advice is limited only by a chronic shortage of funds, older people are ill-served by self-indulgent science fiction. They need practical action to restore their health and they need it yesterday,” he said.
Professor Faragher added: “Our discovery of cell rejuvenation using these simple compounds shows the enormous potential of ageing research to improve the lives of older people”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: Funding provided by Dunhill Medical Trust, University of Brighton, Glenn Foundation for Medical Research, BBSRC.
Source: Marie Woolf – University of Exeter
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to University of Exeter.
Original Research: Full open access research for “Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence” by Eva Latorre, Vishal C. Birar, Angela N. Sheerin, J. Charles C. Jeynes, Amy Hooper, Helen R. Dawe, David Melzer, Lynne S. Cox, Richard G. A. Faragher, Elizabeth L. Ostler and Lorna W. Harries in BMC Cell Biology. Published online October 17 2017 doi:10.1186/s12860-017-0147-7
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Exeter “Old Human Cells Rejuvenated in Breakthrough Discovery on Aging.” NeuroscienceNews. NeuroscienceNews, 7 November 2017.
<http://neurosciencenews.com/old-cell-aging-7890/>.
<http://neurosciencenews.com/old-cell-aging-7890/>.
Abstract
Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence
Background
Altered expression of mRNA splicing factors occurs with ageing in vivo and is thought to be an ageing mechanism. The accumulation of senescent cells also occurs in vivo with advancing age and causes much degenerative age-related pathology. However, the relationship between these two processes is opaque. Accordingly we developed a novel panel of small molecules based on resveratrol, previously suggested to alter mRNA splicing, to determine whether altered splicing factor expression had potential to influence features of replicative senescence.
Results
Treatment with resveralogues was associated with altered splicing factor expression and rescue of multiple features of senescence. This rescue was independent of cell cycle traverse and also independent of SIRT1, SASP modulation or senolysis. Under growth permissive conditions, cells demonstrating restored splicing factor expression also demonstrated increased telomere length, re-entered cell cycle and resumed proliferation. These phenomena were also influenced by ERK antagonists and agonists.
Conclusions
This is the first demonstration that moderation of splicing factor levels is associated with reversal of cellular senescence in human primary fibroblasts. Small molecule modulators of such targets may therefore represent promising novel anti-degenerative therapies.
“Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence” by Eva Latorre, Vishal C. Birar, Angela N. Sheerin, J. Charles C. Jeynes, Amy Hooper, Helen R. Dawe, David Melzer, Lynne S. Cox, Richard G. A. Faragher, Elizabeth L. Ostler and Lorna W. Harries in BMC Cell Biology. Published online October 17 2017 doi:10.1186/s12860-017-0147-7
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Study reveals role of specific lipids in accelerating or curbing bacterial infection
Study reveals role of specific lipids in accelerating or curbing bacterial infection
Lipids appear to play an important role in infections. According to researchers from the University of Maastricht in Maastricht, The Netherlands, and the University of Maryland, Baltimore (UMB) in Baltimore, Md., USA, specific lipids can greatly accelerate bacterial infection.
With the help of mass spectrometry imaging (MSI), researchers showed that specific mammalian lipids could also provide protection against the same infection. Their discovery offers hope for future treatment of vulnerable patients in hospitals or development of preventative treatments for travellers to risk areas in certain parts of the world.
The findings of the research team, led by American researchers Robert Ernst and Alison Scott at UMB and Maastricht University Distinguished Professor Ron Heeren, were published Nov. 6 in the journal, Proceedings of the National Academy of Sciences (PNAS).
Mass Spectrometry Imaging
Mass spectrometry imaging is an imaging technique in which molecular maps of a pathological tissue section can be compiled from a single experiment. Researchers use the technique to determine exactly where certain molecules are located and how their distribution is affected by pathogenic bacteria, for instance. “This technique enables us to analyse thousands of molecules with a single measurement,” Heeren explains. “What is special about our research is that we were able to use this method in order to capture for the first time the molecular changes which occur during a bacterial infection, mainly revealing the role of lipids in the further evolution of such an inflammation. This result means that we’ll be able in future to determine the severity of an infection accurately within half an hour. Based on the type of lipid, we’ll also know how the inflammation will behave in a patient.”
Protect or accelerate
To test their ability to use MSI to track disease progression, the scientists injected a healthy mouse with the highly pathogenic bacteria Francisella novicida (Fn). Through MSI, the researchers were then able to create an accurate molecular map of the infection’s evolution, predominantly based on lipids. In doing so, it became clear that certain lipids significantly accelerated the infection, although these lipids should never be seen as separate from their spatial context in the tissue. “The distribution of lipids in the host – the patient – appears to have a tremendous effect on the immune system. For this reason, lipids are a strong determining factor in the aggressiveness of a bacterial infection,” Heeren concludes. “It is now important to establish a kind of library, in which we can precisely identify which lipids play a role in accelerating infection and which lipids have a positive effect on the immune response.”
Alison Scott PhD, research associate professor at the University of Maryland School of Dentistry (UMSOD) and guest researcher at Maastricht University, hopes that this knowledge will help develop drugs that could be used to treat vulnerable patients and help them form the right lipids in the right places to dampen infection.
Applicability of this study
Although the researchers specifically used MSI to track Fn infection in this study, the techniques could be applied to a wide range of diseases. “The methodology underlying the study is relevant to any infection and positions us to expand work in the field of the role of lipids in both the bacteria and the host. It allows researchers to identify host-based pathways for therapeutic treatment to control bacterial infection and inflammation. I hope to start looking at airway infections such as pseudomonas,” says Scott.
This kind of research is only made possible by collaborations across disciplines. “This study shows the value of highly collaborative projects bringing together microbiologists and mass spectrometry experts to define the finite interactions between a bacteria and a host,” says Robert “Bob” Ernst, PhD, the senior investigator involved in the study and professor and vice chair of the Department of Microbial Pathogenesis at UMSOD and an adjunct professor at the University of Maryland School of Medicine (UMSOM).
The research presented here opens up many research avenues, both into the applicability of MSI for disease studies and the development of therapeutics that target lipids to treat infection, according to Ernst and colleagues, who include Kari Ann Shirey, PhD, assistant professor in UMSOM’s Department of Microbiology and Immunology.
Source:
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Trends in medical health insurance, costs and expenses by state
Employer-sponsored insurance (ESI) is the primary source of health insurance coverage for individuals under age 65
This chartbook uses data for private-sector establishments in the Medical Expenditure Panel Survey-Insurance Component (MEPS-IC) to describe trends in employer coverage, premiums, and benefits from 2003 to 2016.
Medical Expenditure Panel Survey Insurance Component 2016 Chartbook. Rockville, MD:
Agency for Healthcare Research and Quality; September 2017. AHRQ Publication No. 17-0034-EF. https://meps.ahrq.gov/mepsweb/data_files/publications/cb21/cb21.pdf.
The MEPS-IC is an annual survey of private employers and State and local governments and is designed to be representative of all 50 States and the District of Columbia. The large sample size (about 42,000 establishments), combined with a response rate of 67.6 percent in 2016, permits analyses of variations in ESI by firm size and across States that are not readily available from other sources.
Examining trends by firm size and across States is important because of variation in insurance markets along these dimensions. Insurance markets differ by firm size due to smaller firms’ more limited ability to pool risk and their higher administrative costs compared with larger firms. State variation in ESI markets may reflect differences in employment patterns, health care prices, and utilization, as well as differences in State approaches to regulating private insurance and
administering Medicaid.
The period presented in the chartbook, 2003 to 2016, shows trends through a period of change in national health policy that could have affected national ESI trends, as well as trends by firm size.
Starting in 2014, most people were required to either obtain health insurance or make an
individual shared responsibility payment. The employer shared responsibility provisions began to take effect for employers with 100 or more full-time-equivalent employees in 2015 and for employers with 50 or more employees in 2016.
Coinsurance Rates for Physician Office Visits
From 2003 to 2016, the percentage of enrolled employees in plans with coinsurance rates increased from 19.5 percent to 34.9 percent. There were significant year-to-year increases in the percentage of enrolled employees with a coinsurance rate from 2005 to 2006 and from 2009 to 2010 and then each year from 2011 to 2015 (Exhibit 5.7).
The percentage of enrolled employees in a health insurance plan that had a coinsurance rate for physician office visits did not change significantly from 2015 (35.0 percent) to 2016 (34.9 percent) (Exhibit 5.7).
Enrolled employees in large firms (100 or more employees) were more likely to have plans with coinsurance rates than enrolled employees in smaller firms in all years from 2003 to 2016. In 2016, 38.9 percent of enrollees in firms with 100 or more employees had
coinsurance rates compared with 20.6 percent and 21.5 percent in firms with fewer than 50 employees and with 50 to 99 employees, respectively (Exhibit 5.7).
Between 2003 and 2016, the percentage of enrolled employees in health plans with a
coinsurance rate increased for all enrollees, regardless of firm size. However, the increase was more pronounced among enrolled employees in firms with 100 or more employees (17.9 percentage points) than in smaller firms (5.4 and 6.9 percentage point increases at firms with fewer than 50 employees and with 50 to 99 employees, respectively) (Exhibit 5.7).
Among enrolled employees in plans with physician office visit coinsurance rates, average coinsurance rates increased from 18.0 percent in 2003 to 20.5 percent in 2016 (Exhibit 5.8).
Average coinsurance rates rose from 20.1 percent in 2015 to 20.5 percent in 2016, an
increase of 0.4 percentage points. This increase followed increases of 0.6 percentage points from 2013 to 2014 and 0.3 percentage points from 2014 to 2015 (p <0.10) (Exhibit 5.8).
From 2013 to 2014, average coinsurance rates for enrolled employees at firms with 100 or more employees increased from 18.8 to 19.5 percent, but there was no significant change in smaller firms. In contrast, from 2014 to 2015, average coinsurance rates for enrolled employees at firms with fewer than 50 employees increased from 21.5 to 22.6 percent, while there was no significant change at larger employers.
Brain activity ripples linked to creation of long-term memories – sleep more
Brain activity ripples linked to creation of long-term memories
At a Glance
- A study in lab animals showed that communication between two brain regions may be needed for the formation of long-term memories.
- The finding might help researchers discover how long-term memory formation can be enhanced.
An anatomical map with raw sample traces of neocortical ripples, left, color coded to show the brain regions in which they occurred. György Buzsáki, M.D., Ph.D., NYU School of MedicineWhile we’re asleep, the brain is working to store new information as long-term memories. Storing a memory likely involves interactions between the brain’s hippocampus and parts of the cortex. Scientists have been trying to determine the precise connections by examining electrical activity within these regions of the brain.
When hundreds or thousands of nerve cells, or neurons, in the brain become activated at the same moment, the high-frequency electrical activity shows up on recordings as ripples. Previous work by Dr. György Buzsáki at New York University revealed ripples of high-frequency activity in the rat hippocampus during sleep and suggested that ripples play a role in memory storage.
In the current study, Buzsáki’s team set out to record electrical activity in multiple regions of the brain for evidence of cross-talk during sleep. The work was funded in part by NIH’s Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, which is managed and funded by several NIH components including NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and National Institute of Mental Health (NIMH). Results were published on October 20, 2017, in Science.
The researchers created a thin, flexible array of tightly packed, tiny electrodes that can be placed on the surface of the brain. This array can record the electrical activity of single neurons. Using the device, called NeuroGrid, on top of the rat brain along with recording electrodes placed deeper into the brain, the team recorded activity in several brain regions during non-rapid eye movement (NREM) sleep. They noticed activity ripples in the association neocortex, an area on the brain’s surface involved in processing complex information. At the same time, ripples occurred in the hippocampus. The simultaneous ripples suggested that the two regions were communicating.
Six rats were given a memory training session to find water in a maze. The researchers then recorded the rats’ brain activity during NREM sleep. In these trained rats, the learning task increased the cross-talk between the association neocortex and the hippocampus. A second training session boosted the cross-talk even more. Four rats who didn’t undergo memory training were allowed to roam freely through a maze without reward. These untrained rats didn’t have synchronized ripples in the association neocortex and the hippocampus during sleep. The findings suggest that communication between these brain regions is important for the creation and storage of memories.
“Identifying the specific neural patterns that go along with memory formation provides a way to better understand memory and potentially even address disorders of memory,” says co-first author Dr. Jennifer Gelinas of New York University and Columbia University.
The researchers plan to use the NeuroGrid to study whether disrupting the ripples has an effect on memory formation in lab animals. They also plan to use the NeuroGrid to find out whether ripples occur in the same brain regions of people.
Homeless camps contrast with West Coast tech wealth
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