Posts tagged cognitive impairment
Articles and news from the latest research reports.
Are concussions related to Alzheimer’s disease?
A new study suggests that a history of concussion involving at least a momentary loss of consciousness may be related to the buildup of Alzheimer’s-associated plaques in the brain. The research is published in the December 26, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.
"Interestingly, in people with a history of concussion, a difference in the amount of brain plaques was found only in those with memory and thinking problems, not in those who were cognitively normal," said study author Michelle Mielke, PhD, with Mayo Clinic in Rochester, Minn.
For the study, people from Olmsted County in Minnesota were given brain scans; these included 448 people without any signs of memory problems and 141 people with memory and thinking problems called mild cognitive impairment. Participants, who were all age 70 or older, were also asked about whether they had ever experienced a brain injury that involved any loss of consciousness or memory.
Of the 448 people without any thinking or memory problems, 17 percent reported a brain injury and 18 percent of the 141 with memory and thinking difficulties reported a concussion or head trauma.
The study found no difference in any brain scan measures among the people without memory and thinking impairments, whether or not they had head trauma. However, people with memory and thinking impairments and a history of head trauma had levels of amyloid plaques an average of 18 percent higher than those with no head trauma history.
"Our results add merit to the idea that concussion and Alzheimer’s disease brain pathology may be related," said Mielke. "However, the fact that we did not find a relationship in those without memory and thinking problems suggests that any association between head trauma and amyloid is complex."
‘Chemobrain’ linked to disrupted brain networks
For some cancer patients, the mental fogginess that develops with chemotherapy lingers long after treatment ends. Now research in breast cancer patients may offer an explanation.
Patients who experience “chemobrain” following treatment for breast cancer show disruptions in brain networks that are not present in patients who do not report cognitive difficulties, according to researchers at Washington University School of Medicine in St. Louis.
Results of the small study were reported Thursday, Dec. 12 at a poster presentation at the San Antonio Breast Cancer Symposium.
According to the researchers, many breast cancer patients who receive chemotherapy report long-term problems with memory, attention, learning, visual-spatial skills and other forms of information processing. The brain mechanisms contributing to these difficulties are poorly understood.
The investigators used an imaging technique called resting state functional-connectivity magnetic resonance imaging (rs-fcMRI) to assess the wiring among regions of the brain in 28 patients treated at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University. Fifteen patients reported they were “extremely” or “strongly” affected by cognitive difficulties. The remaining 13 reported no cognitive impairment.
The imaging studies suggest that standard chemotherapy given to breast cancer patients may alter connectivity in brain networks, especially in the frontal parietal control regions responsible for executive function, attention and decision-making.
“Chemobrain is most likely a global phenomenon in the brain, but a set of regions involved in executive control, called the frontal-parietal network, is perhaps the most affected brain system,” said Jay F. Piccirillo, MD, professor of otolaryngology and a member of the research team with expertise in the use of brain imaging to study tinnitus, or phantom noise. “We’re confirming previous studies that also have shown this. And we’re developing a solid multidisciplinary working group at Washington University to determine how we can help these women.”
Other studies also have used neuroimaging techniques to observe the neural disruptions associated with Alzheimer’s disease, depression and stroke. Washington University researchers are beginning to investigate whether cancer patients experiencing chemobrain may benefit from therapies similar to those that help patients with other cognitive disorders.
(Source: news.wustl.edu)
Research attributes high rates of smoking among mentally ill to addiction vulnerability
People with mental illness smoke at much higher rates than the overall population. But the popular belief that they are self-medicating is most likely wrong, according to researchers at the Indiana University School of Medicine. Instead, they report, research indicates that psychiatric disease makes the brain more susceptible to addiction.
As smoking rates in the general population have fallen below 25 percent, smoking among the mentally ill has remained pervasive, encompassing an estimated half of all cigarettes sold. Despite the well-known health dangers of tobacco consumption, smoking among the mentally ill has long been widely viewed as “self-medication,” reducing the incentive among health care professionals to encourage such patients to quit.
"This is really a devastating problem for people with mental illness because of the broad health consequences of nicotine addiction," said R. Andrew Chambers, M.D., associate professor of psychiatry at the IU School of Medicine. "Nicotine addiction is the number one cause of premature illness and death in the United States, and most of that morbidity and mortality is concentrated in people with mental illness."
In a report published recently in the journal Addiction Biology, the research team lead by Dr. Chambers reported the results of experiments using an established animal model of schizophrenia in which rats display a neuropsychiatric syndrome that closely resembles the disease.
Both the schizophrenia-model rats and normal rats were given access to intravenous self-administration of nicotine.
"The mentally ill rats acquired nicotine use faster and consumed more nicotine," Dr. Chambers said. "Then when we cut them off from access to nicotine, they worked much harder to restore access to nicotine than did the normal ‘control’ rats."
In additional testing, the researchers found that administration of nicotine provided equal, but minimal, cognitive benefits to both groups of rats when performing a memory test. When the nicotine was withdrawn, however, both groups of rats were more cognitively impaired, so that any cognitive benefits to nicotine administration were “paid for” by cognitive impairments later.
“These results strongly suggest that what has changed in mental illness to cause smoking at such high rates results in a co-morbid addiction to which the mentally ill are highly biologically vulnerable. The evidence suggests that the vulnerability is an involuntary biological result of the way the brain is designed and how it develops after birth, rather than it being about a rational choice to use nicotine as a medicine,” Dr. Chambers said.
The data, he said, point to neuro-developmental mechanisms that increase the risk of addiction. Better understanding of those mechanisms could lead to better prevention and treatment strategies, especially among mentally ill smokers, Dr. Chambers said.
A video interview of Dr. Chambers discussing his research is available here.
(Source: news.medicine.iu.edu)
Study finds link between commonly prescribed statin and memory impairment
New research that looked at whether two commonly prescribed statin medicines, used to lower low-density lipoprotein (LDL) or‘bad cholesterol’ levels in the blood, can adversely affect cognitive function has found that one of the drugs tested caused memory impairment in rats.
Between six and seven million people in the UK take statins daily and the findings follow anecdotal evidence of people reporting that they feel that their newly prescribed statin is affecting their memory. Last year, the US Food and Drug Administration (FDA) insisted that all manufacturers list in their side effects that statins might affect cognitive function.
The study, led by scientists at the University of Bristol and published in the journal PLOS ONE, tested pravastatin and atorvostatin (two commonly prescribed statins) in rat learning and memory models. The findings show that while no adverse cognitive effects were observed in rat performance for simple learning and memory tasks for atorvostatin, pravastatin impaired their performance.
Rats were treated daily with pravastatin (brand name - Pravachol) or atorvostatin (brand name - Lipitor) for 18 days. The rodents were tested in a simple learning task before, during and after treatment, where they had to learn where to find a food reward. On the last day of treatment and following one week withdrawal, the rats were also tested in a task which measures their ability to recognise a previously encountered object (recognition memory).
The study’s findings showed that pravastatin tended to impair learning over the last few days of treatment although this effect was fully reversed once treatment ceased. However, in the novel object discrimination task, pravastatin impaired object recognition memory. While no effects were observed for atorvostatin in either task.
The results suggest that chronic treatment with pravastatin impairs working and recognition memory in rodents. The reversibility of the effects on stopping treatment is similar to what has been observed in patients, but the lack of effect of atorvostatin suggests that some types of statin may be more likely to cause cognitive impairment than others.
Neil Marrion, Professor of Neuroscience at Bristol’s School of Physiology and Pharmacology in the Faculty of Medical and Veterinary Sciences and the study’s lead author, said: “This finding is novel and likely reflects both the anecdotal reports and FDA advice. What is most interesting is that it is not a feature of all statins. However, in order to better understand the relationship between statin treatment and cognitive function, further studies are needed.”
(Source: bris.ac.uk)
Study finds cognitive enhancers do not improve cognition or function in people with mild cognitive impairment but may cause gastrointestinal issues
Cognitive enhancers—drugs taken to enhance concentration, memory, alertness and moods—do not improve cognition or function in people with mild cognitive impairment in the long term, according to a new study by researchers at St. Michael’s Hospital.
In fact, patients on these medications experienced significantly more nausea, diarrhea, vomiting and headaches, according to the study published today in the Canadian Medical Association Journal.
“Our findings do not support the use of cognitive enhancers for mild cognitive impairment,” wrote Dr. Andrea Tricco and Dr. Sharon Straus, who are both scientists in the hospital’s Li Ka Shing Knowledge Institute. Dr. Straus is also a geriatrician at the hospital.
Mild cognitive impairment is a condition characterized by memory complaints without significant limitations in everyday activity. Between 3 and 42 per cent of people are diagnosed with the condition each year, about 4.6 million people worldwide. Each year about 3 to 17 per cent of people with mild cognitive impairment will develop dementia, such as Alzheimer’s disease. Given the aging population, it’s estimated the number of Canadians with dementia will double to more than 1 million in the next 25 years.
It has been hypothesized that cognitive enhancers may delay the onset of dementia. Families and patients are increasingly requesting these drugs even though their efficacy for patients with mild cognitive impairment has not been established. In Canada, cognitive enhancers can be obtained only with special authorization.
Drs. Tricco and Straus conducted a review of existing evidence to understand the efficacy and safety of cognitive enhancers. They looked at eight randomized trials that compared one of four cognitive enhancers (donepezil, rivastigmine, galantamine or memantine) to a placebo among patients diagnosed with mild cognitive impairment.
While they found short-term benefits to using these drugs on one cognition scale, there were no long-term effects after about a year and a half. No other benefits were observed on the second cognition scale or on function, behaviour, and mortality. As well, patients on these medications experienced significantly more nausea, diarrhea, vomiting and headaches. One study also found a higher risk of a heart condition known as bradycardia (slow heartbeat) among patients who received galantamine.
“Our results do not support the use of cognitive enhancers for patients with mild cognitive impairment,” the authors wrote. “These agents were not associated with any benefit and led to an increase in harms. Patients and their families should consider this information when requesting these medications. Similarly, health care decision-makers may not wish to approve the use of these medications for mild cognitive impairment, because these drugs might not be effective and are likely associated with harm.”
This study was funded by the Drug Safety and Effectiveness Network/Canadian Institutes of Health Research.
Another St. Michael’s study published in the CMAJ in April found no evidence that drugs, herbal products or vitamin supplements help prevent cognitive decline in healthy older adults. That review, led by Dr. Raza Naqvi, a University of Toronto resident, found some evidence that mental exercises, such as computerized memory training programs, might help.
Research confirms Mediterranean diet is good for the mind
The first systematic review of related research confirms a positive impact on cognitive function, but an inconsistent effect on mild cognitive impairment.
Over recent years many pieces of research have identified a link between adherence to a Mediterranean diet and a lower risk of age-related disease such as dementia.
Until now there has been no systematic review of such research, where a number of studies regarding a Mediterranean diet and cognitive function are reviewed for consistencies, common trends and inconsistencies.
A team of researchers from the University of Exeter Medical School, supported by the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care in the South West Peninsula (NIHR PenCLAHRC), has carried out the first such systematic review and their findings are published in Epidemiology.
The team analysed 12 eligible pieces of research, 11 observational studies and one randomised control trial. In nine out of the 12 studies, a higher adherence to a Mediterranean diet was associated with better cognitive function, lower rates of cognitive decline and a reduced risk of Alzheimer’s disease.
However, results for mild cognitive impairment were inconsistent.
A Mediterranean diet typically consists of higher levels of olive oil, vegetables, fruit and fish. A higher adherence to the diet means higher daily intakes of fruit and vegetables and fish, and reduced intakes of meat and dairy products.
The study was led by researcher Iliana Lourida. She said: “Mediterranean food is both delicious and nutritious, and our systematic review shows it may help to protect the ageing brain by reducing the risk of dementia. While the link between adherence to a Mediterranean diet and dementia risk is not new, ours is the first study to systematically analyse all existing evidence.”
She added: “Our review also highlights inconsistencies in the literature and the need for further research. In particular research is needed to clarify the association with mild cognitive impairment and vascular dementia. It is also important to note that while observational studies provide suggestive evidence we now need randomized controlled trials to confirm whether or not adherence to a Mediterranean diet protects against dementia.”
(Source: exeter.ac.uk)
Oprah’s and Einstein’s faces help spot dementia
New test designed for younger people reveals early-onset dementia
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, according to new Northwestern Medicine research.
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 lead author Tamar Gefen, a doctoral candidate in neuropsychology at the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg School of Medicine.
Gefen did the research in the lab of senior author Emily Rogalski, assistant research professor at Northwestern’s Cognitive Neurology and Alzheimer’s Disease Center.
Face recognition tests exist to help identify dementia, but they are outdated and more suitable for an older generation.
"The famous faces for this study were specifically chosen for their relevance to individuals under age 65, so that the test may be useful for diagnosing dementia in younger individuals," Rogalski said. An important component of the test is that it distinguishes deficits in remembering the name of a famous person from that of recognizing the same individual, she noted.
The study also used quantitative software to analyze MRI scans of the brains of the individuals who completed the test to understand the brain areas important for naming and recognition of famous faces.
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 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 primary progressive aphasia, a form of 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 the left and right 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.
Increased fluctuation in blood pressure linked to impaired cognitive function in older people
Higher variability in visit-to-visit blood pressure readings, independent of average blood pressure, could be related to impaired cognitive function in old age in those already at high risk of cardiovascular disease, suggests a paper published today on BMJ.
There is increasing evidence that vascular factors contribute in development and progression of dementia. This is of special interest as cardiovascular factors may be amendable and thus potential targets to reduce cognitive decline and the incidence of dementia. Visit-to-visit blood pressure variability has been linked to cerebrovascular damage (relating to the brain and its blood vessels). It has also been shown that this variability can increase the risk of stroke.
It has been suggested that higher blood pressure variability might potentially lead to cognitive impairment through changes in the brain structures.
Researchers from the Leiden University Medical Center (Netherlands), University College Cork (Ireland) and the Glasgow University (UK) therefore investigated the association of visit-to-visit blood pressure variability (independent of average blood pressure) with cognitive function in older subjects at high risk of cardiovascular disease.
All data were obtained from the PROSPER study, which investigated the effect of statins in prevention of vascular events in older men and women. This study took data on 5,461 individuals aged 70-82 years old in Ireland, Scotland and the Netherlands. Average follow-up was three years.
Both systolic (peak pressure) and diastolic (minimum pressure) blood pressures were measured every three months in the same clinical setting. The variability between these measurements were calculated and used in the analyses.
The study used data on cognitive function where the following was tested: selective attention and reaction time; general cognitive speed; immediate and delayed memory performance.
Results showed that visit-to-visit blood pressure variability was associated with worse performance on all cognitive tests. The results were consistent after adjusting for cardiovascular disease and other risk factors.
The main findings of the study were: higher visit-to-visit blood pressure variability is associated with worse performance in different cognitive tests; higher variability is associated with higher risk of stroke and both these associations are independent of various cardiovascular risk factors, in particular, average blood pressure.
Researcher Simon Mooijaart, (Leiden University Medical Centre, Leiden, the Netherlands) says that by using a population of “over five thousand participants and over three years of blood pressure measurements, we showed that high visit-to-visit systolic and diastolic blood pressure variability associates with worse performance in different domains of cognitive function including selection attention, processing speed, immediate verbal memory and delayed verbal memory”. The researchers do add though that it is still unclear whether higher blood pressure variability is a cause or consequence of impaired cognitive function.
They suggest several explanations for their findings: firstly that blood pressure variability and cognitive impairment could stem from a common cause, with cardiovascular risk factors being the most likely candidate; secondly that variability might reflect a long term instability in the regulation of blood pressure and blood flow to the key organs in the body; thirdly that exaggerated fluctuations in blood pressure could result in the brain not receiving enough blood, which can cause brain injury, leading to impairment of cognitive function.
The researchers conclude that “higher visit-to-visit blood pressure variability independent of average blood pressure might be a potential risk factor with worse cognitive performance in older subjects at high risk of cardiovascular disease”. Given that dementia is a major public health issue, they say that further interventional studies are warranted to establish whether reducing blood pressure variability can decrease the risk of cognitive impairment in old age.
(Source: eurekalert.org)
Exercise May be the Best Medicine for Alzheimer’s
New research out of the University of Maryland School of Public Health shows that exercise may improve cognitive function in those at risk for Alzheimer’s by improving the efficiency of brain activity associated with memory. Memory loss leading to Alzheimer’s disease is one of the greatest fears among older Americans. While some memory loss is normal and to be expected as we age, a diagnosis of mild cognitive impairment, or MCI, signals more substantial memory loss and a greater risk for Alzheimer’s, for which there currently is no cure.
The study, led by Dr. J. Carson Smith, assistant professor in the Department of Kinesiology, provides new hope for those diagnosed with MCI. It is the first to show that an exercise intervention with older adults with mild cognitive impairment (average age 78) improved not only memory recall, but also brain function, as measured by functional neuroimaging (via fMRI). The findings are published in the Journal of Alzheimer’s Disease.
“We found that after 12 weeks of being on a moderate exercise program, study participants improved their neural efficiency – basically they were using fewer neural resources to perform the same memory task,” says Dr. Smith. “No study has shown that a drug can do what we showed is possible with exercise.”
Recommended Daily Activity: Good for the Body, Good for the Brain
Two groups of physically inactive older adults (ranging from 60-88 years old) were put on a 12-week exercise program that focused on regular treadmill walking and was guided by a personal trainer. Both groups – one which included adults with MCI and the other with healthy brain function – improved their cardiovascular fitness by about ten percent at the end of the intervention. More notably, both groups also improved their memory performance and showed enhanced neural efficiency while engaged in memory retrieval tasks.
The good news is that these results were achieved with a dose of exercise consistent with the physical activity recommendations for older adults. These guidelines urge moderate intensity exercise (activity that increases your heart rate and makes you sweat, but isn’t so strenuous that you can’t hold a conversation while doing it) on most days for a weekly total of 150 minutes.
Measuring Exercise’s Impact on Brain Health and Memory
One of the first observable symptoms of Alzheimer’s disease is the inability to remember familiar names. Smith and colleagues had study participants identify famous names and measured their brain activation while engaged in correctly recognizing a name – e.g., Frank Sinatra, or other celebrities well known to adults born in the 1930s and 40s. “The task gives us the ability to see what is going on in the brain when there is a correct memory performance,” Smith explains.
Tests and imaging were performed both before and after the 12-week exercise intervention. Brain scans taken after the exercise intervention showed a significant decrease in the intensity of brain activation in eleven brain regions while participants correctly identified famous names. The brain regions with improved efficiency corresponded to those involved in the pathology of Alzheimer’s disease, including the precuneus region, the temporal lobe, and the parahippocampal gyrus.
The exercise intervention was also effective in improving word recall via a “list learning task,” i.e., when people were read a list of 15 words and asked to remember and repeat as many words as possible on five consecutive attempts, and again after a distraction of being given another list of words.
“People with MCI are on a very sharp decline in their memory function, so being able to improve their recall is a very big step in the right direction,” Smith states.
The results of Smith’s study suggest that exercise may reduce the need for over-activation of the brain to correctly remember something. That is encouraging news for those who are looking for something they can do to help preserve brain function.
Dr. Smith has plans for a larger study that would include more participants, including those who are healthy but have a genetic risk for Alzheimer’s, and follow them for a longer time period with exercise in comparison to other types of treatments. He and his team hope to learn more about the impact of exercise on brain function and whether it could delay the onset or progression of Alzheimer’s disease.
Daydreaming simulated by computer model
Scientists have created a virtual model of the brain that daydreams like humans do.
Researchers created the computer model based on the dynamics of brain cells and the many connections those cells make with their neighbors and with cells in other brain regions. They hope the model will help them understand why certain portions of the brain work together when a person daydreams or is mentally idle. This, in turn, may one day help doctors better diagnose and treat brain injuries.
“We can give our model lesions like those we see in stroke or brain cancer, disabling groups of virtual cells to see how brain function is affected,” said senior author Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology at Washington University School of Medicine in St. Louis. “We can also test ways to push the patterns of activity back to normal.”
The study is now available online in The Journal of Neuroscience.
The model was developed and tested by scientists at Washington University School of Medicine in St. Louis, Universitat Pompeu Fabra in Barcelona, Spain, and several other European universities including ETH Zurich, Switzerland; University of Oxford, United Kingdom; Institute of Advanced Biomedical Technologies, Chieti, Italy; and University of Lausanne, Switzerland.
Scientists first recognized in the late 1990s and early 2000s that the brain stays busy even when it’s not engaged in mental tasks. Researchers have identified several “resting state” brain networks, which are groups of different brain regions that have activity levels that rise and fall in sync when the brain is at rest. They have also linked disruptions in networks associated with brain injury and disease to cognitive problems in memory, attention, movement and speech.
The new model was developed to help scientists learn how the brain’s anatomical structure contributes to the creation and maintenance of resting state networks. The researchers began with a process for simulating small groups of neurons, including factors that decrease or increase the likelihood that a group of cells will send a signal.
“In a way, we treated small regions of the brain like cognitive units: not as individual cells but as groups of cells,” said Gustavo Deco, PhD, professor and head of the Computational Neuroscience Group in Barcelona. “The activity of these cognitive units sends out excitatory signals to the other units through anatomical connections. This makes the connected units more or less likely to synchronize their signals.”
Based on data from brain scans, researchers assembled 66 cognitive units in each hemisphere, and interconnected them in anatomical patterns similar to the connections present in the brain.
Scientists set up the model so that the individual units went through the signaling process at random low frequencies that had previously been observed in brain cells in culture and in recordings of resting brain activity.
Next, researchers let the model run, slowly changing the coupling, or the strength of the connections between units. At a specific coupling value, the interconnections between units sending impulses soon began to create coordinated patterns of activity.
“Even though we started the cognitive units with random low activity levels, the connections allowed the units to synchronize,” Deco said. “The spatial pattern of synchronization that we eventually observed approximates very well—about 70 percent—to the patterns we see in scans of resting human brains.”
Using the model to simulate 20 minutes of human brain activity took a cluster of powerful computers 26 hours. But researchers were able to simplify the mathematics to make it possible to run the model on a typical computer.
“This simpler whole brain model allows us to test a number of different hypotheses on how the structural connections generate dynamics of brain function at rest and during tasks, and how brain damage affects brain dynamics and cognitive function,” Corbetta said.