1. Some patients with dementia may experience delayed-onset PTSD

    July 21, 2017 by Ashley

    From the Wiley press release:

    Delayed-onset post-traumatic symptoms in the elderly may be misdiagnosed as falling under the umbrella of behavioural and psychological symptoms of dementia (BPSD), according to a recent review.

    The review describes three cases where post-traumatic stress disorder (PTSD) symptoms are experienced by patients suffering with dementia long after the original traumatic event.

    Considering PTSD in individuals with dementia is important because PTSD is usually associated with working-age adults and is infrequently diagnosed in the elderly. In the early stages of dementia, recognising early life trauma may enable patients to access psychological therapy prior to significant cognitive decline. In patients with more advanced dementias, an awareness of earlier trauma exposure can help clinicians differentiate between delayed PTSD and BPSD in patients suffering with emotional and behavioural disturbances.

    “Every patient with dementia has a unique narrative, which if captured in the earlier stages of the disease, enables clinicians and their families to understand the origin of their distress. Therefore, it is important to look for a history of previous trauma in patients with BPSD as this could be due to delayed onset PTSD,” said Dr. Tarun Kuruvilla, senior author of the Progress in Neurology & Psychiatry review.


  2. Study suggests Alzheimer’s disease patients with psychosis more likely to be misdiagnosed

    July 18, 2017 by Ashley

    From the St. Michael’s Hospital press release:

    People with Alzheimer’s disease who experience psychosis — including delusions and hallucinations — are five times more likely to be misdiagnosed with dementia with Lewy bodies compared to patients who do not, new research suggests.

    Alzheimer’s disease is a type of dementia characterized by protein deposits in the brain including twisted fibers found inside brain cells. Dementia with Lewy bodies is believed to be caused by the buildup of a different abnormal protein aggregate found in nerve cells in the brain. Effective treatments for these conditions are still under development, but will almost certainly be different, according to the authors.

    Researchers also found that Alzheimer’s disease was misdiagnosed in 24 per cent of all cases, with false positive and false negative rates both being 12 per cent. Previous research suggested that the rate of misdiagnosis in Alzheimer’s disease ranged from 12-23 per cent.

    The findings, published online in Alzheimer’s & Dementia: Translational Research & Clinical Interventions, raise concern that there may be an under appreciation of how common psychotic symptoms are in Alzheimer’s disease, said Dr. Corinne Fischer, director of the Memory Disorders Clinic at St. Michael’s Hospital in Toronto and lead author of the study.

    “Psychosis can be a symptom of Alzheimer’s disease, but it is a defining clinical feature in other types of dementia, including Parkinson’s disease related dementia and dementia with Lewy bodies,” she said. “Consequently, clinicians are more reluctant to diagnose a patient with Alzheimer’s disease when they present with delusions or hallucinations.”

    About 36 per cent of people with Alzheimer’s are thought to have delusions and 18 per cent have hallucinations. Psychotic symptoms are significant in Alzheimer’s patients because they have been shown to be associated with increased burden on caregivers, increased functional decline and more rapid progression of the disease.

    Researchers examined 961 people using data from the National Alzheimer’s Coordinating Centre database, collected from 29 Alzheimer’s disease centres in the United States between 2005 and 2012. They included participants who had been clinically diagnosed with Alzheimer’s while they were alive, as well as those whose autopsies showed they the signature physical signs of Alzheimer’s in their brains.

    Patients who experienced psychosis had a higher rate of false negative diagnosis and a lower rate of false positive diagnosis of Alzheimer’s disease compared to those who did not. Whether patients experienced delusions, hallucinations, or a combination of both did not affect the rate of misdiagnosis, according to the authors.

    The Alzheimer’s Society of Canada estimates there are 564,000 people living with dementia in Canada, and that number is expected to almost double over the next 15 years, thus reinforcing the relevance of the study’s findings according to Winnie Qian, a Master’s student in the Neuroscience Research Program at St. Michael’s and an author on the study.

    “An advantage of our study is that we used the final clinical diagnosis after years of follow-up, so the rate of misdiagnosis we described is the rate under ideal conditions,” she said.

    “This means that it should be considered a minimum. If you extrapolate that and apply it to the general population, the magnitude of the problem could be much greater.”

    Dr. Fischer said when patients do not present with psychosis, clinicians should be more careful when considering alternative diagnoses to Alzheimer’s disease.

    “Many dementia patients never receive a definitive clinical diagnosis while they’re alive, so the hope is that by understanding what factors can lead to a misdiagnosis, we can be more accurate and provide patients with the best possible care,” she said.


  3. Alzheimer’s disease risk linked to a network of genes associated with myeloid cells

    July 16, 2017 by Ashley

    From The Mount Sinai Hospital / Mount Sinai School of Medicine press release:

    Many genes linked to late-onset Alzheimer’s disease (AD) are expressed in myeloid cells and regulated by a single protein, according to research conducted at the Icahn School of Medicine at Mount Sinai and published June 19 in the journal Nature Neuroscience.

    Mount Sinai researchers led an international, genome-wide study of more than 40,000 people with and without the disease and found that innate immune cells of the myeloid lineage play an even more central role in Alzheimer’s disease pathogenesis than previously thought.

    Specifically, the research team identified a network of genes that are implicated in AD and expressed by myeloid cells, innate immune cells that include microglia and macrophages. Furthermore, researchers identified the transcription factor PU.1, a protein that regulates gene expression and, thus, cell identity and function, as a master regulator of this gene network.

    “Our findings show that a large proportion of the genetic risk for late-onset AD is explained by genes that are expressed in myeloid cells, and not other cell types,” says Alison Goate, DPhil, Professor of Neuroscience and Director of The Ronald M. Loeb Center for Alzheimer’s Disease at the Icahn School of Medicine at Mount Sinai and principal author of the study. “Dysregulation of this network is certainly a cause of Alzheimer’s, but we have more work to do to better understand this network and regulation by PU.1, to reveal promising therapeutic targets.”

    Using a combination of genetic approaches to analyze the genomes of 14,406 AD patients, and 25,849 control patients who do not have the disease, researchers found that many genes which are known to influence the age at which AD sets in, are expressed in myeloid cells. This work pinpointed SPI1, a gene that encodes the transcription factor PU.1, as a major regulator of this network of AD risk genes and demonstrated that lower levels of SPI1/PU.1 are associated with later age at onset of AD.

    To test the hypothesis that SPI1 expression levels influence expression of other AD risk genes and microglial function, the researchers used a mouse microglial cell line, BV2 cells that can be cultured in a dish. When researchers knocked down expression of SPI1, the gene that produces PU.1 in cells, they found that the cells showed lower phagocytic activity (engulfment of particles), while overexpression of SPI1 led to increased phagocytic activity. Many other AD genes expressed in microglia also showed altered expression in response to this manipulation of SPI1 expression.

    “Experimentally altering PU.1 levels correlated with phagocytic activity of mouse microglial cells and the expression of multiple AD genes involved in diverse biological processes of myeloid cells,” says Dr. Goate. “SPI1/PU.1 expression may be a master regulator capable of tipping the balance toward a neuroprotective or a neurotoxic microglial function.”

    The researchers stress that because the PU.1 transcription factor regulates many genes in myeloid cells, the protein itself may not be a good therapeutic target. Instead, further studies of PU.1’s role in microglia and AD pathogenesis are necessary, as they may reveal promising downstream targets that may be more effective in modulating AD risk without broad effects on microglial function. Increased understanding is crucial to facilitating the development of novel therapeutic targets for a disease that currently has no cure.


  4. Alzheimer’s gene associated with failure to adapt to cognitive challenge in healthy adults

    July 15, 2017 by Ashley

    From the Society for Neuroscience press release:

    Healthy adults carrying the gene APOE4 — the strongest known genetic risk factor for Alzheimer’s disease (AD) — may struggle to adapt their brain activity to increasing cognitive demands as they get older, according to a study published in The Journal of Neuroscience. This age-related effect, which was not observed in people without the risk factor, suggests that interventions targeting cognitive decline in at-risk populations may need to begin many years before any symptoms of the disease emerge in order to be effective.

    Karen Rodrigue and colleagues assessed the performance of 31 adults (ages 20-86) with APOE4 on a distance judgment task at different levels of difficulty while measuring their brain activity. Although these at-risk participants showed similar adjustment in brain activity to the difficulty of the task as non-APOE4 carrying adults of the same age, sex, and education level, this ability declined with increasing age in the individuals with APOE4. These changes occurred in the precuneus, a part of the brain implicated in the early stages of AD, and reduced modulation of this area was associated with poorer performance on the task. These findings may help to inform the identification of individuals at increased risk of developing the disease.


  5. Alzheimer’s and Parkinson’s spurred by same enzyme

    July 12, 2017 by Ashley

    From the Emory Health Sciences press release:

    Alzheimer’s disease and Parkinson’s disease are not the same. They affect different regions of the brain and have distinct genetic and environmental risk factors.

    But at the biochemical level, these two neurodegenerative diseases start to look similar. That’s how Emory scientists led by Keqiang Ye, PhD, landed on a potential drug target for Parkinson’s.

    In both Alzheimer’s (AD) and Parkinson’s (PD), a sticky protein forms toxic clumps in brain cells. In AD, the troublemaker inside cells is called tau, making up neurofibrillary tangles. In PD, the sticky protein is alpha-synuclein, forming Lewy bodies.

    Ye and his colleagues had previously identified an enzyme (asparagine endopeptidase or AEP) that trims tau in a way that makes it more sticky and toxic. Drugs that inhibit AEP have beneficial effects in Alzheimer’s animal models.

    In a new Nature Structural and Molecular Biology paper, Emory researchers show that AEP acts in the same way toward alpha-synuclein.

    “In Parkinson’s, alpha-synuclein behaves much like Tau in Alzheimer’s,” Ye says. “We reasoned that if AEP cuts Tau, it’s very likely that it will cut alpha-synuclein too.”

    A particular chunk of alpha-synuclein produced by AEP’s scissors can be found in samples of brain tissue from patients with PD, but not in control samples, Ye’s team found.

    In control brain samples AEP was confined to lysosomes, parts of the cell with a garbage disposal function. But in PD samples, AEP was leaking out of the lysosomes to the rest of the cell.

    The researchers also observed that the chunk of alpha-synuclein generated by AEP is more likely to aggregate into clumps than the full length protein, and is more toxic when introduced into cells or mouse brains. In addition, alpha-synuclein mutated so that AEP can’t cut it is less toxic.

    Ye cautions that AEP is not the only enzyme that cuts alpha-synuclein into various toxic pieces, and the full-length alpha-synuclein protein is still able to aggregate and cause harm. Nevertheless, he says his team is moving on to testing drugs that inhibit AEP in Parkinson’s animal models.


  6. Interventions to prevent cognitive decline, dementia

    July 11, 2017 by Ashley

    From the National Academies of Sciences, Engineering, and Medicine press release:

    Cognitive training, blood pressure management for people with hypertension, and increased physical activity all show modest but inconclusive evidence that they can help prevent cognitive decline and dementia, but there is insufficient evidence to support a public health campaign encouraging their adoption, says a new report from the National Academies of Sciences, Engineering, and Medicine. Additional research is needed to further understand and gain confidence in their effectiveness, said the committee that conducted the study and wrote the report.

    “There is good cause for hope that in the next several years much more will be known about how to prevent cognitive decline and dementia, as more clinical trial results become available and more evidence emerges,” said Alan I. Leshner, chair of the committee and CEO emeritus, American Association for the Advancement of Science. “Even though clinical trials have not conclusively supported the three interventions discussed in our report, the evidence is strong enough to suggest the public should at least have access to these results to help inform their decisions about how they can invest their time and resources to maintain brain health with aging.”

    An earlier systematic review published in 2010 by the Agency for Healthcare Research and Quality (AHRQ) and an associated “state of the science” conference at the National Institutes of Health had concluded that there was insufficient evidence to make recommendations about any interventions to prevent cognitive decline and dementia. Since then, understanding of the pathological processes that result in dementia has advanced significantly, and a number of clinical trials of potential preventive interventions have been completed and published. In 2015, the National Institute on Aging (NIA) contracted with AHRQ to conduct another systematic review of the current evidence. NIA also asked the National Academies to convene an expert committee to help inform the design of the AHRQ review and then use the results to make recommendations to inform the development of public health messaging, as well as recommendations for future research. This report examines the most recent evidence on steps that can be taken to prevent, slow, or delay the onset of mild cognitive impairment and clinical Alzheimer’s-type dementia as well as steps that can delay or slow age-related cognitive decline.

    Overall, the committee determined that despite an array of advances in understanding cognitive decline and dementia, the available evidence on interventions derived from randomized controlled trials — considered the gold standard of evidence — remains relatively limited and has significant shortcomings. Based on the totality of available evidence, however, the committee concluded that three classes of interventions can be described as supported by encouraging but inconclusive evidence. These interventions are:

    cognitive training — which includes programs aimed at enhancing reasoning and problem solving, memory, and speed of processing — to delay or slow age-related cognitive decline. Such structured training exercises may or may not be computer-based. blood pressure management for people with hypertension — to prevent, delay, or slow clinical Alzheimer’s-type dementia. increased physical activity — to delay or slow age-related cognitive decline.

    Cognitive training has been the object of considerable interest and debate in both the academic and commercial sectors, particularly within the last 15 years. Good evidence shows that cognitive training can improve performance on a trained task, at least in the short term. However, debate has centered on evidence for long-term benefits and whether training in one domain, such as processing speed, yields benefits in others, such as in memory and reasoning, and if this can translate to maintaining independence in instrumental activities of daily living, such as driving and remembering to take medications. Evidence from one randomized controlled trial suggests that cognitive training delivered over time and in an interactive context can improve long-term cognitive function as well as help maintain independence in instrumental activities of daily living for adults with normal cognition. However, results from other randomized controlled trials that tested cognitive training were mixed.

    Managing blood pressure for people with hypertension, particularly during midlife — generally ages 35 to 65 years — is supported by encouraging but inconclusive evidence for preventing, delaying, and slowing clinical Alzheimer’s-type dementia, the committee said. The available evidence, together with the strong evidence for blood pressure management in preventing stroke and cardiovascular disease and the relative benefit/risk ratio of antihypertensive medications and lifestyle interventions, is sufficient to justify communication with the public regarding the use of blood pressure management, particularly during midlife, for preventing, delaying, and slowing clinical Alzheimer’s-type dementia, the report says.

    It is well-documented that physical activity has many health benefits, and some of these benefits — such as stroke prevention — are causally related to brain health. The AHRQ systematic review found that the pattern of randomized controlled trials results across different types of physical activity interventions provides an indication of the effectiveness of increased physical activity in delaying or slowing age-related cognitive decline, although these results were not consistently positive. However, several other considerations led the committee to conclude that the evidence is sufficient to justify communicating to the public that increased physical activity for delaying or slowing age-related cognitive decline is supported by encouraging but inconclusive evidence.

    None of the interventions evaluated in the AHRQ systematic review met the criteria for being supported by high-strength evidence, based on the quality of randomized controlled trials and the lack of consistently positive results across independent studies. This limitation suggests the need for additional research as well as methodological improvements in the future research. The National Institutes of Health and other interested organizations should support further research to strengthen the evidence base on cognitive training, blood pressure management, and increased physical activity, the committee said. Examples of research priorities for these three classes of interventions include evaluating the comparative effectiveness of different forms of cognitive training interventions; determining whether there are optimal blood pressure targets and approaches across different age ranges; and comparing the effects of different forms of physical activity.

    When funding research on preventing cognitive decline and dementia, the National Institutes of Health and other interested organizations should identify individuals who are at higher risk of cognitive decline and dementia; increase participation of underrepresented populations; begin more interventions at younger ages and have longer follow-up periods; use consistent cognitive outcome measures across trials to enable pooling; integrate robust cognitive outcome measures into trials with other primary purposes; include biomarkers as intermediate outcomes; and conduct large trials designed to test the effectiveness of an intervention in broad, routine clinical practices or community settings.


  7. Alzheimer’s disease study links brain health, physical activity

    July 7, 2017 by Ashley

    From the IOS Press press release:

    People at risk for Alzheimer’s disease who do more moderate-intensity physical activity, but not light-intensity physical activity, are more likely to have healthy patterns of glucose metabolism in their brain, according to a new UW-Madison study.

    Results of the research were published online in Journal of Alzheimer’s Disease. Senior author Dr. Ozioma Okonkwo, assistant professor of medicine, is a researcher at the Wisconsin Alzheimer’s Disease Research Center and the Wisconsin Alzheimer’s Institute at the UW School of Medicine and Public Health. First author Ryan Dougherty is a graduate student studying under the direction of Dr. Dane B. Cook, professor of kinesiology and a co-author of the study, and Dr. Okonkwo. The research involved 93 members of the Wisconsin Registry for Alzheimer’s Prevention (WRAP), which with more than 1,500 registrants is the largest parental history Alzheimer’s risk study group in the world.

    Researchers used accelerometers to measure the daily physical activity of participants, all of whom are in late middle-age and at high genetic risk for Alzheimer’s disease, but presently show no cognitive impairment. Activity levels were measured for one week, quantified, and analyzed. This approach allowed scientists to determine the amount of time each subject spent engaged in light, moderate, and vigorous levels of physical activity. Light physical activity is equivalent to walking slowly, while moderate is equivalent to a brisk walk and vigorous a strenuous run. Data on the intensities of physical activity were then statistically analyzed to determine how they corresponded with glucose metabolism — a measure of neuronal health and activity — in areas of the brain known to have depressed glucose metabolism in people with Alzheimer’s disease. To measure brain glucose metabolism, researchers used a specialized imaging technique called 18F-fluorodeoxyglucose positron emission tomography (FDG-PET).

    Moderate physical activity was associated with healthier (greater levels of) glucose metabolism in all brain regions analyzed. Researchers noted a step-wise benefit: subjects who spent at least 68 minutes per day engaged in moderate physical activity showed better glucose metabolism profiles than those who spent less time.

    “This study has implications for guiding exercise ‘prescriptions’ that could help protect the brain from Alzheimer’s disease,” said Dougherty. “While many people become discouraged about Alzheimer’s disease because they feel there’s little they can do to protect against it, these results suggest that engaging in moderate physical activity may slow down the progression of the disease.”

    “Seeing a quantifiable connection between moderate physical activity and brain health is an exciting first step,” said Okonkwo. He explained that ongoing research is focusing on better elucidating the neuroprotective effect of exercise against Alzheimer’s disease.


  8. Extra-virgin olive oil preserves memory, protects brain against Alzheimer’s

    July 4, 2017 by Ashley

    From the Temple University Health System press release:

    The Mediterranean diet, rich in plant-based foods, is associated with a variety of health benefits, including a lower incidence of dementia. Now, researchers at the Lewis Katz School of Medicine at Temple University (LKSOM) have identified a specific ingredient that protects against cognitive decline: extra-virgin olive oil, a major component of the Mediterranean diet. In a study published online June 21 in the Annals of Clinical and Translational Neurology, the researchers show that the consumption of extra-virgin olive oil protects memory and learning ability and reduces the formation of amyloid-beta plaques and neurofibrillary tangles in the brain — classic markers of Alzheimer’s disease.

    The Temple team also identified the mechanisms underlying the protective effects of extra-virgin olive oil. “We found that olive oil reduces brain inflammation but most importantly activates a process known as autophagy,” explained senior investigator Domenico Praticò, MD, Professor in the Departments of Pharmacology and Microbiology and the Center for Translational Medicine at LKSOM. Autophagy is the process by which cells break down and clear out intracellular debris and toxins, such as amyloid plaques and tau tangles.

    “Brain cells from mice fed diets enriched with extra-virgin olive oil had higher levels of autophagy and reduced levels of amyloid plaques and phosphorylated tau,” Dr. Praticò said. The latter substance, phosphorylated tau, is responsible for neurofibrillary tangles, which are suspected of contributing to the nerve cell dysfunction in the brain that is responsible for Alzheimer’s memory symptoms.

    Previous studies have suggested that the widespread use of extra-virgin olive oil in the diets of people living in the Mediterranean areas is largely responsible for the many health benefits linked to the Mediterranean diet. “The thinking is that extra-virgin olive oil is better than fruits and vegetables alone, and as a monounsaturated vegetable fat it is healthier than saturated animal fats,” according to Dr. Praticò.

    In order to investigate the relationship between extra-virgin olive oil and dementia, Dr. Praticò and colleagues used a well-established Alzheimer’s disease mouse model. Known as a triple transgenic model, the animals develop three key characteristics of the disease: memory impairment, amyloid plagues, and neurofibrillary tangles.

    The researchers divided the animals into two groups, one that received a chow diet enriched with extra-virgin olive oil and one that received the regular chow diet without it. The olive oil was introduced into the diet when the mice were six months old, before symptoms of Alzheimer’s disease begin to emerge in the animal model.

    In overall appearance, there was no difference between the two groups of animals. However, at age 9 months and 12 months, mice on the extra virgin olive oil-enriched diet performed significantly better on tests designed to evaluate working memory, spatial memory, and learning abilities.

    Studies of brain tissue from both groups of mice revealed dramatic differences in nerve cell appearance and function.

    “One thing that stood out immediately was synaptic integrity,” Dr. Praticò said. The integrity of the connections between neurons, known as synapses, were preserved in animals on the extra-virgin olive oil diet. In addition, compared to mice on a regular diet, brain cells from animals in the olive oil group showed a dramatic increase in nerve cell autophagy activation, which was ultimately responsible for the reduction in levels of amyloid plaques and phosphorylated tau.

    “This is an exciting finding for us,” explained Dr. Praticò. “Thanks to the autophagy activation, memory and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer’s disease were significantly reduced. This is a very important discovery, since we suspect that a reduction in autophagy marks the beginning of Alzheimer’s disease.”

    Dr. Praticò and colleagues plan next to investigate the effects of introducing extra-virgin olive oil into the diet of the same mice at 12 months of age, when they have already developed plaques and tangles. “Usually when a patient sees a doctor for suspected symptoms of dementia, the disease is already present,” Dr. Praticò added. “We want to know whether olive oil added at a later time point in the diet can stop or reverse the disease.”


  9. Alzheimer’s disease study links brain health and physical activity

    June 30, 2017 by Ashley

    From the IOS Press press release:

    People at risk for Alzheimer’s disease who do more moderate-intensity physical activity, but not light-intensity physical activity, are more likely to have healthy patterns of glucose metabolism in their brain, according to a new UW-Madison study.

    Results of the research were published today online in Journal of Alzheimer’s Disease. Senior author Dr. Ozioma Okonkwo, assistant professor of medicine, is a researcher at the Wisconsin Alzheimer’s Disease Research Center and the Wisconsin Alzheimer’s Institute at the UW School of Medicine and Public Health. First author Ryan Dougherty is a graduate student studying under the direction of Dr. Dane B. Cook, professor of kinesiology and a co-author of the study, and Dr. Okonkwo. The research involved 93 members of the Wisconsin Registry for Alzheimer’s Prevention (WRAP), which with more than 1,500 registrants is the largest parental history Alzheimer’s risk study group in the world.

    Researchers used accelerometers to measure the daily physical activity of participants, all of whom are in late middle-age and at high genetic risk for Alzheimer’s disease, but presently show no cognitive impairment. Activity levels were measured for one week, quantified, and analyzed. This approach allowed scientists to determine the amount of time each subject spent engaged in light, moderate, and vigorous levels of physical activity. Light physical activity is equivalent to walking slowly, while moderate is equivalent to a brisk walk and vigorous a strenuous run. Data on the intensities of physical activity were then statistically analyzed to determine how they corresponded with glucose metabolism–a measure of neuronal health and activity–in areas of the brain known to have depressed glucose metabolism in people with Alzheimer’s disease. To measure brain glucose metabolism, researchers used a specialized imaging technique called 18F-fluorodeoxyglucose positron emission tomography (FDG-PET).

    Moderate physical activity was associated with healthier (greater levels of) glucose metabolism in all brain regions analyzed. Researchers noted a step-wise benefit: subjects who spent at least 68 minutes per day engaged in moderate physical activity showed better glucose metabolism profiles than those who spent less time.

    “This study has implications for guiding exercise ‘prescriptions’ that could help protect the brain from Alzheimer’s disease,” said Dougherty. “While many people become discouraged about Alzheimer’s disease because they feel there’s little they can do to protect against it, these results suggest that engaging in moderate physical activity may slow down the progression of the disease.”

    “Seeing a quantifiable connection between moderate physical activity and brain health is an exciting first step,” said Okonkwo. He explained that ongoing research is focusing on better elucidating the neuroprotective effect of exercise against Alzheimer’s disease. To investigate this further, the team is recruiting individuals with concerns about their memory for a national clinical trial called EXERT to test whether physical exercise can slow the progression of early memory problems caused by Alzheimer’s disease.


  10. Study suggests music sessions may help those with speech difficulties

    June 29, 2017 by Ashley

    From the University of Plymouth press release:

    Tailored music sessions could be crucial in transforming the lives of millions of people whose speech is impacted by learning difficulties, strokes, dementia, brain damage and autism, a new study suggests.

    It could enable individuals and their families to feel less isolated or neglected within society, while enhancing their ability to communicate, both with each other and the wider world.

    But consistent funding and provision needs to be increased, while health and community providers need to implement a more integrated approach to using music in supporting those impacted by strokes and dementia.

    Those are among the key findings of Beyond Words, a project led by the University of Plymouth and Plymouth Music Zone (PMZ) and funded by the Arts Council England Research Grants programme.

    It focused on those who have problems communicating with words — who the researchers now term as being ‘post-verbal’ — and how music might be used to help them.

    The study is the first to focus on post-verbal people and music, and one of the first to explore how music can have a positive effect on a wide range of health-related issues and how future provision might take them all into account rather than focussing on only specific groups within society.

    Jocey Quinn, Professor of Education at the University, led the study which involved a series of interviews, focus groups and arts workshops, as well as observing the regular sessions offered by PMZ.

    She said: “What we have shown is that music can give people a voice, allowing them to explore their creativity as well as communicating both pleasure and pain. In post-verbal children, music can enable carers and families to see the full potential of the individual, while in someone with dementia, a person’s identity can re-emerge when families might have thought it had been lost. This is not simply talking about a minority group, but millions of people who currently do not get good provision, and finding ways to give people hope for the future.”

    Debbie Geraghty is the Executive Director of Plymouth Music Zone, the award-winning charity which was the focus of the groundbreaking longitudinal research. The charity is at the forefront of using music as a powerful tool for inclusion and social change and reaches out to vulnerable children, young people and adults across Plymouth and beyond.

    She added: “This research really shines a light on the tremendous personal and social impacts music can have on individuals and, indeed, how to go about using music to achieve those changes. Surprisingly for us though, it shows just how much those effects really ripple out among families and communities and uncovers the true depth and importance of the work. Plymouth Music Zone willingly opened its doors to researchers because we care so deeply about using the power of music to include and value everyone in society. I hope these valuable insights influence others far and wide as the participants who took part in this research have enrichened our lives and taught us more about the importance of connection, kindness and care than we could ever have imagined possible.”

    For the project, research assistant Claudia Blandon spent 16 months observing sessions delivered by PMZ and following the lives of 25 people who attend sessions at the centre and other community venues like care homes. MPZ’s Training and Research Manager and Music Leader, Anna Batson, was the third member of the research team who brought musical expertise to the findings.

    It also involved interviews with 44 family members, which offered an insight into the richness of the lives led by ‘post-verbal’ people, 30 arts workshops with the post-verbal people and four focus groups with music leaders and volunteers based around current provision and how they felt it might be enhanced.

    The final report is now being communicated to policy makers, charities and others in the hope that the type of sessions offered at Plymouth Music Zone, and other similar centres, can be increased in a sustainable manner.

    Some of its findings have already been communicated during conferences in Plymouth, Poland and the United States, with the hope that the lessons learned could be implemented internationally.

    Phil Gibby, Area Director, South West, Arts Council England, said: “We are delighted to have been able to support the University of Plymouth and Plymouth Music Zone through our National-Lottery funded Research Grants programme to carry out this important project. Our research programme aims to deepen knowledge and understanding of the impact of art and culture, and the complex role it plays in our experience as individuals and a society. We are pleased to see that the results of this study provide credible and robust evidence that demonstrates the wide social benefits of art and culture and hope this goes some way to making the links truly recognised.”