Slow walking speed, memory complaints can predict dementia

A study involving nearly 27,000 older adults on five continents found that nearly 1 in 10 met criteria for pre-dementia based on a simple test that measures how fast people walk and whether they have cognitive complaints. People who tested positive for pre-dementia were twice as likely as others to develop dementia within 12 years. The study, led by scientists at Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center, was published online on July 16, 2014 in Neurology, the medical journal of the American Academy of Neurology.The new test diagnoses motoric cognitive risk syndrome (MCR). Testing for the newly described syndrome relies on measuring gait speed (our manner of walking) and asking a few simple questions about a patient’s cognitive abilities, both of which take just seconds. The test is not reliant on the latest medical technology and can be done in a clinical setting, diagnosing people in the early stages of the dementia process. Early diagnosis is critical because it allows time to identify and possibly treat the underlying causes of the disease, which may delay or even prevent the onset of dementia in some cases.”In many clinical and community settings, people don’t have access to the sophisticated tests — biomarker assays, cognitive tests or neuroimaging studies — used to diagnose people at risk for developing dementia,” said Joe Verghese, M.B.B.S., professor in the Saul R. Korey Department of Neurology and of medicine at Einstein, chief of geriatrics at Einstein and Montefiore, and senior author of the Neurology paper. “Our assessment method could enable many more people to learn if they’re at risk for dementia, since it avoids the need for complex testing and doesn’t require that the test be administered by a neurologist. The potential payoff could be tremendous — not only for individuals and their families, but also in terms of healthcare savings for society. All that’s needed to assess MCR is a stopwatch and a few questions, so primary care physicians could easily incorporate it into examinations of their older patients.”The U.S. …

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Morning rays keep off pounds

A surprising new strategy for managing your weight? Bright morning light.A new Northwestern Medicine study reports the timing, intensity and duration of your light exposure during the day is linked to your weight — the first time this has been shown.People who had most of their daily exposure to even moderately bright light in the morning had a significantly lower body mass index (BMI) than those who had most of their light exposure later in the day, the study found. (BMI is a ratio calculated from a person’s weight and height.)”The earlier this light exposure occurred during the day, the lower individuals’ body mass index,” said co-lead author Kathryn Reid, research associate professor of neurology at Northwestern University Feinberg School of Medicine. “The later the hour of moderately bright light exposure, the higher a person’s BMI.”The influence of morning light exposure on body weight was independent of an individual’s physical activity level, caloric intake, sleep timing, age or season. It accounted for about 20 percent of a person’s BMI.”Light is the most potent agent to synchronize your internal body clock that regulates circadian rhythms, which in turn also regulate energy balance,” said study senior author Phyllis C. Zee, M.D. “The message is that you should get more bright light between 8 a.m. and noon.” About 20 to 30 minutes of morning light is enough to affect BMI.Zee is the Benjamin and Virginia T. Boshes Professor of Neurology and director of the Northwestern Medicine Sleep and Circadian Rhythms Research Program at Northwestern University Feinberg School of Medicine. She also is a neurologist at Northwestern Memorial Hospital.”If a person doesn’t get sufficient light at the appropriate time of day, it could de-synchronize your internal body clock, which is known to alter metabolism and can lead to weight gain,” Zee said. …

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Do obesity, birth control pills raise risk of multiple sclerosis?

The role of the so-called “obesity hormone” leptin and hormones used for birth control in the development of multiple sclerosis (MS) is examined in two new studies that will be presented at the American Academy of Neurology’s 66th Annual Meeting in Philadelphia, April 26 to May 3, 2014.For the obesity study, BMI was calculated for 210 people with MS and 210 people of the same age and sex who did not have MS at ages 15 and 20 and at the time of the study. The study found that people who are obese at age 20 are twice as likely to later develop MS as people who are not obese. The study found that people with higher BMI levels also had higher levels of leptin, a hormone made by fat tissue that regulates weight, appetite and immune response.”Leptin promotes inflammatory responses in the body, which could potentially explain the link between obesity and MS,” said study author Jorge Correale, MD, of the Ral Carrera Institute for Neurological Research in Buenos Aires, Argentina.For the birth control hormone study, researchers identified 305 women who had been diagnosed with MS or its precursor, clinically isolated syndrome, during a three-year period from the membership of Kaiser Permanente Southern California and who had been members for at least three years before the MS symptoms began. Then they compared them to 3,050 women who did not have MS.A total of 29 percent of the women with MS and 24 percent of those without MS had used hormonal contraceptives for at least three months in the three years before symptoms began. The majority used estrogen/progestin combinations.Women who had used hormonal contraceptives were 35 percent more likely to develop MS than those who did not use them. Those who had used the contraceptives but had stopped at least one month before symptoms started were 50 percent more likely to develop MS.”These findings suggest that using hormonal contraceptives may be contributing at least in part to the rise in the rate of MS among women,” said study lead author Kerstin Hellwig, MD, from Bochum Germany, post-doctoral research fellow, Kaiser Permanente Southern California.Story Source:The above story is based on materials provided by American Academy of Neurology (AAN). Note: Materials may be edited for content and length.

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Brain differences linked to insomnia identified by researchers

Johns Hopkins researchers report that people with chronic insomnia show more plasticity and activity than good sleepers in the part of the brain that controls movement.”Insomnia is not a nighttime disorder,” says study leader Rachel E. Salas, M.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine. “It’s a 24-hour brain condition, like a light switch that is always on. Our research adds information about differences in the brain associated with it.”Salas and her team, reporting in the March issue of the journal Sleep, found that the motor cortex in those with chronic insomnia was more adaptable to change — more plastic — than in a group of good sleepers. They also found more “excitability” among neurons in the same region of the brain among those with chronic insomnia, adding evidence to the notion that insomniacs are in a constant state of heightened information processing that may interfere with sleep.Researchers say they hope their study opens the door to better diagnosis and treatment of the most common and often intractable sleep disorder that affects an estimated 15 percent of the United States population.To conduct the study, Salas and her colleagues from the Department of Psychiatry and Behavioral Sciences and the Department of Physical Medicine and Rehabilitation used transcranial magnetic stimulation (TMS), which painlessly and noninvasively delivers electromagnetic currents to precise locations in the brain and can temporarily and safely disrupt the function of the targeted area. TMS is approved by the U.S. Food and Drug Administration to treat some patients with depression by stimulating nerve cells in the region of the brain involved in mood control.The study included 28 adult participants — 18 who suffered from insomnia for a year or more and 10 considered good sleepers with no reports of trouble sleeping. Each participant was outfitted with electrodes on their dominant thumb as well as an accelerometer to measure the speed and direction of the thumb.The researchers then gave each subject 65 electrical pulses using TMS, stimulating areas of the motor cortex and watching for involuntary thumb movements linked to the stimulation. Subsequently, the researchers trained each participant for 30 minutes, teaching them to move their thumb in the opposite direction of the original involuntary movement. They then introduced the electrical pulses once again.The idea was to measure the extent to which participants’ brains could learn to move their thumbs involuntarily in the newly trained direction. …

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Brain cell activity regulates Alzheimer’s protein

Increased brain cell activity boosts brain fluid levels of a protein linked to Alzheimer’s disease, according to new research from scientists at Washington University School of Medicine in St. Louis.Tau protein is the main component of neurofibrillary tangles, one of the hallmarks of Alzheimer’s disease. It has been linked to other neurodegenerative disorders, including frontotemporal dementia, supranuclear palsy and corticobasal degeneration.”Healthy brain cells normally release tau into the cerebrospinal fluid and the interstitial fluid that surrounds them, but this is the first time we’ve linked that release in living animals to brain cell activity,” said senior author David M. Holtzman, MD. “Understanding this link should help advance our efforts to treat Alzheimer’s and other neurodegenerative disorders associated with the tau protein.The study appears online in The Journal of Experimental Medicine.Tau protein stabilizes microtubules, which are long columns that transport supplies from the center of the cell to the distant ends of the cell’s branches. Some tau in the cell is not bound to microtubules. This tau can become altered and clump together inside brain cells, forming structures called tangles. Scientists have tracked the spread of these clumps through brain networks in animal models.”In Alzheimer’s disease, you first see clumps of tau in a region called the entorhinal cortex, and then in the hippocampus, and it continues to spread through the brain in a regular pattern,” said Holtzman, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. …

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Brain’s ‘sweet spot’ for love found in neurological patient

A region deep inside the brain controls how quickly people make decisions about love, according to new research at the University of Chicago.The finding, made in an examination of a 48-year-old man who suffered a stroke, provides the first causal clinical evidence that an area of the brain called the anterior insula “plays an instrumental role in love,” said UChicago neuroscientist Stephanie Cacioppo, lead author of the study.In an earlier paper that analyzed research on the topic, Cacioppo and colleagues defined love as “an intentional state for intense [and long-term] longing for union with another” while lust, or sexual desire, is characterized by an intentional state for a short-term, pleasurable goal.In this study, the patient made decisions normally about lust but showed slower reaction times when making decisions about love, in contrast to neurologically typical participants matched on age, gender and ethnicity. The findings are presented in a paper, “Selective Decision-Making Deficit in Love Following Damage to the Anterior Insula,” published in the journal Current Trends in Neurology.”This distinction has been interpreted to mean that desire is a relatively concrete representation of sensory experiences, while love is a more abstract representation of those experiences,” said Cacioppo, a research associate and assistant professor in psychology. The new data suggest that the posterior insula, which affects sensation and motor control, is implicated in feelings of lust or desire, while the anterior insula has a role in the more abstract representations involved in love.In the earlier paper, “The Common Neural Bases Between Sexual Desire and Love: A Multilevel Kernel Density fMRI Analysis,” Cacioppo and colleagues examined a number of studies of brain scans that looked at differences between love and lust.The studies showed consistently that the anterior insula was associated with love, and the posterior insula was associated with lust. However, as in all fMRI studies, the findings were correlational.”We reasoned that if the anterior insula was the origin of the love response, we would find evidence for that in brain scans of someone whose anterior insula was damaged,” she said.In the study, researchers examined a 48-year-old heterosexual male in Argentina, who had suffered a stroke that damaged the function of his anterior insula. He was matched with a control group of seven Argentinian heterosexual men of the same age who had healthy anterior insula.The patient and the control group were shown 40 photographs at random of attractive, young women dressed in appealing, short and long dresses and asked whether these women were objects of sexual desire or love. The patient with the damaged anterior insula showed a much slower response when asked if the women in the photos could be objects of love.”The current work makes it possible to disentangle love from other biological drives,” the authors wrote. Such studies also could help researchers examine feelings of love by studying neurological activity rather than subjective questionnaires.The full article can be found online at: https://hpenlaboratory.uchicago.edu/sites/caciopponeurolab.uchicago.edu/files/uploads/Cacioppo%20et%20al_Current%20Trends%20in%20Neurology%202013.pdfStory Source:The above story is based on materials provided by University of Chicago. Note: Materials may be edited for content and length.

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Eyemusic sensory substitution device enables the blind to ‘see’ colors and shapes

Using auditory or tactile stimulation, Sensory Substitution Devices (SSDs) provide representations of visual information and can help the blind “see” colors and shapes. SSDs scan images and transform the information into audio or touch signals that users are trained to understand, enabling them to recognize the image without seeing it.Currently SSDs are not widely used within the blind community because they can be cumbersome and unpleasant to use. However, a team of researchers at the Hebrew University of Jerusalem have developed the EyeMusic, a novel SSD that transmits shape and color information through a composition of pleasant musical tones, or “soundscapes.” A new study published in Restorative Neurology and Neuroscience reports that using the EyeMusic SSD, both blind and blindfolded sighted participants were able to correctly identify a variety of basic shapes and colors after as little as 2-3 hours of training.Most SSDs do not have the ability to provide color information, and some of the tactile and auditory systems used are said to be unpleasant after prolonged use. The EyeMusic, developed by senior investigator Prof. Amir Amedi, PhD, and his team at the Edmond and Lily Safra Center for Brain Sciences (ELSC) and the Institute for Medical Research Israel-Canada at the Hebrew University, scans an image and uses musical pitch to represent the location of pixels. The higher the pixel on a vertical plane, the higher the pitch of the musical note associated with it. Timing is used to indicate horizontal pixel location. Notes played closer to the opening cue represent the left side of the image, while notes played later in the sequence represent the right side. Additionally, color information is conveyed by the use of different musical instruments to create the sounds: white (vocals), blue (trumpet), red (reggae organ), green (synthesized reed), yellow (violin); black is represented by silence.”This study is a demonstration of abilities showing that it is possible to encode the basic building blocks of shape using the EyeMusic,” explains Prof. Amir Amedi. …

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Stroke trigger more deadly for African-Americans

Infection is a stronger trigger of stroke death in African- Americans than in whites, a University of Michigan study shows.African-Americans were 39 times more likely to die of a stroke if they were exposed to an infection in the previous month when compared to other time periods while whites were four times more likely and Hispanics were five times more likely to die of stroke after an infection, according to the findings that appear online Feb. 7 in Neurology.The most frequent infections were urinary, skin, and respiratory tract infections and occurred within 30 days of a stroke.”Infection before stroke appears to be most lethal for black Americans,” says lead author Deborah A. Levine, M.D., M.P.H., assistant professor of medicine in the division of general medicine in the U-M Medical School. “We know that African- Americans have a much greater risk of dying from a stroke than white Americans, and we wanted to know if infection — which research suggests is a stroke trigger — might contribute to this disparity.”Infection is believed to promote the formation of blood clots and fat buildup in arteries, which block the artery and stop the flow of blood to the brain causing a stroke.Racial disparities in stroke death continue to widen in the U.S. where blacks are twice as likely to die from stroke as whites. The new findings show that all ethnic and racial groups had a higher risk of stroke following an infection but there were significant disparities in subsequent stroke deaths.Infection appeared to be a trigger of stroke death in whites and Hispanics as well, but it was particularly potent in African-Americans.Infection also occurred more often before stroke death in black Americans, with 70 percent experiencing an infection in the 30 days before stroke death compared to a frequency of 15 percent in months that were not followed by a stroke death. Infection occurred less often before stroke death in white Americans, with 45 percent experiencing an infection in the month before stroke death compared to a frequency of 19 percent in months that were not followed by a stroke death.Although earlier studies suggested that respiratory infections are the most potent triggers of stroke, Levine and colleagues found that urinary tract infections and skin infections seemed to be just as strong of triggers.The study was based on data from the Health and Retirement Study, a nationally-representative sample of older Americans that is conducted by the U-M Institute for Social Research on behalf of the National Institute of Aging.”Because of the higher stroke mortality rate among black Americans, there has been much attention on racial differences in vascular risk factors, like hypertension, and health behaviors but less attention on acute exposures that might contribute to racial differences in stroke deaths,” Levine says.”It is unclear why acute infection is more common, more lethal, or a more powerful trigger for stroke death in black Americans. Genetic risks, clinical, economic or environmental factors, and differences in access to health care are potential reasons. We need further studies to better understand this disparity so we can prevent more black Americans from dying of stroke, particularly after infection,” Levine says.Story Source:The above story is based on materials provided by University of Michigan Health System. Note: Materials may be edited for content and length.

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Women fare worse than men following stroke

The good news: More people survive stroke now than 10 years ago due to improved treatment and prevention. The bad news: Women who survive stroke have a worse quality of life than men, according to a study published in the Feb. 7 online issue of the journal Neurology.Researchers at Wake Forest Baptist Medical Center compared the quality of life in men and women who had a stroke or transient ischemic attack (TIA). A total of 1,370 patients ages 56 to 77 from the AVAIL registry – a national, multicenter, longitudinal registry of ischemic stroke and TIA patients – were included in the study.The patients’ quality of life was measured at three months and one year after a stroke or TIA using a formula that assesses mobility, self-care, everyday activities, depression/anxiety and pain.“We found that women had a worse quality of life than men up to 12 months following a stroke, even after considering differences in important sociodemographic variables, stroke severity and disability,” said Cheryl Bushnell, M.D., associate professor of neurology at Wake Forest Baptist and senior author of the study.“As more people survive strokes, physicians and other healthcare providers should pay attention to quality of life issues and work to develop better interventions, even gender-specific screening tools, to improve these patients’ lives.”The study findings showed that at three months, women were more likely than men to report problems with mobility, pain/discomfort and anxiety and depression, but the difference was greatest in those over age 75. At one year, women still had lower quality of life scores overall than men but the magnitude of those differences had diminished, Bushnell said.“The reason we do these types of studies is to be able to add different variables sequentially to determine what accounts for these gender differences,” Bushnell said. “We found that age, race and marital status accounted for the biggest differences between men and women at three months, with marital status being the most important. Even though the women in the study were older than the men, our study showed that age really had very little effect on quality of life.”The results suggest that further research on mobility, pain or discomfort and anxiety/depression may provide a clearer understanding for how to improve the lives of women after stroke, Bushnell added.The next step for the Wake Forest Baptist team will be to look at the trajectory of cognitive decline in men and women before and after stroke, she said.Story Source:The above story is based on materials provided by Wake Forest Baptist Medical Center. Note: Materials may be edited for content and length.

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Huntington disease prevention trial shows creatine safe, slows progression

The first clinical trial of a drug intended to delay the onset of symptoms of Huntington disease (HD) reveals that high-dose treatment with the nutritional supplement creatine was safe and well tolerated by most study participants. In addition, neuroimaging showed a treatment-associated slowing of regional brain atrophy, evidence that creatine might slow the progression of presymptomatic HD. The Massachusetts General Hospital (MGH) study also utilized a novel design that allowed participants — all of whom were at genetic risk for the neurodegenerative disorder — to enroll without having to learn whether or not they carried the mutation that causes HD.”More than 90 percent of those in the United States who know they are at risk for HD because of their family history have abstained from genetic testing, often because they fear discrimination or don’t want to face the stress and anxiety of knowing they are destined to develop such a devastating disease,” says H. Diana Rosas, MD, of the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND), lead and corresponding author of the paper that will appear in the March 11 issue of Neurology and has been released online. “Many of these individuals would still like to help find treatments, and this trial design allows them to participate while respecting their autonomy, their right not to know their personal genetic information.”Among the ways that the mutated form of the huntingtin protein damages brain cells is by interfering with cellular energy production, leading to a depletion of ATP, the molecule that powers most biological processes. Known to help restore ATP and maintain cellular energy, creatine is being investigated to treat a number of neurological conditions — including Parkinson disease, amyotrophic lateral sclerosis and spinal cord injury. Studies in mouse models of HD showed that creatine raises brain ATP levels and protects against neurodegeneration. Previous clinical trials of creatine in symptomatic HD patients have been limited in scale, involved daily doses of 10 grams or less, and did not provide evidence of potential efficacy. Based on the results of a pilot study at MGH that evaluated doses as high as 40 grams, participants in the current study received doses of up to 30 grams daily.The phase II PRECREST trial enrolled 64 adult participants — 19 who knew they carried the mutated form of the HD gene and 45 with a 50 percent risk of having inherited the HD mutation. Genetic testing, results of which were made available only to the study statistician and not to study staff or participants, confirmed the genetic status of those who had previously been tested and revealed an additional 26 presymptomatic carriers of the mutated gene, for a total of 47 participants with presymptomatic HD and 17 controls.For the first 6 months of the trial, participants were randomized into two groups, regardless of gene status. …

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Gender influences symptoms of genetic disorder NF1

A genetic disorder that affects about 1 in every 2,500 births can cause a bewildering array of clinical problems, including brain tumors, impaired vision, learning disabilities, behavioral problems, heart defects and bone deformities. The symptoms and their severity vary among patients affected by this condition, known as neurofibromatosis type 1 (NF1).Now, researchers at Washington University School of Medicine in St. Louis have identified a patient’s gender as a clear and simple guidepost to help health-care providers anticipate some of the effects of NF1. The scientists report that girls with NF1 are at greater risk of vision loss from brain tumors. They also identified gender-linked differences in male mice that may help explain why boys with NF1 are more vulnerable to learning disabilities.”This information will help us adjust our strategies for predicting the potential outcomes in patients with NF1 and recommending appropriate treatments,” said David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology, who treats NF1 patients at St. Louis Children’s Hospital.The findings appear online in the Annals of Neurology.Kelly Diggs-Andrews, PhD, a postdoctoral research associate in Gutmann’s laboratory, reviewed NF1 patient data collected at the Washington University Neurofibromatosis (NF) Center. In her initial assessment, Diggs-Andrews found that the number of boys and girls was almost equal in a group of nearly 100 NF1 patients who had developed brain tumors known as optic gliomas. But vision loss occurred three times more often in girls with these tumors.With help from David Wozniak, PhD, research professor of psychiatry, the scientists looked for an explanation in Nf1 mice (which, like NF1 patients, have a mutation in their Nf1 gene). …

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Blue light may fight fatigue around the clock

Researchers from Brigham and Women’s Hospital (BWH) have found that exposure to short wavelength, or blue light, during the biological day directly and immediately improves alertness and performance. These findings are published in the February issue of Sleep.”Our previous research has shown that blue light is able to improve alertness during the night, but our new data demonstrates that these effects also extend to daytime light exposure,” said Shadab Rahman, PhD, a researcher in BWH’s Division of Sleep Medicine and lead author of this study. “These findings demonstrate that prolonged blue light exposure during the day has an an alerting effect.”In order to determine which wavelengths of light were most effective in warding off fatigue, the BWH researchers teamed with George Brainard, PhD, a professor of neurology at Thomas Jefferson University, who developed the specialized light equipment used in the study. Researchers compared the effects of blue light with exposure to an equal amount of green light on alertness and performance in 16 study participants for 6.5 hours over a day. Participants then rated how sleepy they felt, had their reaction times measured and wore electrodes to assess changes in brain activity patterns during the light exposure.The researchers found that participants exposed to blue light consistently rated themselves as less sleepy, had quicker reaction times and fewer lapses of attention during the performance tests compared to those who were exposed to green light. They also showed changes in brain activity patterns that indicated a more alert state.”These results contribute to our understanding of how light impacts the brain and open up a new range of possibilities for using light to improve human alertness, productivity and safety,” explained Steven Lockley, PhD, neuroscientist at BWH and senior investigator of the study. “While helping to improve alertness in night workers has obvious safety benefits, day shift workers may also benefit from better quality lighting that would not only help them see better but also make them more alert.”Researchers note that the next big challenge is to figure out how to deliver better lighting. While natural light is ideal, many people do not have access to daylight in their schools, homes or work places. In addition to improvements in daylight access, the advent of new, more controllable lighting technologies may help enable researchers to develop ‘smart’ lighting systems designed to maximize the beneficial effects of light for human health, productivity and safety.Story Source:The above story is based on materials provided by Brigham and Women’s Hospital. Note: Materials may be edited for content and length.

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Pesticides increase risk for Parkinson’s disease: Certain people may be more susceptible

Previous studies have shown the certain pesticides can increase the risk for developing Parkinson’s disease. Now, UCLA researchers have now found that the strength of that risk depends on an individual’s genetic makeup, which in the most pesticide-exposed populations could increase the chances of developing the debilitating disease by two- to six-fold.In a previous study published January 2013 in the Proceedings of the National Academy of Sciences, the UCLA research team discovered a link between Parkinson’s and the pesticide benomyl, a fungicide that has been banned by the U.S. Environmental Protection Agency. That study found that benomyl inhibited an enzyme called aldehyde dehydrogenase (ALDH), which converts aldehydes highly toxic to dopamine cells into less toxic agents, and therefore contributed to the development of Parkinson’s.In this study, UCLA researchers tested a number of other pesticides and found 11 that also inhibit ALDH and increase the risk of Parkinson’s, and at much lower levels than those at which they are currently being used, said study lead author Jeff Bronstein, a professor of neurology and director of movement disorders at UCLA.Bronstein said the team also found that people with a common genetic variant of the ALDH2 gene are particularly sensitive to the effects of ALDH-inhibiting pesticides, and were two to six times more likely to develop Parkinson’s than those without the variant when exposed to these pesticides.The results of the epidemiological study appear Feb. 5, 2014 in the online issue of Neurology, the medical journal of the American Academy of Neurology.”We were very surprised that so many pesticides inhibited ALDH and at quite low concentrations, concentrations that were way below what was needed for the pesticides to do their job,” Bronstein said. “These pesticides are pretty ubiquitous, and can be found on our food supply and are used in parks and golf courses and in pest control inside buildings and homes. So this significantly broadens the number of people at risk.”The study compared 360 patients with Parkinson’s in three agriculture heavy Central California counties to 816 people from the same area who did not have Parkinson’s. Researchers focused their analyses on individuals with ambient exposures to pesticides at work and at home, using information from the California Department of Pesticide Regulation.In the previous PNAS study, Bronstein and his team determined the mechanism that leads to increased risk. Exposure to pesticides starts a cascade of cellular events, preventing ALDH from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When ALDH does not detoxify DOPAL sufficiently, it accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s.”ALDH inhibition appears to be an important mechanism by which these environmental toxins contribute to Parkinson’s pathogenesis, especially in genetically vulnerable individuals,” said study author Beate Ritz, a professor of epidemiology at the Fielding School of Public Health at UCLA. …

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Method of recording brain activity could lead to mind-reading devices, Stanford scientists say

Oct. 15, 2013 — A brain region activated when people are asked to perform mathematical calculations in an experimental setting is similarly activated when they use numbers — or even imprecise quantitative terms, such as “more than” — in everyday conversation, according to a study by Stanford University School of Medicine scientists.Using a novel method, the researchers collected the first solid evidence that the pattern of brain activity seen in someone performing a mathematical exercise under experimentally controlled conditions is very similar to that observed when the person engages in quantitative thought in the course of daily life.”We’re now able to eavesdrop on the brain in real life,” said Josef Parvizi, MD, PhD, associate professor of neurology and neurological sciences and director of Stanford’s Human Intracranial Cognitive Electrophysiology Program. Parvizi is the senior author of the study, published Oct. 15 in Nature Communications. The study’s lead authors are postdoctoral scholar Mohammad Dastjerdi, MD, PhD, and graduate student Muge Ozker.The finding could lead to “mind-reading” applications that, for example, would allow a patient who is rendered mute by a stroke to communicate via passive thinking. Conceivably, it could also lead to more dystopian outcomes: chip implants that spy on or even control people’s thoughts.”This is exciting, and a little scary,” said Henry Greely, JD, the Deane F. and Kate Edelman Johnson Professor of Law and steering committee chair of the Stanford Center for Biomedical Ethics, who played no role in the study but is familiar with its contents and described himself as “very impressed” by the findings. “It demonstrates, first, that we can see when someone’s dealing with numbers and, second, that we may conceivably someday be able to manipulate the brain to affect how someone deals with numbers.”The researchers monitored electrical activity in a region of the brain called the intraparietal sulcus, known to be important in attention and eye and hand motion. Previous studies have hinted that some nerve-cell clusters in this area are also involved in numerosity, the mathematical equivalent of literacy.However, the techniques that previous studies have used, such as functional magnetic resonance imaging, are limited in their ability to study brain activity in real-life settings and to pinpoint the precise timing of nerve cells’ firing patterns. These studies have focused on testing just one specific function in one specific brain region, and have tried to eliminate or otherwise account for every possible confounding factor. …

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Faulty internal recycling by brain’s trash collectors may contribute to Alzheimer’s

Sep. 4, 2013 — A defective trash-disposal system in the brain’s resident immune cells may be a major contributor to neurodegenerative disease, a scientific team from the Stanford University School of Medicine has found.Preliminary observations show that this defect appears in the brains of patients who died of Alzheimer’s disease, so correcting it may someday prove to be an effective way of preventing or slowing the course of the disease.”We were fortunate in being able to compare microglia — the brain’s own immune cells — from five patients who died of Alzheimer’s disease with five who died of other causes,” said Tony Wyss-Coray, PhD, professor of neurology and neurological sciences at the medical school and senior research career scientist at the Veterans Affairs Palo Alto Health Care System. “And we discovered that in Alzheimer’s disease, the microglia are defective. One of these cells’ main functions, removing garbage, is impaired.”Wyss-Coray is the senior author of the study, published Sept. 4 in Neuron. The lead author was postdoctoral scholar Kurt Lucin, PhD.Microglia, one of several important cell types in the brain, serve as both cops and trash collectors. These immune cells continuously police the brain, making sure everything is running smoothly. When they sense a pathogen, they pull out the molecular equivalent of a pistol. If they spot a dead cell or a clump of protein detritus, they don a pair of overalls and hasten to remove it.They do this by engulfing and ingesting the target in a process called phagocytosis. Many cells can do this, but microglia are the pros — and they’d better be, said Wyss-Coray. …

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Alzheimer’s ‘missing link’ found: Promising target for new drugs

Sep. 4, 2013 — Yale School of Medicine researchers have discovered a protein that is the missing link in the complicated chain of events that lead to Alzheimer’s disease, they report in the Sept. 4 issue of the journal Neuron. Researchers also found that blocking the protein with an existing drug can restore memory in mice with brain damage that mimics the disease.”What is very exciting is that of all the links in this molecular chain, this is the protein that may be most easily targeted by drugs,” said Stephen Strittmatter, the Vincent Coates Professor of Neurology and senior author of the study. “This gives us strong hope that we can find a drug that will work to lessen the burden of Alzheimer’s.”Scientists have already provided a partial molecular map of how Alzheimer’s disease destroys brain cells. In earlier work, Strittmatter’s lab showed that the amyloid-beta peptides, which are a hallmark of Alzheimer’s, couple with prion proteins on the surface of neurons. By an unknown process, the coupling activates a molecular messenger within the cell called Fyn.In the Neuron paper, the Yale team reveals the missing link in the chain, a protein within the cell membrane called metabotropic glutamate receptor 5 or mGluR5. When the protein is blocked by a drug similar to one being developed for Fragile X syndrome, the deficits in memory, learning, and synapse density were restored in a mouse model of Alzheimer’s.Strittmatter stressed that new drugs may have to be designed to precisely target the amyloid-prion disruption of mGluR5 in human cases of Alzheimer’s and said his lab is exploring new ways to achieve this.Other Yale authors are Ji Won Um, Adam C. Kaufman, Mikhail Kostylev, Jacqueline K. Heiss, Massimiliano Stagi, Hideyuki Takahashi, Meghan E. …

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Migraine may permanently change brain structure

Aug. 28, 2013 — Migraine may have long-lasting effects on the brain’s structure, according to a study published in the August 28, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.”Traditionally, migraine has been considered a benign disorder without long-term consequences for the brain,” said study author Messoud Ashina, MD, PhD, with the University of Copenhagen in Denmark. “Our review and meta-analysis study suggests that the disorder may permanently alter brain structure in multiple ways.”The study found that migraine raised the risk of brain lesions, white matter abnormalities and altered brain volume compared to people without the disorder. The association was even stronger in those with migraine with aura.For the meta-analysis, researchers reviewed six population-based studies and 13 clinic-based studies to see whether people who experienced migraine or migraine with aura had an increased risk of brain lesions, silent abnormalities or brain volume changes on MRI brain scans compared to those without the conditions.The results showed that migraine with aura increased the risk of white matter brain lesions by 68 percent and migraine with no aura increased the risk by 34 percent, compared to those without migraine. The risk for infarct-like abnormalities increased by 44 percent for those with migraine with aura compared to those without aura. Brain volume changes were more common in people with migraine and migraine with aura than those with no migraines.”Migraine affects about 10 to 15 percent of the general population and can cause a substantial personal, occupational and social burden,” said Ashina. “We hope that through more study, we can clarify the association of brain structure changes to attack frequency and length of the disease. We also want to find out how these lesions may influence brain function.”

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New biomarker could reveal Alzheimer’s disease years before onset

Aug. 14, 2013 — A study published today reported the identification of what may be the earliest known biomarker associated with the risk of developing Alzheimer’s disease (AD). The results suggest that this novel potential biomarker is present in cerebral spinal fluid (CSF) at least a decade before signs of dementia manifest.”If our initial findings can be replicated by other laboratories, the results will change the way we currently think about the causes of Alzheimer’s disease,” said Dr. Ramon Trullas, research professor at the CSIC Institute of Biomedical Research of Barcelona and lead author of the study that was published in Annals of Neurology. “This discovery may enable us to search for more effective treatments that can be administered during the preclinical stage.”Difficult DiagnosisAlzheimer’s disease affects more than five million Americans and is the sixth leading cause of death in the United States. At present, the only way to accurately diagnose the disease is by post-mortem neuropathological analysis. The relationship of currently known biomarkers with the cause of the disease is unclear, making it nearly impossible to diagnose preclinical stages of the disease with any real certainty.The CSIC researchers demonstrated that a decrease in the content of mitochondrial DNA (mtDNA) in CSF may be a preclinical indicator for Alzheimer’s disease; furthermore, there may be a directly causative relationship. The hypothesis is that decreased mtDNA levels in CSF reflect the diminished ability of mitochondria to power the brain’s neurons, triggering their death. The decrease in the concentration of mtDNA precedes the appearance of well-known biochemical Alzheimer’s biomarkers (the Aβ1-42, t-tau, and p-tau proteins), suggesting that the pathophysiological process of Alzheimer’s disease starts earlier than previously thought and that mtDNA depletion may be one of the earliest predictors for the disease.In addition to enabling an investigation of the potential causal relationship of mtDNA and Alzheimer’s progression, the use of mtDNA as an index of preclinical Alzheimer’s disease provides an important advantage over previous biochemical markers: the detection of this novel nucleic acid biomarker is unhampered by the technical difficulties associated with protein detection. mtDNA can be readily quantified by real-time quantitative PCR (qPCR) or droplet digital PCR (ddPCR).Quantitation of mtDNAPrior to this study, researchers had not reported that circulating cell-free mtDNA could be detected in human CSF. …

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From Einstein to Oprah: Famous faces may help spot early dementia

Aug. 12, 2013 — A new study suggests that simple tests that measure the ability to recognize and name famous people such as Albert Einstein, Bill Gates or Oprah Winfrey may help doctors identify early dementia in those 40 to 65 years of age. The research appears in the August 13, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.”These tests also differentiate between recognizing a face and actually naming it, which can help identify the specific type of cognitive impairment a person has,” said study author Tamar Gefen, MS, of Northwestern University Feinberg School of Medicine in Chicago. Gefen worked alongside Emily Rogalski, PhD, also with Northwestern University, for the research.For the study, 30 people with primary progressive aphasia, a type of early onset dementia that mainly affects language, and 27 people without dementia, all with an average age of 62 were given a test. The test includes 20 famous faces printed in black and white, including John F. Kennedy, Lucille Ball, Princess Diana, Martin Luther King, Jr. and Elvis Presley.Participants were given points for each face they could name. If the subject could not name the face, he or she was asked to identify the famous person through description. Participants gained more points by providing at least two relevant details about the person. The two groups also underwent MRI brain scans.Researchers found that the people who had early onset dementia performed significantly worse on the test, scoring an average of 79 percent in recognition of famous faces and 46 percent in naming the faces, compared to 97 percent in recognition and 93 percent on naming for those free of dementia.The study also found that people who had trouble putting names to the faces were more likely to have a loss of brain tissue in the left temporal lobe of the brain, while those with trouble recognizing the faces had tissue loss on both sides of the temporal lobe.”In addition to its practical value in helping us identify people with early dementia, this test also may help us understand how the brain works to remember and retrieve its knowledge of words and objects,” Gefen said.The study was supported by the National Institute on Deafness and Other Communication Disorders, the National Institute on Aging, the National Center for Research Resources, the National Institute of Neurological Disorders and Stroke and the National Center for Research Resources.

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Electrical signatures of consciousness in the dying brain

Aug. 12, 2013 — The “near-death experience” reported by cardiac arrest survivors worldwide may be grounded in science, according to research at the University of Michigan Health System.Whether and how the dying brain is capable of generating conscious activity has been vigorously debated.But in this week’s PNAS Early Edition, a U-M study shows shortly after clinical death, in which the heart stops beating and blood stops flowing to the brain, rats display brain activity patterns characteristic of conscious perception.”This study, performed in animals, is the first dealing with what happens to the neurophysiological state of the dying brain,” says lead study author Jimo Borjigin, Ph.D., associate professor of molecular and integrative physiology and associate professor of neurology at the University of Michigan Medical School.”It will form the foundation for future human studies investigating mental experiences occurring in the dying brain, including seeing light during cardiac arrest,” she says.Approximately 20 percent of cardiac arrest survivors report having had a near-death experience during clinical death. These visions and perceptions have been called “realer than real,” according to previous research, but it remains unclear whether the brain is capable of such activity after cardiac arrest.”We reasoned that if near-death experience stems from brain activity, neural correlates of consciousness should be identifiable in humans or animals even after the cessation of cerebral blood flow,” she says.Researchers analyzed the recordings of brain activity called electroencephalograms (EEGs) from nine anesthetized rats undergoing experimentally induced cardiac arrest.Within the first 30 seconds after cardiac arrest, all of the rats displayed a widespread, transient surge of highly synchronized brain activity that had features associated with a highly aroused brain.Furthermore, the authors observed nearly identical patterns in the dying brains of rats undergoing asphyxiation.”The prediction that we would find some signs of conscious activity in the brain during cardiac arrest was confirmed with the data,” says Borjigin, who conceived the idea for the project in 2007 with study co-author neurologist Michael M. Wang, M.D., Ph.D., associate professor of neurology and associate professor of molecular and integrative physiology at the U-M.”But, we were surprised by the high levels of activity,” adds study senior author anesthesiologist George Mashour, M.D., Ph.D., assistant professor of anesthesiology and neurosurgery at the U-M. ” In fact, at near-death, many known electrical signatures of consciousness exceeded levels found in the waking state, suggesting that the brain is capable of well-organized electrical activity during the early stage of clinical death.­­­”The brain is assumed to be inactive during cardiac arrest. However the neurophysiological state of the brain immediately following cardiac arrest had not been systemically investigated until now.The current study resulted from collaboration between the labs of Borjigin and Mashour, with U-M physicist UnCheol Lee, Ph.D., playing a critical role in analysis.”This study tells us that reduction of oxygen or both oxygen and glucose during cardiac arrest can stimulate brain activity that is characteristic of conscious processing,” says Borjigin. “It also provides the first scientific framework for the near-death experiences reported by many cardiac arrest survivors.”

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