1. Long-term use of opioid patches common among persons with Alzheimer’s disease

    November 15, 2016 by Ashley

    From the University of Eastern Finland media release:

    senior_medicationApproximately seven per cent of persons with Alzheimer’s disease use strong pain medicines, opioids, for non-cancer pain for a period longer than six months, according to a recent study conducted at the University of Eastern Finland. One third of people initiating opioid use became long-term users, and long-term use was heavily associated with transdermal opioid patches. The results were published in PAIN.

    The researchers found that long-term use of opioids was approximately as common among persons with Alzheimer’s disease as it was among those without it. However, long-term use of transdermal patches was twice as common among persons with Alzheimer’s disease, while tablet form opioids were more common among those without Alzheimer’s disease. In addition, long-term opioid use together with benzodiazepines was common, which is worrying as both medicines cause drowsiness. The use of opioids was studied from the date of Alzheimer’s disease diagnosis until death or admission into a long-term care facility. Those with active cancer treatment were excluded from the analysis.

    Long-term opioid use is a problematic practice for non-cancer pain. Evidence of its benefits is limited, and the risk of adverse effects is increased compared to short-term treatment. Further, research on the benefits and adverse effects of long-term opioid use is very scarce among older adults and especially those with dementia. Changing doses and stopping medication when using patch-form opioids requires more time and thus, entails more careful monitoring. Pain, the need for analgesics, and possible adverse effects related to analgesics should be assessed regularly among persons with dementia.

    The study is part of the MEDALZ cohort, which included 67,215 persons with Alzheimer’s disease diagnosed during 2005-2011, of whom 13,111 initiated opioid use. Each person with the disease was matched with a comparison person without Alzheimer’s disease of the same age, gender and region of residence. Data for the study were derived from Finnish nationwide registers.


  2. Alzheimer’s beginnings prove to be a sticky situation

    September 13, 2016 by Ashley

    From the Michigan State University media release:

    mind mazeLaser technology has revealed a common trait of Alzheimer’s disease — a sticky situation that could lead to new targets for medicinal treatments.

    Alzheimer’s statistics are always staggering. The neurodegenerative disease affects an estimated 5 million Americans, one in three seniors dies with Alzheimer’s or a form of dementia, it claims more lives than breast and prostate cancers combined, and its incidence is rising.

    To help fight this deadly disease, Lisa Lapidus, Michigan State University professor of physics and astronomy, has found that peptides, or strings of amino acids, related to Alzheimer’s wiggle at dangerous speeds prior to clumping or forming the plaques commonly associated with Alzheimer’s.

    “Strings of 40 amino acids are the ones most-commonly found in healthy individuals, but strings of 42 are much more likely to clump,” said Lapidus, who published the results in the current issue of ChemPhysChem. “We found that the peptides’ wiggle speeds, the step before aggregation, was five times slower for the longer strings, which leaves plenty of time to stick together rather than wiggle out of the way.”

    This so-called “wiggle” precedes clumping, or aggregating, which is the first step of neurological disorders such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. Lapidus pioneered the use of lasers to study the speed of protein reconfiguration before aggregation.

    If reconfiguration is much faster or slower than the speed at which proteins bump into each other, aggregation is slow. If reconfiguration is the same speed, however, aggregation is fast. She calls the telltale wiggle that she discovered the “dangerous middle.”

    “The dangerous middle is the speed in which clumping happens fastest,” Lapidus said. “But we were able to identify some ways that we can bump that speed into a safer zone.”

    Lapidus and her team of MSU scientists, including Srabasti Acharya, Kinshuk Srivastava and Sureshbabu Nagarajan, found that increasing pH levels kept the amino acids wiggling at fast, safe speeds. Also, a naturally occurring molecule, curcumin (from the spice turmeric), kept the peptide out of the dangerous middle.

    While this is not a viable drug candidate because it does not easily cross the blood-brain barrier, the filter that controls what chemicals reach the brain, they do provide strong leads that could lead to medicinal breakthroughs.

    Along with new drug targets, Lapidus’ research provides a potential model of early detection. By the time patients show symptoms and go to a doctor, aggregation already has a stronghold in their brains. Policing amino acids for wiggling at dangerous speeds could tip off doctors long before the patient begins to suffer from the disease.


  3. New link found between diabetes, Alzheimer’s disease

    June 22, 2016 by Ashley

    From the Diabetologia media release:

    diabetes blood sugarDrugs used to treat diabetes could also be used to treat Alzheimer’s disease, and vice versa, according to new research from the University of Aberdeen.

    This is also the first study of its kind to show that Alzheimer’s disease can lead to diabetes, as opposed to diabetes occurring first as was previously thought.

    The study reports that Alzheimer’s Disease and type 2 diabetes are so closely related that drugs currently used to control glucose levels in diabetes may also alleviate the symptoms and progression of Alzheimer’s disease.

    The paper, published in the journal Diabetologia (the journal of the European Association for the Study of Diabetes), found for the first time that dementia-related complications within the brain can also lead to changes in glucose handling and ultimately diabetes. This is contrary to what was previously thought — that diabetes begins with a malfunction in the pancreas or a high fat, high sugar diet.

    The research was led by Professor Bettina Platt who formed a unique collaboration between her Alzheimer’s research team and the diabetes research team led by Professor Mirela Delibegovic. The teams were keen to investigate why the two diseases are so commonly found together in elderly patients.

    The researchers developed a model of Alzheimer’s disease and were surprised to find that increased levels of a gene involved in the production of toxic proteins in the brain not only led to Alzheimer’s -like symptoms, but also to the development of diabetic complications.

    Professor Platt said of her research: “Many people are unaware of the relationship between diabetes and Alzheimer’s disease, but the fact is that around 80% of people with Alzheimer’s disease also have some form of diabetes or disturbed glucose metabolism. This is hugely relevant as Alzheimer’s is in the vast majority of cases not inherited, and lifestyle factors and comorbidities must therefore be to blame.

    “Our research teams are particularly interested in the impact of lifestyle related factors in dementia and by collaborating with experts in diabetes and metabolism, we have been able to investigate the nature of the link in great detail.

    “Until now, we always assumed that obese people get type 2 diabetes and then are more likely to get dementia — we now show that actually it also works the other way around.

    “Additionally, it was previously believed that diabetes starts in the periphery, i.e. the pancreas and liver, often due to consumption of an unhealthy diet, but here we show that dysregulation in the brain can equally lead to development of very severe diabetes — so again showing that diabetes doesn’t necessarily have to start with your body getting fat — it can start with changes in the brain.

    This study provides a new therapeutic angle into Alzheimer’s disease and we now think that some of the compounds that are used for obesity and diabetic deregulation might potentially be beneficial for Alzheimer’s patients as well. The good news is that there are a number of new drugs available right now which we are testing to see if they would reverse both Alzheimer’s and diabetes symptoms. We will also be able to study whether new treatments developed for Alzheimer’s can improve both, the diabetic and cognitive symptoms.”

     


  4. Genetic variations that boost PKC enzyme contribute to Alzheimer’s disease

    June 3, 2016 by Ashley

    From the University of California – San Diego media release:

    brain scanIn Alzheimer’s disease, plaques of amyloid beta protein accumulate in the brain, damaging connections between neurons. Now, researchers at University of California San Diego School of Medicine and Harvard Medical School have found that the enzyme Protein Kinase C (PKC) alpha is necessary for amyloid beta to damage neuronal connections. They also identified genetic variations that enhance PKC alpha activity in patients with Alzheimer’s disease.

    The study, published May 10 in Science Signaling, may present a new therapeutic target for the disease.

    Until recently, it was thought that PKC helped cells survive, and that too much PKC activity led to cancer. Based on that assumption, many companies tested PKC inhibitors as drugs to treat cancer, but they didn’t work,” said co-senior author Alexandra Newton, PhD, professor of pharmacology at UC San Diego School of Medicine.

    “Instead, we recently found that the opposite is true. PKC serves as the brakes to cell growth and survival, so cancer cells benefit when PKC is inactivated. Now, our latest study reveals that too much PKC activity is also bad, driving neurodegeneration. This means that drugs that failed in clinical trials for cancer may provide a new therapeutic opportunity for Alzheimer’s disease.”

    The study was a three-way collaboration between experts in PKC (Newton), neuroscience (Roberto Malinow, MD, PhD, Distinguished Professor of Neurosciences and Neurobiology at UC San Diego School of Medicine), and genomics (Rudolph Tanzi, PhD, professor of neurology at Harvard Medical School).

    Malinow’s team found that when mice are missing the PKC alpha gene, neurons functioned normally, even when amyloid beta was present. Then, when they restored PKC alpha, amyloid beta once again impaired neuronal function. In other words, amyloid beta doesn’t inhibit brain function unless PKC alpha is active.

    Enter the Tanzi team, which has a database of genetic information for 1,345 people in 410 families with late-onset Alzheimer’s disease. Tanzi and team use this database to look for rare variants — genetic mutations found only in family members with the disease. Here, the team found three variants in one form of the PKC enzyme, PKC alpha that were associated with the disease in five families.

    The researchers replicated these three PKC alpha gene variants in laboratory cell lines. In each instance, PKC alpha activity was increased.

    While this study surfaced only five families with these rare mutations in the PKC alpha gene, there are many ways to influence PKC alpha’s activity, Newton said. She believes there could be many other inherited genetic variations that indirectly boost or inhibit PKC activity, and therefore also influence a person’s likelihood of developing Alzheimer’s disease.

    “Next we want to identify more molecules participating in the pathophysiology,” said Malinow. “The more steps in the mechanism we can understand, the more therapeutic targets we’ll find for Alzheimer’s disease.”


  5. Designing dementia friendly care homes

    May 16, 2016 by Ashley

    From the Bournemouth University media release:

    senior alzheimerAs the population ages and demography changes, the UK is facing an unprecedented challenge of how to care for and support its older people.

    While the fact that people are living longer should be celebrated, the flip side is that age-related illness such as dementia are on the rise and it’s important for us, as a country to find solutions and alleviate the difficulties people may face as a result.

    Under the supervision of Associate Professor Jan Wiener, one of BU’s PhD students, Mary O’Malley, has been exploring how people with dementia learn to navigate unfamiliar environments and what consequences this could have for dementia care home building guidelines.

    “My research is looking at ways to reduce potential spatial disorientation for older adults, both those with memory difficulties and those without,” explained Mary, “By exploring this issue, I hope it will lead to design changes in the living environment that supports successful orientation.”

    I’m looking at people’s wayfinding systems and how navigational tools are used in care homes, and how these might help or hinder people’s abilities to find their way around,” continues Mary, “I’m looking at the strategies people use to learn new environments and I’m also going into retirement developments and asking people how they find their way around and what helps them to navigate unfamiliar places — for me, it’s important to hear the users’ voice when it comes to designing the environment.”

    Mary is undertaking a mixed methods PhD, which is gathering both qualitative and quantitative data. By carrying out a number of studies and drawing on expertise from BU’s Psychology Department, BU’s Dementia Institute (BUDI) and external architecture expertise, Mary is taking a rounded, interdisciplinary approach to her work. For her, bridging the gap between disciplines has been very beneficial.

    “If you were just approaching this from one angle, one discipline, you’d miss so much valuable information,” said Mary, “To be able to improve the design environment, it’s really important to get input from different subject areas. There’s no singular way of doing this, so it’s great to draw on expertise from a spectrum of disciplines.”

    As she explained, “In psychology, we have a lot of knowledge about way-finding and how people navigate around environments, but not a lot of that has been translated into applied settings. There’s lots of potential to apply and test out this knowledge for older people in retirement settings and care homes, both of which are places where this research could make a real impact.”

    While design guidelines are often applied to care homes, there are lots of other spaces used by older people and people with memory problems which could benefit from better wayfinding guidelines — hospitals, retirement homes and shopping centres are just a few examples. Given the prominence of the idea of dementia friendly communities, Mary’s research is very timely.

    In order to carry out her research, Mary has been going out to retirement homes and care homes, and learning from their residents about their experiences of navigating their environments. She has also been using some of the state-of-the-art technology available in the Psychology Department to create virtual environments which older people navigate their way around.

    One of her studies looked at how people learn a new route and which navigational strategies people use when learning it. “The results showed that older adults who performed lower on a neuropsychological assessment, suggesting possible atypical aging, had difficulties with some specific measures of route memory– they found it hard to translate and to identify a recently learned route from a map perspective, and interestingly, there were significant differences between two separate forms of landmark memory which we would like to further investigate,” explained Mary.

    “We want to follow-up these findings with a second study which will explore how useful ‘you are here’ maps are for certain demographics and in certain environments,” said Mary, “Additionally, we want to see whether a certain placement of landmarks would make a difference in how well a route is learned. For this we are going to be using a virtual care home environment, which will allow us to change the variables, such as corridor layout and where landmarks are placed.”

    Mary’s research is already having an impact, as one of the retirement homes where she has been carrying out her qualitative research is intending to have a full re-design based on the findings and reports made by the residents living there. Ultimately, Mary’s aim is to use her research to influence designers and architects to create built environments which are easier for older people and people with memory loss to navigate. The main tool for achieving this will be through informing building guidelines and regulations — something Mary is keen to develop.


  6. Study shows how the brain switches into memory mode

    May 11, 2016 by Ashley

    From the University of Bonn media release:

    brain scanResearchers from Germany and the USA have identified an important mechanism with which memory switches from recall to memorization mode.

    The study may shed new light on the cellular causes of dementia. The work was directed by the University of Bonn and the German Center for Neurodegenerative Diseases (DZNE). It is being published in the journal Neuron.

    Because of its shape, the control center of memory bears the poetic name of “hippocampus” (seahorse). New sensations to be stored continually enter this region of the brain. But at the same time, the hippocampus is also the guardian of memories: It retrieves stored information from the depths of memory.

    The hippocampus is also an important transport junction. And just like rush hour in a major city, it also needs a regulating hand to control the opposing flows of information. The researchers from Bonn, Los Angeles and Palo Alto have now identified such a memory traffic policeman. Certain cells in the brain, the hippocampal astrocytes, ensure that the new information is given priority. The mind thus switches into memorization mode; by contrast, the already saved memories must wait.

    However, the astrocytes themselves only take orders: They react to the neurotransmitter acetylcholine, which is released in particular in novel situations. It has been known for several years that acetylcholine promotes the storage of new information. How this happens has only been partly understood. “In our work, we were able to show for the first time that acetylcholine stimulates astrocytes which then are induced to release the transmitter glutamate,” explains Milan Pabst, who is a doctoral candidate at the Laboratory for Experimental Epileptology of the University of Bonn. “The released glutamate then activates inhibitory nerve cells which inhibit a pathways mediating the retrieval of memories.”

    The researchers working with the neuroscientist Prof. Dr. Heinz Beck genetically modified nerve cells so that they could be activated by light and then release acetylcholine. Using this trick, they were able to clarify the mechanism using recordings in living brain tissue sections. “However, we also show that, in the brains of living mice, acetylcholine has the same effect on the activity of the neurons,” explains Pabst’s colleague, Dr. Holger Dannenberg.

    Astrocytes have long since been underestimated

    Another reason this result is interesting is because astrocytes themselves are not nerve cells. They belong to what are known as glial cells. Until the turn of the millennium, they were still considered to merely serve as mechanical support to the real stars of the brain, the neurons.

    In recent decades, however, it has become increasingly clearer that this image is far from correct. It is known by now that astrocytes can release neurotransmitters — the messengers by which neurons communicate with each other — or even remove them from the brain. “It was previously unknown that the astrocytes are involved in central memory processes through the mechanism which has now been discovered,” explains Prof. Beck. However, an observation made by US scientists in 2014 fits into this context: If astrocytes’ function is inhibited, this has a negative effect on the recognition of objects.

    The results may also shed new light on the cellular causes of memory disorders. Thus there are indications that the controlled secretion of acetylcholine is disrupted in patients with Alzheimer’s dementia. “However, we have not investigated whether the mechanism we discovered is also impacted,” stresses Pabst.


  7. New cases of dementia in the UK fall by 20 percent over two decades

    April 25, 2016 by Ashley

    From the University of Cambridge media release:

    seniors_companionshipThe UK has seen a 20% fall in the incidence of dementia over the past two decades, according to new research from England, led by the University of Cambridge, leading to an estimated 40,000 fewer cases of dementia than previously predicted. However, the study, published today in Nature Communications, suggests that the dramatic change has been observed mainly in men.

    Reports in both the media and from governments have suggested that the world is facing a dementia ‘tsunami’ of ever-increasing numbers, particularly as populations age. However, several recent studies have begun to suggest that the picture is far more complex. Although changing diagnostic methods and criteria are identifying more people as having dementia, societal measures which improve health such as education, early- and mid-life health promotion including smoking reduction and attention to diet and exercise may be driving a reduction in risk in some countries. Prevalence (the proportion of people with dementia) has been reported to have dropped in some European countries but it is incidence (the proportion of people developing dementia in a given time period) that provides by far the most robust evidence of fundamental change in populations.

    As part of the Medical Research Council Cognitive Function and Ageing Study (CFAS), researchers at the University of Cambridge, Newcastle University, Nottingham University and the University of East Anglia interviewed a baseline of 7,500 people in three regions of the UK (Cambridgeshire, Newcastle and Nottingham) between 1991 and 1994 with repeat interviews at two years to estimate incidence. Then 20 years later a new sample of over 7,500 people from the same localities aged 65 and over was interviewed with a two year repeat interview again. This is the first time that a direct comparison of incidence across time in multiple areas, using identical methodological approaches, has been conducted in the world.

    The researchers found that dementia incidence across the two decades has dropped by 20% and that this fall is driven by a reduction in incidence among men at all ages. These findings suggest that in the UK there are just under 210,000 new cases per year: 74,000 men and 135,000 women — this is compared to an anticipated 250,000 new cases based on previous levels. Incidence rates are higher in more deprived areas.

    Even in the presence of an ageing population, this means that the number of people estimated to develop dementia in any year has remained relatively stable, providing evidence that dementia in whole populations can change. It is not clear why rates among men have declined faster than those among women, though it is possible that it is related to the drop in smoking and vascular health improving in men.

    Professor Carol Brayne, Director of the Cambridge Institute of Public Health, University of Cambridge, says: “Our findings suggest that brain health is improving significantly in the UK across generations, particularly among men, but that deprivation is still putting people at a disadvantage. The UK in earlier eras has seen major societal investments into improving population health and this appears to be helping protect older people from dementia. It is vital that policies take potential long term benefits into account. ”

    Professor Fiona Matthews from the Institute of Health and Society, Newcastle University and the MRC Biostatistics Unit, Cambridge adds: “Public health measures aimed at reducing people’s risk of developing dementia are vital and potentially more cost effective in the long run than relying on early detection and treating dementia once it is present. Our findings support a public health approach for long term dementia prevention, although clearly this does not reduce the need for alternative approaches for at-risk groups and for those who develop dementia.”

    The researchers argue that while influential reports continue to promote future scenarios of huge increases of people with dementia across the globe, their study shows that global attention and investment in reducing the risk of dementia can help prevent such increases.

    “While we’ve seen investment in Europe and many other countries, the lack of progress in access to education, malnutrition in childhood and persistent inequalities within and across other countries means that dementia will continue to have a major impact globally,” says Professor Brayne. “Our evidence shows that the so-called dementia ‘tsunami’ is not an inevitability: we can help turn the tide if we take action now.”

    Dr Rob Buckle, director of science programmes at the Medical Research Council, which funded the study, added: “It is promising news that dementia rates, especially amongst men, have dropped by such a significant amount over the last twenty years, and testament to the benefits of an increased awareness of a brain-healthy lifestyle. However, the burden of dementia will continue to have significant societal impact given the growing proportion of elderly people within the UK population and it is therefore as important as ever that we continue to search for new ways of preventing and treating the disease. This study does, however, reinforce the importance of long-term, quality studies that create a wealth of data of invaluable resource for researchers.”


  8. Remote Italian village could harbor secrets of healthy aging

    April 14, 2016 by Ashley

    From the University of California, San Diego Health Sciences media release:

    mediterranean diet fishThe average life expectancy in the United States is approximately 78 years old. Americans live longer, with better diets and improved health care, than ever before, but only 0.02 percent will hit the century mark.

    To understand how people can live longer throughout the world, researchers at University of California, San Diego School of Medicine have teamed up with colleagues at University of Rome La Sapienza to study a group of 300 citizens, all over 100 years old, living in a remote Italian village nestled between the ocean and mountains on the country’s coast.

    “We are the first group of researchers to be given permission to study this population in Acciaroli, Italy,” said Alan Maisel, MD, lead UC San Diego School of Medicine investigator and professor of medicine in the Division of Cardiovascular Medicine.

    The Acciaroli study group is known to have very low rates of heart disease and Alzheimer’s. It favors a Mediterranean diet markedly infused with the herb rosemary. Due to the location of the village, Maisel said locals also walk long distances and hike through the mountains as part of their daily activity.

    The goal of this long-term study is to find out why this group of 300 is living so long by conducting a full genetic analysis and examining lifestyle behaviors, like diet and exercise,” said Maisel. “The results from studying the longevity of this group could be applied to our practice at UC San Diego and to patients all over the world.”

    Maisel and his research team will work with their Italian counterparts to collect blood samples and distribute questionnaires to the group over the next six months.

    The study will also involve tests to look at metabolomics, biomes, cognitive dysfunction and protein biomarkers for risk of heart disease, Alzheimer’s, kidney disease and cancer.

    “This project will not only help to unlock some of the secrets of healthy aging, but will build closer ties with researchers across the globe, which will lead to more science and improved clinical care in our aging population,” said Salvatore DiSomma, MD, lead Italian investigator and professor of emergency medicine at University of Rome La Sapienza.

    Co-authors include Nicholas Schork, Robert Rissman, Chris Benner, Tatianna Kisseleva, William Kemen, Rob Knight, Dillip Jeste, Lori Daniels, and Mohit Jain, all with UC San Diego.

    The study is supported, in part, from European grants.


  9. Brain study reveals how long-term memories are erased

    March 31, 2016 by Ashley

    From the University of Edinburgh media release:

    mri scanVital clues about how the brain erases long term memories have been uncovered by researchers.

    The study in rats reveals how forgetting can be the result of an active deletion process rather than a failure to remember.

    It points towards new ways of tackling memory loss associated with conditions such as Alzheimer’s disease and other types of dementia.

    The findings could also help scientists to understand why some unwanted memories are so long-lasting — such as those of people suffering from post-traumatic stress disorders.

    Memories are maintained by chemical signalling between brain cells that relies on specialised receptors called AMPA receptors. The more AMPA receptors there are on the surface where brain cells connect, the stronger the memory.

    The team led by the University of Edinburgh found that the process of actively wiping memories happens when brain cells remove AMPA receptors from the connections between brain cells.

    Over time, if the memory is not recalled, the AMPA receptors may fall in number and the memory is gradually erased.

    The researchers also showed that actively forgetting information in this way helps the animals to adapt their behaviour according to their surroundings.

    Blocking the removal of AMPA receptors with a drug that keeps them at the surface of the cell stopped the natural forgetting of memories, the study found.

    Drugs that target AMPA receptor removal are already being investigated as potential therapies to prevent memory loss associated with diseases such as Alzheimer’s and dementia.

    However, researchers say that active forgetting could be an important facet of learning and memory. Further research is needed to understand what consequences blocking this process could have on the ability to take on new information and retrieve existing memories.

    Dr Oliver Hardt, of the Centre for Cognitive and Neural Systems at the University of Edinburgh, said: “Our study looks at the biological processes that happen in the brain when we forget something. The next step is to work out why some memories survive whilst others are erased. If we can understand how these memories are protected, it could one-day lead to new therapies that stop or slow pathological memory loss.”

    The study is published in The Journal of Neuroscience.


  10. Transmissibility of Alzheimer’s: No clinical symptoms

    by Ashley

    From the Medical University of Vienna media release:

    memory lossMedUni Vienna researchers have published the results of a clarifying research study on the potential transmissibility of Alzheimer’s disease. Although the protein associated with Alzheimer’s disease, amyloid-?, might be transmissible under very unusual circumstances, this does not go along with a transmission of the clinical manifestation of Alzheimer’s disease. The affected persons develop no clinical symptoms of the disease.

    Deposits of amyloid-? together with the tau protein in the brain constitute a distinctive biomarker of Alzheimer’s disease. In the last months, researchers from the UK and a research team from Switzerland and Austria attracted attention by stating that the amyloid-? protein might be transmitted to healthy persons in the context of medical procedures such as brain surgery. They examined the brain tissue of deceased persons who had received human growth hormone or dura mater transplants. This raised fears that the protein might be able to transmit the disease.

    The research group of Gabor G. Kovacs of the Institute of Neurology of MedUni Vienna could now for the first time microscopically examine and compare archived dura mater (the thick membrane covering of the brain) of donors. The results confirm that amyloid-? is transmissible from the dura mater to another brain. However, the microscopic appearance of the amyloid-? deposits differs from the usual appearance in Alzheimer’s disease.

    The amyloid-? protein remains in the vicinity of the operated tissue and does not spread considerably or affect other brain regions. There were also no clinical symptoms of Alzheimer’s disease and no characteristic deposits of the tau protein were seen.

    To determine if amyloid-? deposits can be found in the dura mater, the research group also examined the dura mater of elderly individuals. In this context, the researchers demonstrated for the first time that amyloid-? can also be stored by the dura mater. This was previously only known for cerebral tissue.

    “The study allows us to obtain a balanced opinion of the transmissibility of Alzheimer’s disease,” explained the principal investigator of the research study, Gabor G. Kovacs. “Despite the fact that it looks as if amyloid-?, the protein associated with Alzheimer’s, might be transmissible under very unusual circumstances, the clinical manifestation of Alzheimer’s disease is not transmitted. It is certainly not correct to talk of a transmissibility of the disease.”