Tag Archives: research

Caring for Someone with Alzheimer’s Disease

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Are you caring for someone with Alzheimer’s disease? Here’s what you should know.

 

Caring for someone with Alzheimer's diseaseIt is common knowledge that Alzheimer’s disease affects a person’s memory, cognition and ability to reason. People with Alzheimer’s disease can however also become listless, agitated, stubborn, depressed, anxious and even violent. Furthermore, they may suffer from hallucinations – experienced as pleasant and/or frightening. During the final stages of the disease, Alzheimer’s patients need full-time care and supervision, as they aren’t able to perform even relatively simple tasks, such as taking a bath, dressing, shopping, cooking or using the phone.

Are you caring for someone with Alzheimer’s disease? The tips below will help you with what can be a challenging journey. Just remember that each person with Alzheimer’s is as unique as a snowflake – which means that the tips given here may not work for everyone.

Tips for caregivers:

  • If the person becomes angry or present with combative behaviour, give them space by leaving the room. Only return when they have calmed down.
  • Don’t try to argue. People with Alzheimer’s disease have lost their ability to reason.
  • Allow strange behaviour if it doesn’t affect others. It’s their way to make sense of their “new” environment among “new” people. Typical behaviour may include repeatedly packing and unpacking a suitcase, sorting out a wardrobe, or hiding a handbag under the bed. Always ask yourself, “Does it matter?”
  • Be aware that strange behaviour could be their way of telling you, the carer, that something is wrong. The person might suddenly shout, hit something, swear, cry or laugh out loudly. Try to work out what is wrong, respond to possible emotions they’re feeling at the time of the incident, and then try to distract them.
  • If you can determine what triggers these reactions, you can try to prevent it or keep the person calm when the trigger occurs. This can be anything – from a hallucination to being thirsty or wanting to go to the toilet.
  • People with Alzheimer’s disease often get agitated because they struggle to complete simple tasks. When you show or tell them how to do something, it’s important that you relay the steps one by one, allowing enough time between each step for the person to absorb the information. Be patient!
  • Don’t give the patient too many choices. Rather ask, “Do you want to wear this dress?” instead of “Which dress would you like to wear?”
  • Don’t change familiar routines.

 

If the person with Alzheimer’s disease tends to wander or walk away:

  • Try to find a solution to let them do so safely, for example allow then to wander into a secure garden.
  • If the person is determined to leave, don’t confront them, as this could cause extreme anxiety, which may result in aggression. Rather accompany them for a short way, then divert their attention so you can both return.
  • Make sure the person carries some form of identification such as a MedicAlert bracelet, or a card with a name and contact details.
  • Attach a little bell to outside doors to alert you when they’re opened.
  • Tell your neighbours about the situation and ask them to give you a call if/when they spot the patient outside.
  • Lock the door, if absolutely necessary, but never lock a person with dementia alone in the home. The decision must be taken in the best interest of the patient. A too restricted environment causes boredom with resulting frustration that may lead to aggressive outbursts.
  • Encourage friends and family to come and visit. Alzheimer’s patients often walk away in the hope of getting to see their loved ones. These visits also help to allay boredom.

 

Source: http://www.health24.com/Medical/Alzheimers/Looking-after-your-loved-one/Caring-for-someone-with-Alzheimers-disease-20130909

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Decreased Autism Rates Found with Healthy Fats During Pregnancy

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By Chris Weller

Consuming various healthy fats during pregnancy may reduce a woman’s risk of having a child with autism, new research finds.

Published in the Journal of American Epidemiology by the Harvard School for Public Health, the study examined maternal intake of certain fatty acids across mothers whose children have autism and those whose do not. The study found that women who consumed linoleic acid — a type of omega-6 acid found in vegetable oils, nuts, and seeds — were 34 percent less likely to birth a child with autism, while women who consumed low levels of omega-3 fatty acids — those found in fish — were more 53 percent more likely.

“Our results provide preliminary evidence that increased maternal intake of omega-6 fatty acids could reduce risk of offspring [autism spectrum disorder],” the researchers wrote, “and that very low intakes of omega-3 fatty acids and linoleic acid could increase risk.”

The researchers point to the fatty acids’ importance in the fetus’ brain development, coupled with the mother’s stores of fatty acid toward the end of the pregnancy, as contributing to the decreased risks. However, they could only draw associative links, no causal claims, between the two behavior patterns.

The study included 317 mothers whose children have autism spectrum disorder and 17,728 mothers whose children do not. The mothers all completed surveys about their diets during pregnancy, with some filling out the information while pregnant and others completing it one year after birth.

One standout figure from the research was that women who consumed more omega-3 fatty acids than other women did not necessarily reduce their child’s risk for autism. At a certain point, the benefits reached a threshold.

This suggests that although getting too little omega-3 fatty acids may increase the risk of autism, once a certain threshold is reached, further consumption doesn’t provide an extra benefit, the researchers said.

Because of the limited sample size and correlative link, the researchers recommended further testing be done.
Read more at http://www.medicaldaily.com/articles/17077/20130702/healthy-fats-autism-risk-fetus-brain-development-omega-3-fatty-acids-pregnancy.htm#zHJkvEcXGqufHxwU.99

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Antidepressants May Fail to Help Some Autistic Kids

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About a quarter of children with autism may be taking antidepressants that won’t help them, a new study suggests.

Antidepressants may fail to help some autistic kidsAutistic children are sometimes prescribed antidepressants to reduce repetitive behaviors, but the new findings suggest the drugs may not be as effective for this use as they seem.

Researchers at the University of Michigan analyzed results from both published and unpublished studies (unpublished studies have been completed, but have not appeared in a scientific journal). In all studies, children with autism were randomly assigned to receive serotonin receptor inhibitors (SRIs) or a placebo for at least four weeks.

When the researchers looked at results from the published studies alone, they saw a small but real benefit to the drugs. But when the results were adjusted to take into account the role of unpublished studies, the benefit of the drugs disappeared.

The researchers said the purported benefit of taking SRIs for kids with autism could be due to publication bias, a term used to refer to the selective publication of studies with positive results — or those that show a drug works.

“This research made it clear that the effects of SRI treatment in [autism spectrum disorder] are considerably overrated because of publication bias,” the researchers write in an article published today (April 23) in the journal Pediatrics.

Finding effective treatments for autistic children will be difficult if publication bias persists, the researchers said, because it will remain unclear whether drugs are actually effective.

It’s also unclear why five of the studies went unpublished. It could be that journals would rather publish studies with positive results, or that studies with negative results tend to take a longer time to get published. The Michigan researchers were able to obtain results from only one of the unpublished studies — the researchers who worked on the other four would not provide this information when it was requested.

It is not uncommon for studies involving children to go unpublished. Another study, also published today in Pediatrics, found that, of the 3,400 clinical trials involving children that have taken place since 2000 and have been registered with the government, about 70 percent have been completed, but less than one-third have been published.

When information from studies is not made available, “trials may be unnecessarily repeated, and the information cannot be used to guide therapy,” Dr. Scott Denne, of Indiana University School of Medicine, wrote in a comment about the new Pediatrics studies.

This problem could be solved by mandating that researchers post information from their trials to the same government website that is used to document trial registration (ClinicalTrials.gov), according to the researchers of the study on child clinical trials. Currently, registration of studies involving children and posting of results on the site is voluntary.

Source: http://www.foxnews.com/health/2012/04/23/antidepressants-may-fail-to-help-some-autistic-kids/#ixzz1sssp1NMq

Sleep Less, Eat More, Gain Weight

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By Carrie Gann

Obesity linked to hormonal changes, lack of sleep

We’ve all heard about the importance of getting a good night’s sleep, and now scientists offer more evidence to back that up. A new study found that people who get less sleep may be inclined to eat more, move less and gain weight.

Scientists at the Mayo Clinic in Rochester, Minn., studied a group of 17 healthy volunteers between the ages 18 and 40 for a week in their homes, monitoring how much each one typically slept and ate. Then, they brought the volunteers into the clinic’s research lab for eight days: Half of the volunteers were allowed to sleep according to their usual pattern, and the other half got only two-thirds of their usual shut-eye.

All the volunteers were allowed to eat as much food as they wanted from the hospital cafeteria or from outside the research center. The researchers also measured how much energy each volunteer expended each day.

The sleep-deprived participants wolfed down an average of 549 calories beyond their usual intake but burned no more calories than their well-rested peers.

“A lot of people have this idea that if they’re up late, working hard, they’re burning more energy. But we found no change in how much they moved when sleep deprived,” said Dr. Andrew Calvin, lead author of the study and an assistant professor of medicine at the Mayo Clinic. “They’re consuming an additional 549 calories per day, but not burning any of them off.”

Those excess of unburned calories is a surefire way to gain weight, which numerous studies have connected to a variety of chronic health problems.

The volunteers who got less sleep also had higher levels of leptin, a hormone that suppresses appetite, and lower levels of ghrelin, a hormone that stimulates appetite, in their blood. The findings seem counterintuitive to what researchers would expect in people who are hungrier, but Calvin said the hormones were most likely an outcome, rather than a cause of people eating more.

Scientists have previously studied the physical downsides of getting too little sleep.

In 2011, Australian researchers found that adolescents and teenagers were more likely to be slimmer if they went to bed earlier, while those who stayed up late were more likely to engage in sedentary activities.

Previous studies have also found that workers covering late and overnight shifts were more likely to be obese and have type 2 diabetes, which may be associated with unhealthy eating habits, according to an editorial published in December.

The connection between sleep and weight may be important for the more than one-quarter of Americans who get six hours of sleep or less every night. Calvin said the future research on how sleep affects eating habits may give scientists useful insights into two of America’s biggest health problems: sleep deprivation and obesity.

“This study, while small, suggests that these two may indeed be linked, and if the findings are confirmed, they may suggest that sleep is a powerful factor in how much we eat and our chances of gaining weight,” he said.

Source: http://abcnews.go.com/blogs/health/2012/03/14/sleep-less-eat-more-gain-weight/

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Latest Alzheimer’s Research Progress Report Released

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2010 Alzheimer’s Disease Progress Report: A Deeper Understanding2010 Alzheimer’s Disease Progress Report: A Deeper Understanding, the latest annual Alzheimer’s research report from the National Institutes of Health (NIH), is now available online. Prepared by the National Institute on Aging, which leads the NIH effort conducting and supporting research on age-related cognitive decline and Alzheimer’s disease, the report highlights important developments and directions in NIH-funded research, including:

  • risk for developing Alzheimer’s
  • genes that play a role in the disease
  • neuroimaging and biomarkers that detect and track the disease
  • research into new treatments
  • lifestyle factors that may worsen or protect against the disease
  • help for caregivers

Special features include animation showing the progression of Alzheimer’s in the brain and video interviews highlighting new insights into the disease.

Read online or download @ http://www.nia.nih.gov/alzheimers/publication/2010-alzheimers-disease-progress-report-deeper-understanding.

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Skin Cancer Drug Reverses Alzheimer’s in Mice

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Skin cancer drug reverses Alzheimer's in miceScientists say they “serendipitously” discovered that a drug used to treat a type of cancer quickly reversed Alzheimer’s disease in mice. “I want to say as loudly and clearly as possible that this was a study in mice, not in humans,” he said. “We’ve fixed Alzheimer’s in mice lots of times, so we need to move forward expeditiously but cautiously.”
Via edition.cnn.com

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Using Structural MRI to Map the Functional Anatomy of Language and Reading

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Free Video Resource from the NIH

Using structural MRI to map the functional anatomy of language and reading [electronic resource] / Cathy Price.

Click on image to view video

Dr. Price’s research program aims to establish a functional anatomical model of language that predicts how speech and reading are lost and recovered following neurological damage or developmental delay. The hypothesis is that there are multiple ways that the brain can perform each language task (degeneracy). If this is true, then the effect of damage or developmental delay will depend on whether there is a surviving system available to sustain the task.

To dissociate the neuronal systems for the same task, they use structural and functional MRI of subjects who vary in their cognitive abilities, demographics and neurological status. This allows them to characterize individual variability in the neuronal networks of neurologically normal populations and to examine how brain damage affects cognitive abilities in patient populations. In particular, Dr. Price’s lab aims to determine how the impact of damage to one system depends on the integrity of another.

The language tasks they use are designed to tap various aspects of reading, speech perception, speech production and language control (e.g. in bilinguals). Their studies typically compare the neuronal networks for verbal stimuli to those involved in perceptual, conceptual or motor processing of non-verbal stimuli such as music, environmental sounds, numerals and pictures of objects.

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Alzheimer’s Disease – eUpdate

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Studies Find Possible New Genetic Risk Factors for Alzheimer’s Disease

NIH-funded genome-wide association study is largest ever conducted in Alzheimer’s research

from the Alzheimer’s Disease Education and Referral Center:

Studies find possible new genetic risk factors for Alzheimer's Disease

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Scientists have confirmed one gene variant and have identified several others that may be risk factors for late-onset Alzheimer’s disease, the most common form of the disorder. In the largest genome-wide association study, or GWAS, ever conducted in Alzheimer’s research, investigators studied DNA samples from more than 56,000 study participants and analyzed shared data sets to detect gene variations that may have subtle effects on the risk for developing Alzheimer’s. The National Institutes of Health funded the study appearing April 3, 2011, in the online issue of Nature Genetics.

“New technologies are allowing us to look at subtle genetic differences among large groups of study participants. By comparing people diagnosed with Alzheimer’s with people free of disease symptoms, researchers are now able to discern elusive genetic factors that may contribute to risk of developing this very devastating disease,” said Richard J. Hodes, M.D., director of the National Institute on Aging (NIA). “We are entering an exciting period of discoveries in genetics that may provide new insights about novel disease pathways that can be explored for development of therapies.”

The Alzheimer’s Disease Genetics Consortium (ADGC), a collaborative body established and funded by the NIA, part of the NIH, coordinated the study. The research reported today involved investigators at universities and research centers across the country. Datasets were funded in part by the NIA, the National Institute of Mental Health, the National Institute of Neurological Disorders and Stroke, and the National Center for Research Resources, all part of the NIH. The Alzheimer’s Association, U.S. Department of Veterans Affairs, Wellcome Trust, Howard Hughes Medical Institute, and the Canadian Institute of Health Research also lent support. Gerard Schellenberg, Ph.D., University of Pennsylvania School of Medicine, Philadelphia, directs the ADGC, which also received Recovery Act funds in 2009.

Until recently, only one gene variant, Apolipoprotein E-e4 (APOE-e4), had been confirmed as a significant risk factor gene for the common form of late-onset Alzheimer’s disease, which typically occurs after age 60. In 2009 and 2010, however, researchers confirmed additional gene variants of CR1, CLU and PICALM as possible risk factors for late-onset Alzheimer’s. This newest GWAS confirms that a fifth gene variant, BIN 1, affects development of late-onset Alzheimer’s. It also identified genetic variants significant for Alzheimer’s at EPHA 1, MS4A, CD2AP, and CD33. The genes identified by this study may implicate pathways involved in inflammation, movement of proteins within cells, and lipid transport as being important in the disease process.

In addition, a second paper appearing online in the journal presented GWAS findings for Alzheimer’s by another scientific team. The United Kingdom-based group, led by Julie Williams, Ph.D., Cardiff University School of Medicine, Wales, found the same genes as risk factors and identified a gene variant ABCA7 as an additional gene of interest. Components of the NIH involved in or supporting the study included the NIA, the National Heart, Lung and Blood Institute, and the National Institute of Diabetes and Digestive and Kidney Diseases. Some private support came through the independent Foundation for the National Institutes of Health.

“Researchers conducting GWAS are looking for genetic variations that may have a smaller effect but still play a role in the disease,” said Schellenberg. “Our findings bring us one step closer to a fuller understanding of the genetic basis of this complex disease, although more study is needed to determine the role these genetic factors may play in the onset and progression of Alzheimer’s.”

Schellenberg said the study was made possible by the research infrastructures established and funded by the NIA, including 29 Alzheimer’s Disease Centers, the National Alzheimer’s Coordinating Center, the Genetics of Alzheimer’s Disease Data Storage Site, the Late-onset Alzheimer’s Disease Family Study, and the National Cell Repository for Alzheimer’s Disease. They collect, store and make available to qualified researchers DNA samples, datasets containing biomedical and demographic information about participants, and genetic analysis data.

References:

Naj, A.C., et al. Common variants of MS4A4/MS4A6E, CD2AP, CD33 and EPHA 1 are associated with late-onset Alzheimer’s Disease. Nature Genetics. Epub April 3, 2011.

Hollingworth, P., et al. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA 1, CD33 and CD2AP are associated with Alzheimer’s disease. Nature Genetics. Epub April 3, 2011.

The NIA leads the federal government effort conducting and supporting research on aging and the health and well being of older people. For more on health and on aging generally, go to www.nia.nih.gov. The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer’s Disease Education and Referral (ADEAR) Center at www.nia.nih.gov/Alzheimers. To sign up for e-mail alerts about new findings or publications, please visit either website.

The NIH—The Nation’s Medical Research Agency—includes 27 institutes and centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

The activities described in this release are being funded through the American Recovery and Reinvestment Act (ARRA). To track the progress of HHS activities funded through the ARRA, visit www.hhs.gov/recovery. To track all federal funds provided through the ARRA, visit www.recovery.gov.