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FactsheetsAge-related hearing loss (presbyacusis)Age-related hearing loss (known medically as presbyacusis) is the most common cause of hearing loss in older people. An interview with the chair of the IMPC, Professor Steve Brown, has been published in the science magazine International Innovation, a global dissemination resource that provides insight and analysis on current scientific research trends.
Dr Acevedo-Arozena led research on a mouse with the same mutation as a familial form of amyotrophic lateral sclerosis, which may provide new insights into the how the disease develops.
Indicators of neurodegeneration (red, green) seen in the lumbar spinal cord of 52 week old Sod1 mutant mice. Amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, is a neurodegenerative disease that affects motor neurons. A newly discovered mouse line, which shares the same gene mutation as found in a type of ALS, has been described for the first time by a team led by Abraham Acevedo-Arozena together with collaborators from the UCL Institute of Neurology.
Familial ALS accounts for around 10% of all cases, caused by gene mutations that can be inherited.
While there are already numerous mouse models of SOD1 ALS in existence, all overexpress the human gene, producing excessive amounts of the mutant protein.
This is the first mouse model described that has the equivalent of a human ALS mutation in the mouse Sod1 gene. Down’s syndrome is an extremely debilitating condition, caused by the whole or partial presence of a third copy of chromosome 21. While there are many mouse models of Down’s syndrome, none fully replicate all of the symptoms, so different models are used to study different aspects of the condition.
The Tc1 model is trans-species, expressing most of human chromosome 21, which adds to the two copies of the equivalent chromosome that mice already have. The researchers used two complementary methods, circadian wheel running and video tracking, to monitor a group of male Tc1 mice and compare their behaviour to a set of ordinary male mice. Taken together, these findings point towards Tc1 as a model that could prove extremely useful for future research into the sleep patterns of those with Down’s syndrome, helping us understand why so many people with the condition have trouble getting a good night’s sleep. MRC Harwell is an International Centre for Mouse Genetics at the forefront of studies in mouse functional genomics and mouse models of human disease.
MRC Harwell offers first class opportunities for PhD students including a formal training programme.
The Mary Lyon Centre at MRC Harwell is one of the best state-of-the-art SPF mouse facilities in Europe. Award of an MRC-funded studentship within the Unit is conditional on achieving a first-class or 2.1 honours degree, or equivalent, in a biological science or related discipline. Being out of sync with your body clock may affect your metabolism, leading to obesity and disease. Just as travelling to a different time zone can make you feel more inclined to curl up in bed at midday than grab a bite for lunch, you can get ‘social jetlag’ from living slightly out of sync with your body clock on a weekly basis. Social jetlag occurs when you have a mismatch between the times that you sleep during the working week and on your days off. While the rise of obesity in the West is generally attributed to high calorie diets and a sedentary lifestyle, there is growing evidence that disruptions to our internal body clock such as those caused by social jetlag may also play a role. To investigate the effects of social jetlag on obesity and risk factors for associated diseases such as type 2 diabetes, Michael Parsons and Pat Nolan joined forces with researchers in London, the USA and New Zealand. When they were 38 years old, these participants underwent a series of tests to assess their BMI, fat mass and girth, as well as indicators of inflammation and diabetes, used to determine if they were obese and showed any signs of obesity-related disease. While more research is required to determine the underlying cause for this correlation, this research suggests that cutting down on social jetlag could help us stay healthy. It is with great sadness that we have learnt of the death of Mary Lyon, aged 89, on Christmas Day.
Mary was a colleague and friend to all of us, and was pivotal in leading and developing mouse genetics at Harwell.
In her own quiet way, she was a tremendous inspiration and supporter of young scientists and all those who were starting out in a career in genetics.
Her legacy will be recognised through the Mary Lyon Centre and the continuing work in mouse genetics at MRC Harwell. So far, genetic research into age-related hearing loss in patients has yielded little insight.
Loss of hair cells in the inner ear of the trombone mouse model aged 6 months (left) and 9 months (right).
It is now possible to study the genetics of large cohorts of patients using techniques such as genome-wide association studies and exome sequencing, which enable links to be made between gene variants and disease. This is especially true for age-related hearing loss, where the results from such studies with patients have been difficult to interpret. A mini review by Mike Bowl, published in Gerontology, has investigated how we can combine our knowledge from mouse and human studies to further research into the genetics of age-related hearing loss. Establishing good mouse models will allow researchers to investigate the onset and progression of the disease at the cellular level, something which is not possible in patients.
Often mistakenly assumed to be an inherent part of the ageing process, progressive hearing loss in old age is the most common kind of sensory loss experienced by the elderly. Beginning with high-pitched noises and progressing to deeper sounds, the person gradually loses the ability to hear.
During age-related hearing loss, these vital hair cells are lost and the person loses the ability to hear. Such knowledge is crucial for developing better treatments, such as gene therapy, antioxidant treatments or stem cell therapy, which hold the potential to prevent, lessen or even reverse hearing loss in old age. Research into age-related hearing loss presents a number of challenges, not least of which is that all of the interesting changes happen in the cochlea, which is encased within the temporal bone - the hardest bone in the body. To add to this, age-related hearing loss is extremely complex and likely to have multiple causes, including a variety of genetic and environmental factors. This reciprocal, integrated approach, combining our knowledge from studies in both patients and animals, has the potential to reveal new insights into this complex and common disease. Old age affects our circadian clocks, disturbing our sleep at night and increasing the frequency of daytime naps. It’s well known that old people have a tendency to drop off in their armchair and stir during the night, but exactly why this happens is still somewhat puzzling. One way in which we can investigate it is to use the mouse, specifically strains that are tested over their lifetime to monitor the ageing process.
The mammalian circadian clock will continue to maintain a sleep-wake cycle in the absence of any cues, but it is only really useful when it is ‘entrained’ to work in response to light. To assess the circadian system in the mouse strains, the researchers used a variety of methods. As all of the mouse strains aged, their sleep became more fragmented and they woke more often. This strain could therefore be used to study exactly what happens to alter our circadian system as we age, and potentially develop a way to alleviate the more disruptive aspects, allowing people to make the most of their golden years.
Nodal cilia from wild type mice (left), compared to Atmin and Dynll1 mutants (middle and right). Cilia are small hair-like protrusions that extend from the surface of cells, and are known to play diverse roles in the body, from being required for certain kinds of cell-to-cell signalling to acting as flow sensors. Both Atmin and Dynll1 mutant cells had fewer and shorter cilia than normal, and any present appeared stunted.
To explain how the stunted cilia in these mutant mice lead to abnormal lung development, the researchers considered their role in signalling. This discovery has begun to unravel the vital role of cilia in mammalian development and disease. Age-related hearing loss is on the rise and, on average, it takes 7-10 years for someone with a hearing loss to start looking for help.
Having hearing loss leads someone to be less aware of their surroundings and therefore more likely to fall. If either #2 or 3 are right, then getting a hearing aid or hearing implant could reduce the chances of falling. Having hearing loss tends to mean that someone does less physical activity.4 A moderate or worse hearing loss is associated with lower levels of physical activity. As we’ve said, studies are indicating that hearing aids and hearing implants might help someone deal with these effects. For someone who’s eligible to receive a hearing implant, implantation is a routine procedure and there’s no upper age limit.6 Some recipients have been older than 90 when they got their hearing implant.
About this blog:This is the official blog of MED-EL, a leader in implantable hearing loss solutions. Sensory presbycusis: This refers to epithelial atrophy with loss of sensory hair cells and supporting cells in the organ of Corti.
Mechanical (ie, cochlear conductive) presbycusis: This condition results from thickening and secondary stiffening of the basilar membrane of the cochlea. The rest of my answer is based on this book, some parts of which exist online (which I'll quote).
As you can see from the graph, severity of age-related hearing loss depends on sound frequency: older people need high-pitched sounds to be displayed more loudly, in order to hear them. It's not described much on the website, but the book explains that there is a relationship between how loud a sound has to be to harm you, and which frequency it is.
Here's a plot of the connection between loudness and frequency in auditory perception, in which you can see that sounds around 4kHz can most easily harm us. Does this explain that when I was younger, I was more sensitive to sound and slept less well?
Not the answer you're looking for?Browse other questions tagged medical-science or ask your own question. If a caster uses a higher level slot for Enhance Ability, can they specify different effects for different targets?

New employer wants me to pay for ISO 9001 accreditation before employment begins - is this a scam?
The article contemplates the curious phenomenon that, while glasses are acceptable and widely used to correct defective vision, hearing aids seem to imply to many people that their wearers are past it. Things are quite different with hearing, which can deteriorate considerably before we have the slightest inkling that things were not what they used to be. Yet by the time we are into our 40's many if not most of us will have lost a distinct and easily measurable amount of our hearing abilities compared to when we were younger - in our 20's and earlier - and the effects are progressive thereafter. This societal phenomenon results in some in middle age and beyond insisting there is nothing wrong with their hearing despite the fact they need the TV turned up so loud that it drives everybody else to distraction, or blaming others for speaking indistinctly when they do nothing of the sort, or having no idea what turn the conversation has taken in a noisy restaurant. In the UK one reason why consultations with audiologists are far too rare is because of the inexcusable lack of investment in diagnosing and treating hearing problems.
It is a salutary experience to perform a rough check on one's hearing by employing the services of the younger members of the family.
The curves in Figure 1 below show how we progressively lose the ability to hear the higher frequencies as we age.
The sensitivity measurement on the vertical axis can be thought of as the amplitude of a pure tone (sine wave) at a given frequency which, when applied to headphones, just results in the perception of a sound at that frequency.
The lowest curve in Figure 1, labelled "20", is an average plot of the performance of a healthy ear of around that age.
By the time men are 60 the difference is about 45 dB (the voltage now needs to be nearly 200 times larger than at age 20, a considerable amount). A feature of high frequency deafness for either gender is that it becomes total beyond a certain cut-off frequency - no matter how loud the sound beyond that point, we cannot hear it at all. A practical consequence of all this is that if you need the sound turned up more loudly than those with better hearing before you can follow the dialogue on TV programmes, it is virtually certain you will also have more difficulty hearing the top notes of an organ than they do. Professional musicians and musical instrument technicians are potentially more at risk from another form of hearing degradation than members of the general population because of the high sound levels many of them are subjected to during the course of their work. Pipe organ voicers and tuners are similarly at risk, particularly when called on to spend hours or days on end voicing and regulating loud reeds or mixtures. The four short mp3 sound samples of an organ piece below are an attempt to demonstrate the progressive effects of age related hearing loss so that the foregoing remarks can perhaps be related to real life more easily. The file entitled "age 20" represents the more or less perfect hearing which someone of that age or younger would normally enjoy.
The sound sample entitled "age 40" is exactly the same extract as that above but now processed to represent the sound which an average male around age 40 might perceive.
The "age 60" and "age 80" sample files were produced in the same way, by processing the original "age 20" file in each case but with the progressive hearing deterioration suggested by the corresponding data in Figure 1.
It should be noted that the effects you perceive when listening to these samples will only have meaning if your hearing is good to start with (corresponding to the age 20 data in Figure 1). As a rough guide of what to expect, I played these sound files to some people with excellent hearing but with varying experience of (and liking for!) organ music. It goes without saying that your sound system should be very good when listening to these samples, with loudspeakers of a quality comparable to audiophile headphones such as the Sennheiser HD 650. There are two main implications of age related hearing loss for organists and the listeners in their audience. The second implication of age-impaired hearing concerns tone quality or timbre, which is strongly influenced by the relative proportions of harmonics in the sounds. It is also important to consider the effects of hearing loss on an organ builder, and particularly a voicer. In the previous section the effects of hearing loss on organists and listeners were discussed by relating it to the regulation and tonal characteristics of the organ being played.
Eventually it is quite possible that the voicer would cease to be able to hear such a pipe.
At quite an early stage in the ageing process, by mid-career, a voicer's aural judgement of the timbre of pipes much lower in the keyboard will have probably changed also.
Therefore the sound samples discussed earlier are just as relevant to the voicer's situation as they are to the player and the listener. As well as regulation and the timbre of the pipes, there is a third implication for organ builders of high frequency deafness, and this concerns tuning. Fortunately we need take the discussion on tuning no further in view of the widespread use of electronic tuning aids, which enable tuners to continue to tune pipes which they can no longer hear.
The tonal quality of organs is frequently and sometimes hotly debated, and it must surely be the case that some of the issues involve genuine differences in the hearing abilities of some of those who participate in the discussions. Another reason is that many of the participants in the discussions are probably blithely unaware of the importance that the state of their hearing plays in the positions they adopt, and only a minority will have visited an audiologist. However one or two examples do exist where one can legitimately enquire as to whether failing hearing played a role. Interestingly, the organ in Manchester's Bridgewater Hall (see above) which has been heavily censured by a number of players and experts is also by Marcussen.
If the answer to either is in the affirmative, it begs the additional question of whether the individuals involved are actually aware of the state of their hearing. There are many implications of this unfortunate dichotomy relating to two of our principal senses. Until society stands its current values relating to defective hearing on its head, we will not be able to emerge from the miasma of uncertainty outlined in this article.
In the article, he explains the consortium's achievements to date, our intentions for the future, and why it will be an unparalleled resource for research into mouse genetics and human disease. It causes muscle weakness and paralysis, and gradually worsens over time, typically lasting for around three to five years before death. Mutations in the gene for superoxide dismutase 1 (SOD1) are known to cause a large proportion of these familial ALS cases, and some research has indicated that defects in SOD1 may also underlie other forms of sporadic ALS.
They identified a mouse line with a chemically induced point mutation in the mouse gene Sod1, and found it to be exactly the same as one seen in patients with a type of familial SOD1 ALS. It provides a new model, which can be used to study the early stages of ALS and develop new treatments to reduce the burden of this terrible disease. New research by Pat Nolan’s group shows this is shared by Tc1 mice, providing a model for future studies.
It affects about 1 in 700 babies born, and comes with a whole host of health issues, including intellectual disability, early onset dementia and heart and gut problems.
Pat Nolan led research at MRC Harwell and the Nuffield Department of Clinical Neurosciences, published in Genes, Brain and Behavior, to investigate whether the Tc1 mouse model could be used to study these sleep disturbances.
It is the most complete genetic model of Down’s syndrome, with many characteristics of someone with the condition, including learning and memory problems. The circadian wheel method tracks when they are running on their wheel and uses this as measure of their activity, whereas video monitoring tracked when they were immobile and took this as a measure of sleep.
During the night, the Tc1 mice displayed an initial period of total hyperactivity, barely stopping at all for the first six hours and had a lower number of sleep episodes (our equivalent of a nap) during their active phase. We are engaged in lifetime studies – from developmental abnormalities through to diseases of ageing.
Students join a 4-year PhD programme that includes an initial six-month induction and rotation across two laboratories of their choice before selecting and embarking on their research project. While this may have less of an obvious effect than travel jetlag, in the long term it could harm our health. Perhaps you prefer to lie in at the weekends, but during the week you have to get up early for work. They gave 815 New Zealanders who were part of the Dunedin Longitudinal Study a questionnaire to fill in to assess their sleeping habits.
This adds to growing evidence for a link between social jetlag and obesity, and particularly highlights how social jetlag could increase our risk of obesity-related diseases. She was one of the foremost geneticists of the 20th century, and with the discovery of X inactivation and her work on the t complex, she brought fundamental and profound insights to mammalian genetics and the genetic bases of disease.
She would never fail to give good advice and forthright opinions to all who sought her counsel.
She remained very involved in science after retirement, and continued to follow and contribute to current developments in mammalian genetics.
A reciprocal approach, combining patient data with results from mouse models, could provide the answer. However, these approaches only indicate which genes might be involved, and cannot tell us how these could lead to the disease. While these studies have identified possible contributory genes, none of the associations have been particularly pronounced. This will improve our understanding of the causes of one of the most common forms of hearing loss. Age-related hearing loss, also known as presbycusis, affects 31% of people in their sixties and 63% of those over 70, and our ageing population means that these are expected to rise. Less able to hear conversations, people with age-related hearing loss can experience social isolation, depression and cognitive decline. These vibrations are transferred along a chain of tiny bones, causing the last in the chain to knock against a small window in a fluid-filled structure shaped like a snail’s shell. However, we lack detailed knowledge of the underlying processes that cause these hair cells to be lost, meaning more research is needed to understand exactly how and why this happens. This means that the inner ear can only be examined post-mortem in patients, making it difficult to determine if what you see is the primary cause of the hearing loss or a secondary event occurring much later. However, if you have a good model, every mouse within that line should have the same genetic makeup and live in the same environment, so should develop hearing loss in the same way.

Perhaps, with our ageing population, it will lead to new treatments at a time when we need them most. And because we are now living so much longer than previous generations, it’s in all our interests to discover what is really going on. Pat Nolan has led research, published in Neurobiology of Aging, which compared how the sleep patterns of four inbred mouse strains change as they age, and identified how these can model sleep in human ageing. While daylight is the trigger for us to wake up, mice are nocturnal, so it instead results in them falling asleep. They tested the visual health of the mice by placing them in enclosure surrounded by computer monitors and measuring how well they could track a pattern that rotated around them. Shortened, stumpy cilia can be seen in the Atmin mutant, while Dynll1 cilia bulge at their base.
Research led by Dominic Norris, published in Development, into the underlying genetics of mouse lines with short cilia and underdeveloped lungs has helped explain the essential role of the Atmin gene in lung development.
Some cilia are motile, such as those lining the wind pipe, which beat so as to clear mucus from the lungs. In order for cilia to grow, proteins must be carried to the tip, where they are added onto the cilium.
Yet when functional DYNLL1 protein was added to Atmin mutant cells, the cilia were ‘rescued’. Particularly puzzling was the bulges they observed at the bottom of the Dynll1 mutant cilia – if retrograde transport is disrupted, you would expect everything to get stuck at the tip of the cilia, and therefore would expect to see a bulge at the top. Someone with age-related hearing loss relies more on assistance from friends and family, is less likely to participate in group activities, and goes to the doctor less frequently than they should. It makes sense that someone who can’t hear well has difficulties communicating in many environments like social activities and family gatherings.
It is a place where you can connect with MED-EL and learn all about hearing and hearing implants. Characteristically, presbycusis involves bilateral high-frequency hearing loss associated with difficulty in speech discrimination and central auditory processing of information.
This process originates in the basal turn of the cochlea and slowly progresses toward the apex.
The thickening is more severe in the basal turn of the cochlea where the basilar membrane is narrow. The question is being unable to hear ranges as we get older, starting from childhood, while presbycusis is specific to post middle-aged people. Sounds that are near our auditory thresholds (under 20 Hz and above 20.000 Hz in the normal, healthy hearing range) can't harm us even if they are extremely loud.
People with ALS have a weak grip, difficulty moving and walking, and problems breathing and swallowing. Normally, the main function of SOD1 is to remove superoxide radicals, preventing their accumulation from causing oxidative damage to the cell. This raises concerns about whether the neurodegeneration and other effects seen in these models are actually due to the mutation, or just the fact that the gene is overexpressed. As the mice aged, they developed signs of reactive gliosis (an indicator of damaged neurons), gradual degeneration of their motor neurons, and a loss of nerve contact with muscles in the hind limbs.
A less well known feature of Down’s syndrome is an unusual sleep pattern - patients with Down’s syndrome tend to be sleepier during the day, wake more during the night and take longer to get to sleep. It also avoids the confounding issue found in other models of additional, irrelevant chromosome regions also being duplicated.
When the researchers later added a 3 hour pulse of light in the middle of the night, which normally triggers sleep, they found it had little effect in inducing sleep on the Tc1 mice - they stayed active and took much longer to settle down and go to sleep. It is an exciting time for the IMPC, with over 1,500 lines now phenotyped and big plans being put in place for Stage 2, and it was great to catch up with mouse network members from all over the UK. Research by Parsons et al., published in the International Journal of Obesity, suggests those with social jetlag run a higher risk of developing obesity-related diseases. This mismatch is thought that to set your circadian clock off kilter, which not only controls when you fall asleep and wake up, but also keeps your metabolism in check.
This could be due to many different factors – perhaps these people just have a greater tendency to eat a poor diet and do less exercise, or maybe social jetlag causes changes in the expression of genes that regulate our metabolism. Since these diseases include some of the biggest killers in the western world, cutting down on social jetlag and working in sync with our body clock could help us live a long and healthy life. Her accomplishments were widely recognised by many international honours and prizes, and she was a formidable icon to all woman making their way in science. We celebrate her life and contributions to genetics - she was one of the greats of British science. By taking a human-to-mouse approach, it is possible to see whether mice with the same genes as those identified in patients develop the disease symptoms, therefore proving that the disease is caused by these genes.
This is the cochlea, which houses the tiny hair cells that detect the vibrations and transmit the signal to the brain to interpret. This means that you can investigate the progression of the disease at various stages, from the initial trigger to the end result, and record the effect it has on their ability to hear.
Despite this, in all other respects the sleep pattern of mice closely resembles that of humans, making them an excellent model to study the effect of ageing on this system. They also tested for cataracts and the ability of the pupil to constrict in response to light.
With these varied roles, it is perhaps unsurprising that the symptoms of ciliopathies can vary considerably. Molecular motors ‘walk’ up and down the cilium to transport these proteins as cargo - kinesin transports cargo up to the tip (‘anterograde’ transport), whereas cytoplasmic-dynein-2 transports cargo down to the base (‘retrograde’ transport). One of these, the ‘hedgehog’ signalling pathway, is known to require fully developed cilia. They suggest that this might be due to another motor protein component taking up the slack, or possibly that the only aspect disrupted is the release from the base of the cilium. Surprisingly, they’re often the last person to recognize how hearing loss is affecting them and their loved ones.
Scientists are studying whether getting a hearing aid or hearing implant can delay or prevent dementia. This can make them feel removed from friends and family and can be the first step towards social isolation and, many times, towards depression. Association between hearing impairment and lower levels of physical activity in older adults. These changes correlate with a precipitous drop in the high-frequency thresholds, which begins after middle age. This correlates with a gradually sloping high-frequency sensorineural hearing loss that is slowly progressive.
The wiki page does refer to the issue as presbycusis, yet every reliable source on presbycusis lists it as being limited to post middle-aged people. We don't hear them because they cause no mechanical change in our ear that responds to those frequencies, and consequently no harm is done. However, the mutant variety of SOD1 takes on a new, toxic function that ultimately leads to the death of the motor neurons that control muscle movement. The mice lost grip strength, developed tremors and an odd gait, and become severely hunched as their back muscles weakened.
And while most people recover from travel jetlag within a day or two, social jetlag can continue for a person’s entire life, so could have long-lasting effects on your health.
This pathway and was found to be working less efficiently in their lungs, and deficient signalling due to stunted cilia almost certainly interfered with normal lung development in these embryos.
The abrupt downward slope of the audiogram begins above the speech frequencies; therefore, speech discrimination is often preserved. It seems the wiki page is the only source referring to range of audible frequencies in young people as presbycusis?
In the case of age-related hearing loss, the hair cells in the inner ear that should respond to high-frequency sounds, have already stopped responding, so there is nothing left to harm.
However, mutant mice do not progress to end-stage disease, and therefore do not become paralysed. Together the many junior members of the Unit contribute to a vibrant atmosphere providing a supportive environment for the development of future leaders in mouse genetics and the life sciences. Histologically, the atrophy may be limited to only the first few millimeters of the basal end of the cochlea.
As a young person in their teens, he or she will usually have been able to hear frequencies up to 16 kHz or beyond with no difficulty.
The researchers also found indicators that the mitochondria in their motor neurons were malfunctioning, often considered an important factor in the development of ALS in patients. This was done at five different stages of their life, and the results were used to determine what happened to their circadian system as they got older.
One theory proposes that these changes are due to the accumulation of lipofuscin pigment granules.

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29.04.2016 admin

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