Source: Research Suggests Association Between Gut Bacteria and Emotion
Stiff Vessels and Low Blood Flow in the Brain Forewarn of Dementia
New York Times
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Social Status of Listener Alters Our Voice
Summary: According to researchers, people tend to change the pitch of their voice depending on who they are talking to and how dominant they feel. The study found that a person’s vocal characteristics altered in response to people of different social status. When a person was believed to be more dominant, people’s voices became more high pitched.
Source: University of Stirling.
People tend to change the pitch of their voice depending on who they are talking to, and how dominant they feel, a study by the University of Stirling has found.
The psychology research, published in PLOS ONE, put participants through a simulated job interview task and discovered that individuals’ vocal characteristics – particularly pitch – are altered in response to people of different social status.
Regardless of self-perceived social status, people tend to talk to high status individuals using a higher pitch.
Dr Viktoria Mileva, a Postdoctoral Researcher at the University of Stirling, said: “A deep, masculine voice sounds dominant, especially in men, while the opposite is true of a higher pitched voice. So, if someone perceives their interviewer to be more dominant than them, they raise their pitch. This may be a signal of submissiveness, to show the listener that you are not a threat, and to avoid possible confrontations.
“These changes in our speech may be conscious or unconscious but voice characteristics appear to be an important way to communicate social status. We found both men and women alter their pitch in response to people they think are dominant and prestigious.”
The researchers also found that participants who think they are dominant – who use methods like manipulation, coercion, and intimidation to acquire social status – are less likely to vary their pitch and will speak in a lower tone when talking to someone of a high social status.
Individuals who rate themselves as high in prestige – they believe people look up to them and value their opinions, thereby granting them social status – do not change how loud they are speaking, no matter who they are speaking to. This may signal that they are more calm and in control of a situation.
The participants responded to introductory, personal, and interpersonal interview questions. They lowered the pitch of their voice most in response to the more complex, interpersonal questions, for example when explaining a conflict situation to an employer.
Dr Mileva added: “Signals and perceptions of human social status have an effect on virtually every human interaction, ranging from morphological characteristics – such as face shape – to body posture, specific language use, facial expressions and voices.
“Understanding what these signals are, and what their effects are, will help us comprehend an essential part of human behaviour.”
Experts believe the vocal changes identified in this study could be true for other situations where there are perceived social status differences between two people talking. This includes talking with a rival on the football pitch or interacting with a colleague.
Source: University of Stirling
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Perceived differences in social status between speaker and listener affect the speaker’s vocal characteristics” by Juan David Leongómez, Viktoria R. Mileva, Anthony C. Little, and S. Craig Roberts in PLOS ONE. Published online June 14 2017 doi:10.1371/journal.pone.0179407
<http://neurosciencenews.com/voice-social-status-7008/>.
Abstract
Perceived differences in social status between speaker and listener affect the speaker’s vocal characteristics
Non-verbal behaviours, including voice characteristics during speech, are an important way to communicate social status. Research suggests that individuals can obtain high social status through dominance (using force and intimidation) or through prestige (by being knowledgeable and skilful). However, little is known regarding differences in the vocal behaviour of men and women in response to dominant and prestigious individuals. Here, we tested within-subject differences in vocal parameters of interviewees during simulated job interviews with dominant, prestigious, and neutral employers (targets), while responding to questions which were classified as introductory, personal, and interpersonal.
We found that vocal modulations were apparent between responses to the neutral and high-status targets, with participants, especially those who perceived themselves as low in dominance, increasing fundamental frequency (F0) in response to the dominant and prestigious targets relative to the neutral target. Self-perceived prestige, however, was less related to contextual vocal modulations than self-perceived dominance.
Finally, we found that differences in the context of the interview questions participants were asked to respond to (introductory, personal, interpersonal), also affected their vocal parameters, being more prominent in responses to personal and interpersonal questions. Overall, our results suggest that people adjust their vocal parameters according to the perceived social status of the listener as well as their own self-perceived social status.
“Perceived differences in social status between speaker and listener affect the speaker’s vocal characteristics” by Juan David Leongómez, Viktoria R. Mileva, Anthony C. Little, and S. Craig Roberts in PLOS ONE. Published online June 14 2017 doi:10.1371/journal.pone.0179407
Researchers Find Link Between Food Allergies and Childhood Anxiety
Summary: A new study reveals a link between a food allergy diagnosis and social anxiety in children of low socioeconomic status. The study found 57% of children with food allergies report anxiety symptoms. Researchers suggest food allergies are linked to elevated social anxiety, fear of social rejection and also humiliation in children.
Source: Columbia University.
Researchers at Columbia University’s Mailman School of Public Health and Albert Einstein College of Medicine studied the link between food allergy and childhood anxiety and depression among a sample of predominantly low socioeconomic status minority children. The results showed that children with a food allergy had a significantly higher prevalence of childhood anxiety. Food allergies were not associated with symptoms of childhood depression or with symptoms of anxiety or depression among their caregivers. The results are published in the Journal of Pediatrics.
Food allergies are increasingly common among youth in the U.S. with recent estimates as high as 8 percent. Until nowlittle was known about the prevalence of food allergy in low socioeconomic ethnic minority populations.
The researchers studied 80 pediatric patients ages 4-12 years, 8 years old on average, with and without food allergy and their caregivers from urban pediatric outpatient clinics in the Bronx, New York. They controlled for an asthma diagnosis in the children, as anxiety and mood disorders are more prevalent among youth with asthma and especially more common in low socioeconomic minority children.
Among the children with a food allergy, 57 percent reported having symptoms of anxiety compared to 48 percent of children without a food allergy. Approximately 48 percent of the children had symptoms of depression with or without a food allergy.
“Management of food allergy can be expensive both in terms of food shopping, meal preparation, and the cost of epinephrine auto-injectors, which expire annually,” said Renee Goodwin, PhD, in the Department of Epidemiology at the Mailman School of Public Health and lead author. “These demands could result in higher levels of anxiety for those with fewer financial resources and further heighten anxiety symptoms in children and their caregivers.”
The results suggest that food allergy is particularly linked to elevated social anxiety and fear of social rejection and humiliation. “There are a number of possible explanations for the relationship found between food allergy diagnosis and increased social anxiety issues in this sample of pediatric patients,” noted Dr. Goodwin. “Management of a potentially life-threatening condition may be anxiety provoking, and some children may experience increased social anxiety about being “different” from other children depending on their age and how food allergy is managed by adults in a particular setting.”
The researchers also point out a possible explanation for not finding a link between food allergy and depression in children. The sample was young, and the mean age of onset for depression is significantly later than anxiety. “It would be worthwhile to examine these relationships among older adolescents and young adults with food allergy who are at the peak of risk for depression onset, especially because early anxiety is associated with increased risk for subsequent onset of depression,” said Jonathan Feldman, PhD, professor at Ferkauf Graduate School of Psychology, Yeshiva University and Albert Einstein College of Medicine.
“With the high prevalence of food allergies today, education in schools remains a priority,” said Dr. Goodwin. “Given the strong association between food allergy and social anxiety in children future investigations on the food allergy-mental health relationship are also warranted in clinical, school, and community-based settings which could aid in the development of interventions.”
Co-authors: Sandra Rodgin, Rachel Goldman, and Jonathan Feldman, Ferkauf Graduate School of Psychology, Yeshiva University; Juliana Rodriguez, Department of Pediatrics, Albert Einstein College of Medicine; Gabriele deVos and Denise Serebrisky, Jacobi Medical Center, Bronx, NY. The authors declare no conflicts of interest.
NeuroscienceNews would like to thank Stephanie Berger for submitting this article for inclusion.
Source: Stephanie Berger – Columbia University
Image Source: NeuroscienceNews.com image is credited to Columbia University.
Original Research: Abstract for “Food Allergy and Anxiety and Depression among Ethnic Minority Children and Their Caregivers” by Renee D. Goodwin, PhD, MPH, Sandra Rodgin, MA, Rachel Goldman, MA, Juliana Rodriguez, MD, Gabriele deVos, MD, Denise Serebrisky, MD, and Jonathan M. Feldman, PhD in Journal of Pediatrics. Published online June 5 2017 doi:10.1016/j.jpeds.2017.04.055
<http://neurosciencenews.com/food-allergies-anxiety-7011/>.
Abstract
Food Allergy and Anxiety and Depression among Ethnic Minority Children and Their Caregivers
Objective
To investigate the relationship between food allergy and symptoms of anxiety and depression among ethnic minority, low socioeconomic status (SES) children and their caregivers.
Study design
Pediatric patients ages 4-12 years with and without food allergy and their caregivers were recruited from urban pediatric outpatient clinics. Statistical analyses were used to examine the prevalence of symptoms of anxiety and depression among patients and their caregivers with and without food allergy, adjusting for asthma.
Results
Eighty patients ranging from ages 4 to 12 years, with a mean age of 8.1 years, and their caregivers participated in the study. Food allergy was associated with significantly higher t scores on the Multidimensional Anxiety Scale for Children (MASC) Total (P = .007), MASC Humiliation Rejection, (P = .02) and MASC Social Anxiety (P = .02) among pediatric patients, adjusting for asthma. Food allergy was not associated with child depression symptoms, nor was there a significant difference in anxiety or depression symptoms among caregivers of patients with and without food allergy.
Conclusions
Food allergy appears to be associated with increased symptoms of social anxiety and higher levels of anxiety overall, but not depression, in ethnic minority children of lower socioeconomic status. This finding was not due to confounding by asthma. Food allergy was not associated with higher levels of depression or anxiety symptoms among caregivers of pediatric patients with food allergy. Future studies should investigate potential pathways between food allergy and anxiety that may be unique to children in underserved populations, and develop interventions to reduce anxiety in children with food allergy.
“Food Allergy and Anxiety and Depression among Ethnic Minority Children and Their Caregivers” by Renee D. Goodwin, PhD, MPH, Sandra Rodgin, MA, Rachel Goldman, MA, Juliana Rodriguez, MD, Gabriele deVos, MD, Denise Serebrisky, MD, and Jonathan M. Feldman, PhD in Journal of Pediatrics. Published online June 5 2017 doi:10.1016/j.jpeds.2017.04.055
Research Suggests Association Between Gut Bacteria and Emotion
Summary: A new study identifies gut bacteria that appears to interact with brain areas associated with mood and behavior.
Source: UCLA.
Researchers have identified gut microbiota that interact with brain regions associated with mood and behavior. This may be the first time that behavioral and neurobiological differences associated with microbial composition in healthy humans have been identified.
BACKGROUND
Brain-gut-microbiota interactions may play an important role in human health and behavior. Previous research suggests that microbiota, a community of microorganisms in the gut, can influence behavior and emotion. Rodent models have demonstrated the effects of gut microbiota on emotional and social behaviors, such as anxiety and depression. There is, however, little evidence of this in humans.
For this study the researchers sought to identify brain and behavioral characteristics of healthy women clustered by gut microbiota profiles.
METHOD
Forty women supplied fecal samples for profiling, and magnetic resonance images were taken of their brains as they viewed images of individuals, activities or things that evoked emotional responses. The women were divided by their gut bacteria composition into two groups: 33 had more of a bacterium called Bacteroides; the remaining seven had more of the Prevotella bacteria. The Bacteroides group showed greater thickness of the gray matter in the frontal cortex and insula, brain regions involved with complex processing of information. They also had larger volumes of the hippocampus, a region involved in memory processing. The Prevotella group, by contrast, showed more connections between emotional, attentional and sensory brain regions and lower brain volumes in several regions, such as the hippocampus. This group’s hippocampus was less active while the women were viewing negative images. They also rated higher levels of negative feelings such as anxiety, distress and irritability after looking at photos with negative images than did the Bacteroides group.
IMPACT
These results support the concept of brain-gut-microbiota interactions in healthy humans. Researchers do not yet know whether bacteria in the gut influence the development of the brain and its activity when unpleasant emotional content is encountered, or if existing differences in the brain influence the type of bacteria that reside in the gut. Both possibilities, however, could lead to important changes in how one thinks about human emotions.
Funding: This research was supported by grants from Danone Research and from the National Institutes of Health, including R01 DK048351, P50 DK64539, P30 DK041301 and R01 HD076756. In addition, pilot funds were provided for brain scanning by the Ahmanson-Lovelace Brain Mapping Center.
DISCLOSURE Tillisch received funding from Danone Research. Mayer is on the advisory boards for yogurt product company Dannon and its parent company Danone. Derrien, Le Nevé, Guyonnet and Brazeilles are or were employed by Danone Research at the time of the study. The remaining authors disclose no conflicts.
Source: Enrique Rivero – UCLA
Image Source: NeuroscienceNews.com image is credited to NIH.
Original Research: The study will appear in Psychosomatic Medicine: Journal of Behavioral Medicine.
Stiff Vessels and Low Blood Flow in the Brain Forewarn of Dementia
Summary: Researchers report harmful plaques associated with Alzheimer’s disease may build up in the brain as a result of high blood pressure and decreased cerebral blood flow.
Source: USC Dornsife.
USC researchers plan to explore whether this early sign could be targeted by drugs already approved for treating other health conditions.
A combination of high blood pressure and decreased blood flow inside the brain may spur the build-up of harmful plaque and signal the onset of dementia, USC researchers have found.
“If you have problems with the blood vessels in the brain, then you’re going to end up with difficulty with thinking skills, cognition, memory, and ultimately this can be related to other brain pathologies such as Alzheimer’s disease,” said Daniel Nation, lead author of the study and an assistant professor of psychology at USC Dornsife.
For the study published June 1 in the journal Brain, Nation used patient data from a national medical database, the Alzheimer’s Disease Neuroimaging Initiative housed at Keck School of Medicine at USC, to explore whether constricted blood flow contributes to the build-up of amyloid plaque and, consequently, to the onset of dementia. He also determined a new way to calculate cerebrovascular resistance — a stiffening of the vessels that results from high blood pressure and low blood flow.
The brain’s blood vessels function as a plumbing system that delivers nutrients and oxygen to feed the brain cells, and then flushes away any waste that the cells cannot use. The metabolic waste secreted by cells includes protein fragments — called amyloid — that a healthy brain breaks down and expels by pulsating blood through its vessels.
The brain tightens or relaxes its vessels to maintain blood flow as it adjusts for changes in blood pressure. However, the brain vessels in Alzheimer’s patients are stiff and tight, inhibiting blood flow and enabling the sticky amyloid to accumulate, Nation found.
“The idea of cerebrovascular resistance converges on the notion that the blood vessels in Alzheimer’s brains are in this hyper-contracted state,” Nation said. “For many different reasons, the contracting blood vessels are resistant to opening up and really letting the blood in.”
Blood pressure and blood flow measures alone do not predict dementia as well as when they are examined together.
“When blood pressure goes up or down, the brain vessels accommodate so that blood flow will remain fixed,” Nation said. “So if you don’t measure blood pressure and blood flow together, then it is basically masking all of these important changes in vascular resistance, and it is very difficult to see the vessel changes that underlie this.”
Dementia and Alzheimer’s: A rising health crisis
Alzheimer’s is considered one of the greatest health challenges of the century. Alzheimer’s affects an estimated 5.4 million Americans — about 1 in 3 seniors. As a research institution devoted to promoting lifelong health, USC researchers across a range of disciplines are examining the health, societal and political effects and implications of the disease.
Nation’s lab at USC Dornsife is part of the multidisciplinary effort. He focuses on understanding cognitive decline associated with age-related changes in vascular structure and function.
High resistance in Alzheimer’s patients
To measure resistance in the brain’s vessels, Nation developed an index that represents a ratio of average blood pressure to regional cerebral blood flow. A high index ranking for resistance indicates that amyloid is building up and that the patient is progressing toward dementia, Nation said.
The Alzheimer’s Disease Neuroimaging Initiative database used for the study is an extensive repository of medical data from an estimated 1,000 volunteers age 55–90. The data include results of genetic, memory and cognitive tests, brain scans and blood biomarker information.
Nation used data on three groups of volunteer men and women: those who did not have any amyloid buildup in their brains, those who did, and those who had Alzheimer’s disease.
Nation found that the people with Alzheimer’s disease had lower blood flow in their brains than the people without dementia. These blood flow changes were undetectable in the earlier stages of disease, when amyloid was accumulating but there were no obvious signs of memory loss.
The people with Alzheimer’s disease also measured much higher on the cerebrovascular resistance index.
Amyloid-positive patients’ cognition worsened over time. Nation found that just two years after their initial examination, they were more likely to experience accelerated cognitive decline and progression to clinical dementia.
“Our findings suggest that change in resistance may be an early and key phenomenon in the brain that’s closely linked to the symptoms of cognitive decline in the future,” Nation said.
Potential dementia blockers
In recent months, major pharmaceutical companies aiming for a cure have halted testing of Alzheimer’s drugs mid-trial due to poor results. However, recent studies point to a promising option to delay the onset of dementia or Alzheimer’s: drugs already on the market and approved by the U.S. Food and Drug Administration for other purposes.
Among the most promising are cholesterol-lowering statins and blood pressure-lowering drugs known as angiotensin receptor blockers. The latter were highlighted by Nation in a recent study published in Alzheimer’s Research & Therapy.
He found that people taking blood pressure-lowering drugs have better memories than people who have elevated blood pressure and are taking other drugs. A subclass of these drugs can cross the blood-brain barrier — the filtration mechanism in the capillaries that prevents toxins from entering the brain.
Nation said he aims to refine how he measures vascular resistance so that he can test it in older adults in the lab. By measuring the index dynamically with brain scanners, he will track how blood pressure-lowering drugs affect vascular resistance from moment to moment in the brains of people at risk of Alzheimer’s disease.
Then, he will work toward answering the next important question: If vascular resistance can be managed with treatments, will that lower someone’s risk for developing dementia?
USC graduate student Belinda Yew was a co-author of the cerebrovascular resistance study published in Brain, and USC graduate student Jean Ho was a co-author on the blood-pressure-lowering drugs study published in Alzheimer’s Research & Therapy. The research was supported by National Institutes of Health grants P50 AG005142 (an estimated $7.1 million grant that covered 10 percent of the study’s costs) and P01 AG052350 (an estimated $8.9 million grant that covered 20 percent of the study’s costs). The NIH grants also support a series of studies by Nation.
The remaining 70 percent of the Brain study’s costs were covered by the Alzheimer’s Disease Neuroimaging Initiative and a U.S. Department of Defense grant (W81XWH-12-2-0012).
Source: Michelle Boston and Emily Gersema – USC Dornsife
Image Source: NeuroscienceNews.com image is credited to Daniel Nation.
Original Research: Abstract for “Cerebrovascular resistance: effects on cognitive decline, cortical atrophy, and progression to dementia” by Belinda Yew, Daniel A. Nation, for the Alzheimer’s Disease Neuroimaging Initiative in Brain. Published online June 1 2017 doi:10.1093/brain/awx112
<http://neurosciencenews.com/dementia-stiff-vessel-blood-flow-7015/>.
Abstract
Cerebrovascular resistance: effects on cognitive decline, cortical atrophy, and progression to dementia
Evidence for vascular contributions to Alzheimer’s disease has been increasingly identified, with increased blood pressure and decreased cerebral blood flow both linked to in vivo biomarkers and clinical progression of Alzheimer’s disease. We therefore hypothesized that an elevated ratio of blood pressure to cerebral blood flow, indicative of cerebrovascular resistance, would exhibit earlier and more widespread associations with Alzheimer’s disease than cerebral blood flow alone. Further, we predicted that increased cerebrovascular resistance and amyloid retention would synergistically influence cognitive performance trajectories, independent of neuronal metabolism. Lastly, we anticipated associations between cerebrovascular resistance and later brain atrophy, prior to amyloid accumulation. To evaluate these hypotheses, we investigated associations between cerebrovascular resistance and amyloid retention, cognitive decline, and brain atrophy, controlling for neuronal metabolism. North American older adults (n = 232) underwent arterial spin labelling magnetic resonance imaging to measure regional cerebral blood flow in brain regions susceptible to ageing and Alzheimer’s disease. An estimated cerebrovascular resistance index was then calculated as the ratio of mean arterial pressure to regional cerebral blood flow. Positron emission tomography with 18F-florbetapir and fludeoxyglucose was used to quantify amyloid retention and neuronal metabolism, respectively. Cognitive performance was evaluated via annual assessments of global cognition, memory, and executive function. Results indicated diminished inferior parietal and temporal cerebral blood flow for patients with Alzheimer’s disease (n = 33) relative to both non-demented groups, but no cerebral blood flow differences between non-demented amyloid-positive (n = 87) and amyloid-negative (n = 112) cases. In contrast, the cerebrovascular resistance index was significantly elevated in amyloid-positive versus amyloid-negative cases, with additional elevation in patients with Alzheimer’s disease. Furthermore, cerebrovascular resistance index group differences were of greater statistical effect size and encompassed a greater number of brain regions than those for cerebral blood flow alone. Cognitive decline over 2-year follow-up was accelerated by elevated baseline cerebrovascular resistance index, particularly for amyloid-positive individuals. Increased baseline cerebrovascular resistance index also predicted greater progression to dementia, beyond that attributable to amyloid-positivity. Finally, increased cerebrovascular resistance index predicted greater regional atrophy among non-demented older adults who were amyloid-negative. Findings suggest that increased cerebrovascular resistance may represent a previously unrecognized contributor to Alzheimer’s disease that is independent of neuronal hypometabolism, predates changes in brain perfusion, exacerbates and works synergistically with amyloidosis to produce cognitive decline, and drives amyloid-independent brain atrophy during the earliest stage of disease.
“Cerebrovascular resistance: effects on cognitive decline, cortical atrophy, and progression to dementia” by Belinda Yew, Daniel A. Nation, for the Alzheimer’s Disease Neuroimaging Initiative in Brain. Published online June 1 2017 doi:10.1093/brain/awx112
Military’s resilience during the transition to widowhood
We use the Health and Retirement Study and linked Veterans Mail Survey to address respondents while they are continuously married (T1) and at widowhood four years later (T2) using Ordinary Least Squares (OLS) regression. To address our hypotheses, we examine whether military experience without exposure to death, and/or military experience with exposure to death moderates the overall negative effect of widowhood for loneliness relative to civilians.
There is a significantly lower level of loneliness among veterans with exposure to death relative to civilians who become widowed; however, veterans without exposure to death remain similar to civilian widowers. Social engagement does not explain the benefits associated with military exposures for widowers.
Although exposure to death early in life is traumatic, our research suggests that such adversity within the specific context of the military may help enhance resilience during the transition to widowhood
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Key Mechanism Behind Some Forms of Deafness Identified
Key Mechanism Behind Some Forms of Deafness Identified
Summary: Researchers have identified a new protein, CIB2, that is key to helping the auditory system to turn soundwaves into meaningful brain signals. Mutations of this gene leave people unable to convert the soundwaves into signals that the brain can interpret, and are deaf.
Source: University of Maryland.
Study identifies a new protein that is essential to the process of turning sound waves into meaningful brain signals.
Although the basic outlines of human hearing have been known for years – sensory cells in the inner ear turn sound waves into the electrical signals that the brain understands as sound – the molecular details have remained elusive.
Now, new research from the University of Maryland School of Medicine (UM SOM), has identified a crucial protein in this translation process.
The findings were published today in the latest issue of Nature Communications. The study is the first to illuminate in detail how a particular protein, which is known as CIB2, allows hearing to work.
“We are very excited by these results,” said the senior author of the study, Zubair Ahmed, professor in the Department of Otorhinolaryngology-Head and Neck Surgery at UM SOM. “This tells us something new about the fundamental biology of how hearing works on a molecular level.”
CIB2, which is short for calcium and integrin-binding protein 2, is essential for the structure of stereocilia, the structures at the top of the sensory hair cells in the inner ear. Stereocilia are extremely small, less than a half a micrometer in diameter, which is about the wavelength of a visible light. Each ear contains 18,000 hair cells that do not divide or regenerate.
Dr. Ahmed and his colleague Saima Riazuddin, professor in the Department of Otorhinolaryngology-Head and Neck Surgery at UM SOM, along with their collaborators, discovered five years ago that CIB2 was involved in hearing. Since then, they have studied this protein in flies, mice, zebrafish and humans. The new study is the first to explain the mechanism behind CIB2 in hearing.
In this study, they genetically engineered mice without CIB2, as well as mice in which a human CIB2 gene mutation had been inserted. The researchers found that the human mutation affects the ability of the CIB2 protein to interact with two other proteins, TMC1 and TMC2, which are crucial in the process of converting sound to electrical signals. This process is known as mechanotransduction.
People with this mutation cannot turn soundwaves into signals that the brain can interpret, and so are deaf. When the researchers inserted the human CIB2 mutation into the mouse, they found that the mice were deaf.
“This is a big step in determining the identity of key components of the molecular machinery that converts sound waves into electrical signals in the inner ear,” said the study’s co-senior author, Gregory Frolenkov, of the Department of Physiology at the University of Kentucky.
Dr. Ahmed and his colleagues are now looking for other molecules beyond CIB2 that play a key role in the process. In addition, they are exploring potential therapies for CIB2-related hearing problems. In mice, they are using the gene editing tool CRISPR to modify dysfunctional CIB2 genes. They suspect that if this modification occurs in the first few weeks after birth, these mice, which are born deaf, will be able to hear. The scientists are also experimenting with gene therapy, using a harmless virus to deliver a normal copy of the normal CIB2 gene to baby mice that have the mutated version. Dr. Ahmed says the early results of these experiments are intriguing.
Nearly 40 million Americans suffer from some level of hearing loss. This includes around 74,000 children with profound, early-onset deafness. At least 50 percent of these deafness cases are due to genetic causes.
It is not clear how common CIB2 mutations are in the US population, or how large a role these mutations play in deafness in humans worldwide. In his research on a group of families in Pakistan that have a higher risk of deafness, Dr. Ahmed has found that about 8 to 9 percent seem to have mutations in CIB2. Overall, he says, the gene could play a role in tens of thousands of cases of deafness, and perhaps many more than that. He is also studying CIB2 among the general population. It may be that some versions of the gene also play a role in deafness caused by environmental conditions, creating a predisposition to hearing loss.
Arnaud Giese, a Post-Doc Fellow at UM SOM, and Yi-Quan Tang, from Cambridge University in England, are the first co-authors of this study. Other significant contributors include Dr. Riazuddin, William Schafer, from Cambridge University, Steve S.D. Brown, from the MRC Harwell Institute, UK, and Robert Fettiplace, from the University of Wisconsin.
Source: David Kohn – University of Maryland
Image Source: NeuroscienceNews.com image is credited to BruceBlaus, licences CC BY 3.0.
Original Research: Full open access research for “CIB2 interacts with TMC1 and TMC2 and is essential for mechanotransduction in auditory hair cells” by Arnaud P. J. Giese, Yi-Quan Tang, Ghanshyam P. Sinha, Michael R. Bowl, Adam C. Goldring, Andrew Parker, Mary J. Freeman, Steve D. M. Brown, Saima Riazuddin, Robert Fettiplace, William R. Schafer, Gregory I. Frolenkov & Zubair M. Ahmed in Nature Communications. Published online June 29 2017 doi:10.1038/s41467-017-00061-1
<http://neurosciencenews.com/deafness-auditory-neuroscience-7006/>.
Abstract
CIB2 interacts with TMC1 and TMC2 and is essential for mechanotransduction in auditory hair cells
Inner ear hair cells detect sound through deflection of stereocilia, the microvilli-like projections that are arranged in rows of graded heights. Calcium and integrin-binding protein 2 is essential for hearing and localizes to stereocilia, but its exact function is unknown. Here, we have characterized two mutant mouse lines, one lacking calcium and integrin-binding protein 2 and one carrying a human deafness-related Cib2 mutation, and show that both are deaf and exhibit no mechanotransduction in auditory hair cells, despite the presence of tip links that gate the mechanotransducer channels. In addition, mechanotransducing shorter row stereocilia overgrow in hair cell bundles of both Cib2 mutants. Furthermore, we report that calcium and integrin-binding protein 2 binds to the components of the hair cell mechanotransduction complex, TMC1 and TMC2, and these interactions are disrupted by deafness-causing Cib2 mutations. We conclude that calcium and integrin-binding protein 2 is required for normal operation of the mechanotransducer channels and is involved in limiting the growth of transducing stereocilia.
“CIB2 interacts with TMC1 and TMC2 and is essential for mechanotransduction in auditory hair cells” by Arnaud P. J. Giese, Yi-Quan Tang, Ghanshyam P. Sinha, Michael R. Bowl, Adam C. Goldring, Andrew Parker, Mary J. Freeman, Steve D. M. Brown, Saima Riazuddin, Robert Fettiplace, William R. Schafer, Gregory I. Frolenkov & Zubair M. Ahmed in Nature Communications. Published online June 29 2017 doi:10.1038/s41467-017-00061-1
Trump Thinks Healthcare Is Something You Can Win
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