1. Researchers focus on cell membranes to develop Alzheimer’s treatments

    March 31, 2017 by Ashley

    From the University of Michigan press release:

    Thin parts of the cell membranes of neurons turn out to be particularly vulnerable to a protein that collects in the brain of people with Alzheimer’s disease, according to a University of Michigan researcher.

    The discovery could open an avenue for developing treatments for Alzheimer’s disease that work within the cell’s membrane.

    The protein amyloid-beta builds up in the brains of people with Alzheimer’s disease, ultimately aggregating into sticky clumps called plaque on the surface of neurons. U-M researcher Ayyalusamy Ramamoorthy, the Robert W. Parry Collegiate Professor of Chemistry and Biophysics, found that thinner parts of the neuronal membranes give access points to amyloid-beta, allowing the protein to puncture and kill those cells, and destroying the patient’s ability to make and retain memory. This kind of build-up is also implicated in disorders such as Huntington’s and type 2 diabetes.

    These thin spots are composed of short fatty acid chains whereas the thicker parts of the membrane are composed of long fatty acid chains. The research team thinks that the formation of lipids with short chains — caused by aging or other physiological means that result in Alzheimer’s — can promote cell death from the accumulation of amyloid-beta.

    “We’re trying to understand how components of the cell membrane and the physical and chemical properties of the lipid membrane would influence the aggregation of amyloid-beta by a variety of biophysical techniques,” Ramamoorthy said. “The thickness of cell membranes is very important not only for Alzheimer’s disease, but also for diabetes and other aging-related diseases.”

    The group investigated three types of lipids that varied in thickness. The thicker lipid membranes that were composed of longer fatty acid chains seemed to attract and promote the growth of plaque. The thinner membrane acted sometimes like a lipid and sometimes like a detergent, Ramamoorthy said.

    The researchers found that the detergent-like fatty acid chains interact with the plaque, allowing that plaque to penetrate the cell membrane. A technique called phosphorus-31 nuclear magnetic resonance, which can reveal details at the atomic level within bilayers similar to the way a physician would use an MRI machine to look at tissues in the human body, allowed the researchers to examine how the collection of amyloid-beta in thinner membrane fragmented the cellular membrane.

    The study was done in what’s called a phospholipid bilayer, which consists of two layers of lipids. These layers are made up of hydrophobic, or water-hating, and hydrophilic, or water-loving phases, and look similar to a mixture of oil and water. This lipid bilayer replicates the cell membranes found in neurons. To measure amyloid-beta’s toxicity, the researchers used neuronal cells.

    “Many other labs are investigating the amyloid inhibition by small molecules in solution, but we are doing it in a membrane environment. From our study it is clear that the cell membrane is the hot spot where amyloid-beta becomes crazy,” Ramamoorthy said. “The cell membrane is definitely not like a coffee filter that filters biological events — rather, it is the place where a plethora of biological actions happen.”

    Currently, Ramamoorthy’s team is screening libraries of small molecular compounds that could target the aggregation of amyloid-beta within a person’s cell membrane.

    “These findings could be significant in the potential development of compounds to treat the aging-related diseases,” he said.


  2. Daily consumption of tea may protect the elderly from cognitive decline

    March 29, 2017 by Ashley

    From the National University of Singapore press release:

    A cup of tea a day can keep dementia away, and this is especially so for those who are genetically predisposed to the debilitating disease, according to a recent study led by Assistant Professor Feng Lei from the Department of Psychological Medicine at National University of Singapore’s (NUS) Yong Loo Lin School of Medicine.

    The longitudinal study involving 957 Chinese seniors aged 55 years or older has found that regular consumption of tea lowers the risk of cognitive decline in the elderly by 50 per cent, while APOE e4 gene carriers who are genetically at risk of developing Alzheimer’s disease may experience a reduction in cognitive impairment risk by as much as 86 per cent.

    The research team also discovered that the neuroprotective role of tea consumption on cognitive function is not limited to a particular type of tea — so long as the tea is brewed from tea leaves, such as green, black or oolong tea.

    “While the study was conducted on Chinese elderly, the results could apply to other races as well. Our findings have important implications for dementia prevention. Despite high quality drug trials, effective pharmacological therapy for neurocognitive disorders such as dementia remains elusive and current prevention strategies are far from satisfactory. Tea is one of the most widely consumed beverages in the world. The data from our study suggests that a simple and inexpensive lifestyle measure such as daily tea drinking can reduce a person’s risk of developing neurocognitive disorders in late life,” explained Asst Prof Feng.

    He added, “Based on current knowledge, this long term benefit of tea consumption is due to the bioactive compounds in tea leaves, such as catechins, theaflavins, thearubigins and L-theanine. These compounds exhibit anti-inflammatory and antioxidant potential and other bioactive properties that may protect the brain from vascular damage and neurodegeneration. Our understanding of the detailed biological mechanisms is still very limited so we do need more research to find out definitive answers.”

    In this study, tea consumption information were collected from the participants, who are community-living elderly, from 2003 to 2005. At regular intervals of two years, these seniors were assessed on their cognitive function using standardised tools until 2010. Information on lifestyles, medical conditions, physical and social activities were also collected. Those potential confounding factors were carefully controlled in statistical models to ensure the robustness of the findings.

    The research team published their findings in scientific journal The Journal of Nutrition, Health & Aging in December 2016.

    Future Research

    Asst Prof Feng and his team are planning to embark on further studies to better understand the impact of Asian diet on cognitive health in aging. They are also keen to investigate the effects of the bioactive compounds in tea and test them more rigorously through the assessment of their biological markers and by conducting randomised controlled trials or studies that assign participants into experimental groups or control groups randomly to eliminate biased results.


  3. Brain cells show teamwork in short-term memory

    March 23, 2017 by Ashley

    From the University of Western Ontario press release:

    Nerve cells in our brains work together in harmony to store and retrieve short-term memory, and are not solo artists as previously thought, Western-led brain research has determined.

    The research turns on its head decades of studies assuming that single neurons independently encode information in our working memories.

    “These findings suggest that even neurons we previously thought were ‘useless’ because they didn’t individually encode information have a purpose when working in concert with other neurons,” said researcher Julio Martinez-Trujillo, based at the Robarts Research Institute and the Brain and Mind Institute at Western University.

    “Knowing they work together helps us better understand the circuits in the brain that can either improve or hamper executive function. And that in turn may have implications for how we work though brain-health issues where short-term memory is a problem, including Alzheimer disease, schizophrenia, autism, depression and attention deficit disorder.”

    Working memory is the ability to learn, retain and retrieve bits of information we all need in the short term: items on a grocery list or driving directions, for example. Working memory deteriorates faster in people with dementia or other disorders of the brain and mind.

    In the past, researchers have believed this executive function was the job of single neurons acting independently from one another — the brain’s version of a crowd of people in a large room all singing different songs in different rhythms and different keys. An outsider trying to decipher any tune in all that white noise would have an extraordinarily difficult task.

    This research, however, suggests many in the neuron throng are singing from the same songbook, in essence creating chords to strengthen the collective voice of memory. With neural prosthetic technology — microchips that can “listen” to many neurons at the same time — researchers are able to find correlations between the activity of many nerve cells. “Using that same choir analogy, you can start perceiving some sounds that have a rhythm, a tune and chords that are related to each other: in sum, short-term memories,” said Martinez-Trujillo, who is also an associate professor at Western’s Schulich School of Medicine & Dentistry.

    And while the ramifications of this discovery are still being explored, “this gives us good material to work with as we move forward in brain research. It provides us with the necessary knowledge to find ways to manipulate brain circuits and improve short term memory in affected individuals,” Martinez-Trujillo said.

    “The microchip technology also allows us to extract signals from the brain in order to reverse-engineer brain circuitry and decode the information that is in the subject’s mind. In the near future, we could use this information to allow cognitive control of neural prosthetics in patients with ALS or severe cervical spinal cord injury,” said Adam Sachs, neurosurgeon and associate scientist at The Ottawa Hospital and assistant professor at the University of Ottawa Brain and Mind Research Institute.


  4. Head injuries can alter hundreds of genes and lead to serious brain diseases

    by Ashley

    From the UCLA press release:

    Head injuries can harm hundreds of genes in the brain in a way that increases people’s risk for a wide range of neurological and psychiatric disorders, UCLA life scientists report.

    The researchers identified for the first time master genes that they believe control hundreds of other genes which are linked to Alzheimer’s disease, Parkinson’s disease, post-traumatic stress disorder, stroke, attention deficit hyperactivity disorder, autism, depression, schizophrenia and other disorders.

    Knowing what the master genes are could give scientists targets for new pharmaceuticals to treat brain diseases. Eventually, scientists might even be able to learn how to re-modify damaged genes to reduce the risk for diseases, and the finding could help researchers identify chemical compounds and foods that fight disease by repairing those genes.

    “We believe these master genes are responsible for traumatic brain injury adversely triggering changes in many other genes,” said Xia Yang, a senior author of the study and a UCLA associate professor of integrative biology and physiology.

    Genes have the potential to become any of several types of proteins, and traumatic brain injury can damage the master genes, which can then lead to damage of other genes.

    That process can happen in a couple of ways, said Yang, who is a member of UCLA’s Institute for Quantitative and Computational Biosciences. One is that the injury can ultimately lead the genes to produce proteins of irregular forms. Another is to change the number of expressed copies of a gene in each cell. Either change can prevent a gene from working properly. If a gene turns into the wrong form of protein, it could lead to Alzheimer’s disease, for example.

    “Very little is known about how people with brain trauma — like football players and soldiers — develop neurological disorders later in life,” said Fernando Gomez-Pinilla, a UCLA professor of neurosurgery and of integrative biology and physiology, and co-senior author of the new study. “We hope to learn much more about how this occurs.”

    The research appears in EBioMedicine, a journal published by Cell and The Lancet.

    The researchers trained 20 rats to escape from a maze. They then used a fluid to produce a concussion-like brain injury in 10 of the rats; the 10 others did not receive brain injuries. When the rats were placed in the maze again, those that had been injured took approximately 25 percent longer than the non-injured rats to solve it.

    To learn how the rats’ genes had changed in response to the brain injury, the researchers analyzed genes from five animals in each group. Specifically, they drew RNA from the hippocampus, which is the part of the brain that helps regulate learning and memory, and from leukocytes, white blood cells that play a key role in the immune system.

    In the rats that had sustained brain injuries, there was a core group of 268 genes in the hippocampus that the researchers found had been altered, and a core group of 1,215 genes in the leukocytes that they found to have been changed.

    “A surprise was how many major changes occurred to genes in the blood cells,” Yang said. “The changes in the brain were less surprising. It’s such a critical region, so it makes sense that when it’s damaged, it signals to the body that it’s under attack.”

    Nearly two dozen of the altered genes are present in both the hippocampus and the blood, which presents the possibility that scientists could develop a gene-based blood test to determine whether a brain injury has occurred, and that measuring some of those genes could help doctors predict whether a person is likely to develop Alzheimer’s or other disorders. The research could also lead to a better way to diagnose mild traumatic brain injury.

    More than 100 of the genes that changed after the brain injury have counterparts in humans that have been linked to neurological and psychiatric disorders, the researchers report. For example, 16 of the genes affected in the rats have analogs in humans, and those genes are linked to a predisposition for Alzheimer’s, the study reports. The researchers also found that four of the affected genes in the hippocampus and one in leukocytes are similar to genes in humans that are linked to PTSD.

    Yang said the study not only indicated which genes are affected by traumatic brain injury and linked to serious disease, but also might point to the genes that govern metabolism, cell communication and inflammation — which might make them the best targets for new treatments for brain disorders.

    The researchers now are studying some of the master genes to determine whether modifying them also causes changes in large numbers of other genes. If so, the master genes would be even more promising as targets for new treatments. They also plan to study the phenomenon in people who have suffered traumatic brain injury.

    In a 2016 study, Yang, Gomez-Pinilla and colleagues reported that hundreds of genes can be damaged by fructose and that an omega-3 fatty acid called docosahexaenoic acid, or DHA, seems to reverse the harmful changes produced by fructose. One of the genes they identified in that study, Fmod, also was among the master regulator genes identified in the new research.

    Not everyone with traumatic brain injuries develops the same diseases, but more severe injuries can damage more genes, said Gomez-Pinilla, who also is a member of UCLA’s Brain Injury Research Center.

     


  5. Might smartphones help to maintain memory in patients with mild Alzheimer’s disease?

    March 20, 2017 by Ashley

    From the IOS Press press release:

    The patient is a retired teacher who had reported memory difficulties 12 months prior to the study. These difficulties referred to trouble remembering names and groceries she wanted to purchase, as well as frequently losing her papers and keys. According to the patient and her husband, the main difficulties that she encountered were related to prospective memory (e.g., forgetting medical appointments or to take her medication).

    To help her with her symptoms, Mohamad El Haj, a psychologist and assistant professor at the University of Lille, proposed Google Calendar, a time-management and scheduling calendar service developed by Google. The patient accepted as she was already comfortable using her smartphone. She also declared that she preferred the application as it offers more discrete assistance than a paper-based calendar.

    With the patient and her husband, Dr. El Haj and his colleagues defined several prospective omissions in the patient, such as forgetting her weekly medical appointment, forgetting her weekly bridge game in the community club, and forgetting to go to weekly mass at the church. These omissions were targeted by sending automatic alerts, prompted by Google Calendar, at different times before each event (e.g., the medical appointment).

    The researchers compared omissions before after the use of Google Calendar, they observed less omission after implementing the application.

    The study is the first to suggest positive effects of smartphones applications on everyday life prospective memory in Alzheimer’s disease. The findings, published in Journal of Alzheimer’s disease, are encouraging, however, Dr. El Haj notes that this is a case study and therefore entails a few limitations, including generalizability of the results. The current, anecdotal findings require a larger study, not only to confirm or refute the findings reported here, but also to address challenges such as the long-term benefits of Google calendar.

    Regardless of its potential limitations, Dr. El Haj notes that this study addresses memory loss, the main cognitive hallmark of Alzheimer’s disease and the major concern of the patients and their families. By demonstrating positive effect of Google Calendar on prospective memory in this patient, Dr. El Haj hopes that his study paves the way for exploring the potential of smartphone-integrated memory aids in Alzheimer’s disease. The future generation of patients may be particularly sensitive to the use of smartphones as a tool to alleviate their memory compromise.


  6. Mild cognitive impairment (MCI) detected with brain training game

    March 17, 2017 by Ashley

    From the IOS Press press release:

    Greek researchers demonstrated the potential of a self-administered virtual supermarket cognitive training game for remotely detecting mild cognitive impairment (MCI), without the need for an examiner, among a sample of older adults. MCI patients suffer from cognitive problems and often encounter difficulties in performing complex activities such as financial planning. They are at a high risk for progressing to dementia however early detection of MCI and suitable interventions can stabilize the patients’ condition and prevent further decline.

    It has been shown that virtual reality game-based applications and especially virtual supermarkets can detect MCI. Past studies have utilized user performance in such applications along with data from standardized neuropsychological tests in order to detect MCI. The team that conducted this study was the first scientific team to achieve reliable MCI detection using a virtual reality game-based application on its own. In that previous study , administration of the virtual super market (VSM) exercise was conducted by an examiner. The present study eliminated the need for an examiner by calculating the average performance of older adults using a special version of the VSM application, the VSM Remote Assessment Routine (VSM-RAR), at home on their own, for a period of one month. It is the first instance where a self-administered virtual reality application was used to detect MCI with a high degree of reliability.

    The research team included scientists from the Aristotle University of Thessaloniki (AUTH), the Centre for Research and Technology Hellas/Information Technologies Institute (CERTH/ITI), the Greek Association of Alzheimer’s Disease and Related Disorders (GAADRD) and the Network Aging Research (NAR) of the University of Heidelberg.

    In an article published in the Journal of Alzheimer’s Disease, the researchers have indicated that the virtual supermarket remote assessment routine (VSM-RAR) application displayed a correct classification rate (CCR) of 91.8% improving VSM’s CCR as assessed in the previous VSM study while achieving a level of diagnostic accuracy similar to the most accurate standardized neuropsychological tests, which are considered the gold standard for MCI detection.

    Self-administered computerized cognitive training exercises/games are gaining popularity among older adults as an easy and enjoyable means of maintaining cognitive health. Such applications are especially popular among older adults who consider themselves healthy and are not inclined to visit specialized memory clinics for cognitive assessment. If self-administered games and exercises could also detect cognitive disorders, initial cognitive screening could be conducted remotely. The wide implementation of this method of remote screening would facilitate the detection of cognitive impairment at the MCI stage thus allowing for more efficient therapeutic interventions.

    This preliminary study indicates that automated, remote MCI screening is feasible. This method could be utilized to screen the majority of the older adult population, as it dramatically lowers examination-related costs. The social and economic benefits, especially caregiver and healthcare service burden, of the early detection of cognitive disorders could be enormous. At the same time, as older adults are becoming increasingly computer savvy, it is important to create software that meets their needs and allows them to remain healthy and active. Out team continues its research on the VSM with the aim of improving its usability, shortening its administration time and supplementing the science behind VSM with additional data.


  7. Benzodiazepines, related drugs increase stroke risk among persons with Alzheimer’s disease

    January 25, 2017 by Ashley

    From the University of Eastern Finland media release:

    memory lossThe use of benzodiazepines and benzodiazepine-like drugs was associated with a 20 per cent increased risk of stroke among persons with Alzheimer’s disease, shows a recent study from the University of Eastern Finland. Benzodiazepines were associated with a similar risk of stroke as benzodiazepine-like drugs.

    The use of benzodiazepines and benzodiazepine-like drugs was associated with an increased risk of any stroke and ischemic stroke, whereas the association with hemorrhagic stroke was not significant. However, due to the small number of hemorrhagic stroke events in the study population, the possibility of such an association cannot be excluded. The findings are important, as benzodiazepines and benzodiazepine-like drugs were not previously known to predispose to strokes or other cerebrovascular events. Cardiovascular risk factors were taken into account in the analysis and they did not explain the association.

    The findings encourage a careful consideration of the use of benzodiazepines and benzodiazepine-like drugs among persons with Alzheimer’s disease, as stroke is one of the leading causes of death in this population group. Earlier, the researchers have also shown that these drugs are associated with an increased risk of hip fracture.

    The study was based on data from a nationwide register-based study (MEDALZ) conducted at the University of Eastern Finland in 2005-2011. The study population included 45,050 persons diagnosed with Alzheimer’s disease, and 22 per cent of them started using benzodiazepines or benzodiazepine-like drugs.

    The findings were published in International Clinical Psychopharmacology.


  8. The lasting effects of ministrokes may contribute to dementia

    January 24, 2017 by Ashley

    From the Medical University of South Carolina media release:

    hospital emergency signEvidence overwhelmingly supports a link between cognitive decline and cerebrovascular diseases such as atherosclerosis, arteriolosclerosis, and cerebral amyloid angiopathy.

    Not only do individuals with cerebrovascular diseases have a much higher incidence of cortical microinfarcts (mini-strokes), but post-mortem histological and in vivo radiological studies also find that the burden of microinfarcts is significantly greater among people with vascular cognitive impairment and dementia (VCID) than in age-matched, non-demented individuals.

    Until now, the mechanisms by which these miniscule lesions (~0.05 to 3 millimeters in diameter) contribute to cognitive deficits including dementia have been poorly understood.

    Findings from a recent study by investigators at the Medical University of South Carolina (MUSC) provide crucial information for better understanding the impact of microinfarcts, showing that the functional deficits caused by a single microinfarct can affect a larger area of brain tissue and last longer than was previously thought to be the case.

    The functional effects of microinfarcts are extremely difficult to study. Not only are most microinfarcts difficult to detect with standard neuroimaging techniques, mismatches between in vivo functional data and post-mortem histological evidence make it nearly impossible to connect microinfarcts to the timeline of cognitive decline.

    These infarcts are so small and unpredictable, we just haven’t had good tools to detect them while the person was still alive,” said Andy Shih, Ph.D., Assistant Professor of Neurosciences and senior author on the article. “So, until now, we basically just had post-mortem snapshots of these infarcts at the end of the dementia battle as well as measures of the person’s cognitive decline, which might have been taken years before the brain became available for study.”

    Intrigued by the mounting evidence linking cognitive decline and microinfarct burden, Shih’s group hypothesized that microinfarcts might disrupt brain function beyond what was visible by histology or magnetic resonance imaging (MRI).

    Even though a person may experience hundreds of thousands of microinfarcts in their lifetime, each event is extremely small and thought to resolve in a matter of days,” said Shih. “It’s been estimated that, overall, microinfarcts affect less than 2% of the entire human brain. But those estimates of tissue loss are based only on the ‘core’ of the microinfarct, the area of dead or dying tissue that we can see in routine, post-mortem, histological stains.”

    To investigate their theory of broader impacts, the team developed a mouse model so that they could examine the effects of individual cortical microinfarcts on surrounding tissue function in vivo over several weeks post-event. “We needed a preclinical model to create very predictable lesions that we could follow over time,” said Shih. “Also, we needed to be able to obtain readouts of brain activity that were consistent over time.”

    The team used photothrombosis to occlude a single arteriole in the barrel cortex of mice fitted with cranial windows. They then compared functional readouts of sensory-evoked brain activity, indicated by activity-dependent c-Fos expression or in vivo two-photon imaging of single vessel hemodynamic responses, to the location of the microinfarct core.

    Post-mortem, c-Fos immunostaining revealed that an area estimated to be at least 12-times greater in volume than the microinfarct core had been affected by the event. Furthermore, in vivo, two-photon imaging of single vessel, sensory-evoked hemodynamics found that neuronal activity across the affected tissue area remained partially depressed for 14 to 17 days after the microinfarct.

    Together, these data indicate that functional deficits caused by a single microinfarct occur across a much larger area of viable peri-lesional tissue than was previously understood and that the resulting deficits are much longer-lasting.

    I knew larger strokes could have distant effects, but I was surprised that something of this scale could have such a large effect,” said Shih.

    The duration of effect from a single microinfarct was also a surprise for Shih’s team. “The MRI signal increased and then went away as we’d expected, but we were surprised on autopsy to see that there was still lots going on — tissue damage and neuroinflammation,” Shih explained. “Even after three weeks the neurally evoked blood flow responses had only partially recovered. So, that means a microinfarct can come and go and you can see it briefly with MRI but it leaves a lasting impression on brain function-possibly for months.”

    Importantly, a person with VCID is likely to experience other microinfarcts during this recovery time. Furthermore, these tiny infarcts occur not only in the brain’s grey matter, where this study was conducted, but also in the white matter, which sends messages from one part of the brain to another.

    “Over time, after you have a lot of microinfarcts, there may be enough accumulated damage in the brain’s circuitry to equal the impact of a larger event,” said Shih.

    According to Shih, one of the most important messages from this study is that conventional methods used in clinical trials do not reveal the entire impact that microinfarcts have on brain function. He hopes that his team’s contribution to illuminating microinfarct pathology will help inform MRI interpretation in humans and help researchers better explain some of the relationships that they see in clinical studies.

    These findings might also lead to new preventive protocols. “On a clinical level, maybe it’s a situation where therapeutics can play a bigger role. Maybe drugs that we already have can mitigate the cumulative damage of microinfarcts,” speculated Shih. “The neuro-protective idea hasn’t flown very far for acute stroke, in part, because the window of time for protecting the brain from stroke damage is very narrow. But, for microinfarcts, you don’t have to know exactly when they occur. If an MRI shows a person is at high risk for microinfarcts, maybe one day we can put them on a drug for a while to reduce the impacts of these lesions.”


  9. Living near major traffic linked to higher risk of dementia

    January 13, 2017 by Ashley

    From the Public Health Ontario media release:

    night trafficPeople who live close to high-traffic roadways face a higher risk of developing dementia than those who live further away, new research from Public Health Ontario (PHO) and the Institute for Clinical Evaluative Sciences (ICES) has found.

    Led by PHO and ICES scientists, the study found that people who lived within 50 metres of high-traffic roads had a seven per cent higher likelihood of developing dementia compared to those who lived more than 300 meters away from busy roads.

    Published in The Lancet, the researchers examined records of more than 6.5 million Ontario residents aged 20-85 to investigate the correlation between living close to major roads and dementia, Parkinson’s disease and multiple sclerosis.

    Scientists identified 243,611 cases of dementia, 31,577 cases of Parkinson’s disease, and 9,247 cases of multiple sclerosis in Ontario between 2001 and 2012. In addition, they mapped individuals’ proximity to major roadways using the postal code of their residence. The findings indicate that living close to major roads increased the risk of developing dementia, but not Parkinson’s disease or multiple sclerosis, two other major neurological disorders.

    “Little is known in current research about how to reduce the risk of dementia. Our findings show the closer you live to roads with heavy day-to-day traffic, the greater the risk of developing dementia. With our widespread exposure to traffic and the greater tendency for people to live in cities these days, this has serious public health implications,” says Dr. Hong Chen, environmental and occupational health scientist at PHO and an adjunct scientist at ICES. Dr. Chen is lead author on the paper titled Living Near Major Roads and the Incidence of Dementia, Parkinson’s Disease, and Multiple Sclerosis: A Population-based Cohort Study.

    Our study is the first in Canada to suggest that pollutants from heavy, day-to-day traffic are linked to dementia. We know from previous research that air pollutants can get into the blood stream and lead to inflammation, which is linked with cardiovascular disease and possibly other conditions such as diabetes. This study suggests air pollutants that can get into the brain via the blood stream can lead to neurological problems,” says Dr. Ray Copes, chief of environmental and occupational health at PHO and an author on the paper.

    As urban centres become more densely populated and more congested with vehicles on major roads, Dr. Copes suggests the findings of this paper could be used to help inform municipal land use decisions as well as building design to take into account air pollution factors and the impact on residents.

    This research was conducted in collaboration with scientists from the University of Toronto, Carleton University, Dalhousie University, Oregon State University, and Health Canada. The study was funded by Health Canada.

    Key findings:

    • Using data held at ICES, the researchers examined records of more than 6.5 million Ontario residents, aged 20-85, and mapped them according to residential postal codes five years before the study started.
    • Between 2001 and 2012, 243,611 cases of dementia, 31,577 cases of Parkinson’s disease, and 9,247 cases of multiple sclerosis were identified in Ontario.
    • People who lived within 50 metres of high-traffic roads had a seven per cent higher likelihood of dementia than those who lived more 300 meters away from busy roads.
    • The increase in the risk of developing dementia went down to four per cent if people lived 50-100 metres from major traffic, and to two per cent if they lived within 101-200 metres. At over 200 metres, there was no elevated risk of dementia.
    • There was no correlation between major traffic proximity and Parkinson’s disease or multiple sclerosis.

     


  10. Mediterranean diet may have lasting effects on brain health

    by Ashley

    From the American Academy of Neurology (AAN) media release:

    healthy, vital seniorA new study shows that older people who followed a Mediterranean diet retained more brain volume over a three-year period than those who did not follow the diet as closely.

    The study is published in the January 4, 2017, online issue of Neurlogy®, the medical journal of the American Academy of Neurology. But contrary to earlier studies, eating more fish and less meat was not related to changes in the brain.

    The Mediterranean diet includes large amounts of fruits, vegetables, olive oil, beans and cereal grains such as wheat and rice, moderate amounts of fish, dairy and wine, and limited red meat and poultry.

    As we age, the brain shrinks and we lose brain cells which can affect learning and memory,” said study author Michelle Luciano, PhD, of the University of Edinburgh in Scotland. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.”

    Researchers gathered information on the eating habits of 967 Scottish people around age 70 who did not have dementia. Of those people, 562 had an MRI brain scan around age 73 to measure overall brain volume, gray matter volume and thickness of the cortex, which is the outer layer of the brain. From that group, 401 people then returned for a second MRI at age 76. These measurements were compared to how closely participants followed the Mediterranean diet.

    The participants varied in how closely their dietary habits followed the Mediterranean diet principles. People who didn’t follow as closely to the Mediterranean diet were more likely to have a higher loss of total brain volume over the three years than people who followed the diet more closely. The difference in diet explained 0.5 percent of the variation in total brain volume, an effect that was half the size of that due to normal aging.

    The results were the same when researchers adjusted for other factors that could affect brain volume, such as age, education and having diabetes or high blood pressure [hypertension].

    There was no relationship between grey matter volume or cortical thickness and the Mediterranean diet.

    The researchers also found that fish and meat consumption were not related to brain changes, which is contrary to earlier studies.

    It’s possible that other components of the Mediterranean diet are responsible for this relationship, or that it’s due to all of the components in combination,” Luciano said.

    Luciano noted that earlier studies looked at brain measurements at one point in time, whereas the current study followed people over time.

    “In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain,” said Luciano. “Still, larger studies are needed to confirm these results.”