1. Some patients with dementia may experience delayed-onset PTSD

    July 27, 2017 by Ashley

    From the Wiley press release:

    Delayed-onset post-traumatic symptoms in the elderly may be misdiagnosed as falling under the umbrella of behavioural and psychological symptoms of dementia (BPSD), according to a recent review.

    The review describes three cases where post-traumatic stress disorder (PTSD) symptoms are experienced by patients suffering with dementia long after the original traumatic event.

    Considering PTSD in individuals with dementia is important because PTSD is usually associated with working-age adults and is infrequently diagnosed in the elderly. In the early stages of dementia, recognising early life trauma may enable patients to access psychological therapy prior to significant cognitive decline. In patients with more advanced dementias, an awareness of earlier trauma exposure can help clinicians differentiate between delayed PTSD and BPSD in patients suffering with emotional and behavioural disturbances.

    “Every patient with dementia has a unique narrative, which if captured in the earlier stages of the disease, enables clinicians and their families to understand the origin of their distress. Therefore, it is important to look for a history of previous trauma in patients with BPSD as this could be due to delayed onset PTSD,” said Dr. Tarun Kuruvilla, senior author of the Progress in Neurology & Psychiatry review.


  2. Healthy lifestyle may help older adults preserve their independence

    July 26, 2017 by Ashley

    From the Wiley press release:

    In a study of men with an average age of 71 years, lifestyle factors such as never smoking, maintaining a healthy diet, and not being obese were associated with survival and high functionality over the next 16 years.

    The study included 1104 men who completed a questionnaire. High functionality was defined as preserved ability in personal activities of daily living and cognitive function.

    Additional studies are needed to investigate whether lifestyle changes after the age of 70 years may also lead to preserved independence.

    The findings are published in the Journal of the American Geriatrics Society.


  3. Traumatic brain injury associated with dementia in working-age adults

    by Ashley

    From the University of Helsinki press release:

    According to a study encompassing the entire Finnish population, traumatic brain injury associated with an increased risk for dementia in working-age adults. Yet, no such relationship was found between traumatic brain injury and later onset of Parkinson’s disease or ALS.

    The researchers believe that these results may play a significant role for the rehabilitation and long-term monitoring of traumatic brain injury patients.

    Traumatic brain injuries (TBI) are among the top causes of death and disability, particularly among the young and middle aged. Approximately one in three that suffer from moderate-to-severe TBI die, and approximately half of the survivors will suffer from life-long disabilities.

    Degenerative brain diseases include memory disorders such as Alzheimer’s disease as well as Parkinson’s disease and amyotrophic lateral sclerosis (ALS). While the connection between TBI and degenerative brain diseases has been known, no comprehensive research data exist on the impact of TBI on degenerative brain diseases among adults of working age.

    Researchers from the University of Helsinki and the Helsinki University Hospital have now examined the relationship between TBI and degenerative brain diseases in a study encompassing the entire Finnish population. The study combined several nationwide registers to monitor more than 40,000 working-age adults, who survived the initial TBI, for ten years. Importantly, the persons´ level of education and socioeconomic status were accounted for.

    “It seems that the risk for developing dementia after TBI is the highest among middle-aged men. The more severe the TBI, the higher the risk for subsequent dementia. While previous studies have identified good education and high socioeconomic status as protective factors against dementia, we did not discover a similar effect among TBI survivors,” explains Rahul Raj, docent of experimental neurosurgery and one of the primary authors of the study.

    A significant discovery is that the risk of dementia among TBI survivors who have seemingly recovered well remains high for years after the injury. Raj points out that TBI patients may occasionally be incorrectly diagnosed with dementia due to the damage caused by the TBI itself, but such possible errors were considered in the study.

    “According to our results, it might be so that the TBI triggers a process that later leads to dementia.”

    “These results are significant for the rehabilitation and monitoring of TBI patients. Such a reliable study of the long-term impact of TBI has previously been impossible,” says Professor Jaakko Kaprio, a member of the research group.

    The WHO has predicted that TBI will become a leading cause of death and long-term illness during the next ten years. Already one per cent of the population in the United States suffers from a long-term disability caused by TBI. In western countries, the ageing of the population and age-related accidents increase the amount of TBIs, while in Asia, TBIs caused by traffic accidents are on the rise.

    Dementia is commonly seen as a problem of the elderly. However, the Finnish study shows that TBI may cause dementia to develop before old age, and that dementia caused by injuries are much more common than was thought.

    “It is a tragedy when an adult of working age develops dementia after recovering from a brain injury, not just for the patient and their families, but it also negatively impacts the whole society. In the future, it will be increasingly important to prevent TBIs and to develop rehabilitation and long-term monitoring for TBI patients,” says Docent Raj.


  4. Well-being in later life: The mind plays an important role

    July 25, 2017 by Ashley

    From the Helmholtz Zentrum München – German Research Center for Environmental Health press release:

    Aging itself is not inevitably associated with a decline in mood and quality of life,” says Prof. Karl-Heinz Ladwig, summarizing the results. “It is rather the case that psychosocial factors such as depression or anxiety impair subjective well-being, the Head of the Mental Health Research Group at the Institute of Epidemiology II, Helmholtz Zentrum München and Professor of Psychosomatic Medicine at the TUM University Hospital explains. “And in the case of women, living alone also plays an important role.”

    “To date the impact of emotional stress has barely been investigated”

    For the current study, Prof. Ladwig and his team relied on data derived from about 3,600 participats with an average age of 73 who had taken part in the population-based KORA-Age Study. “What made the study particularly interesting was the fact that the impact of stress on emotional well-being has barely been investigated in a broader, non-clinical context,” explains PD Dr. Karoline Lukaschek, epidemiologist in the Mental Health Research Group and lead author of the paper. “Our study therefore explicitly included anxiety, depression and sleep disorders.”

    Generally high levels of well-being but…

    To ascertain levels of subjective well-being, the scientists used a questionnaire devised by the World Health Organization (the WHO-5 Well-Being Index) with a score range of 0 to 100. For the purpose of analysis, they divided the respondents’ results into two categories: ‘high’ (score > 50) and ‘low’ (score ? 50). The subsequent evaluation revealed a high level of subjective well-being in the majority (79 percent) of the respondents. The average values were also above the threshold set by the WHO. In the ‘low’ group, however, there was a conspicuously high number of women: about 24 percent compared to 18 percent for men.

    Depression and anxiety disorders are the biggest risk

    Trying to uncover the most important causes for subjective well-being, the scientists mainly identified psychosocial factors: above all, depression and anxiety disorders had the strongest effect on well-being. Low income and sleep disorders also had a negative effect. However, poor physical health (for example, low physical activity or so-called multimorbidity) seemed to have little impact on perceived life satisfaction. Among women, living alone also significantly increased the probability of a low sense of well-being.

    “The findings of the current study clearly demonstrate that appropriate services and interventions can play a major role for older people, especially for older women living on their own,” Prof. Ladwig says, categorizing the results. “And this is all the more important, given that we know that high levels of subjective well-being are linked to a lower mortality risk.”


  5. Sleep problems may be early sign of Alzheimer’s

    July 24, 2017 by Ashley

    From the American Academy of Neurology press release:

    Poor sleep may be a sign that people who are otherwise healthy may be more at risk of developing Alzheimer’s disease later in life than people who do not have sleep problems, according to a study published in the July 5, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. Researchers have found a link between sleep disturbances and biological markers for Alzheimer’s disease found in the spinal fluid.

    “Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways,” said study author Barbara B. Bendlin, PhD, of the University of Wisconsin-Madison. “For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.”

    Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer’s disease.

    For the study, researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer’s, either having a parent with the disease or being a carrier of a gene that increases the risk for Alzheimer’s disease called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer’s disease.

    Researchers found that people who reported worse sleep quality, more sleep problems and daytime sleepiness had more biological markers for Alzheimer’s disease in their spinal fluid than people who did not have sleep problems. Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.

    “It’s important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save $367 billion in health care spending,” said Bendlin.

    While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea.

    The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.

    “It’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep,” said Bendlin. “More research is needed to further define the relationship between sleep and these biomarkers.”

    Bendlin added, “There are already many effective ways to improve sleep. It may be possible that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”

    One limitation of the study was that sleep problems were self-reported. Monitoring of sleep patterns by health professionals may be beneficial in future studies.


  6. No link seen between traumatic brain injury and cognitive decline

    by Ashley

    From the Boston University Medical Center press release:

    Although much research has examined traumatic brain injury (TBI) as a possible risk factor for later life dementia from neurodegenerative diseases such as Alzheimer’s disease (AD), little is known regarding how TBI influences the rate of age-related cognitive change. A new study now shows that history of TBI (with loss of consciousness) does not appear to affect the rate of cognitive change over time for participants with normal cognition or even those with AD dementia.

    These findings appear in the Journal of Alzheimer’s Disease.

    More than 10 million individuals worldwide are affected annually by TBI, however the true prevalence is likely even greater given that a majority of TBIs are mild in severity and may not be recognized or reported. TBI is a major public health and socioeconomic concern resulting in $11.5 billion in direct medical costs and $64.8 billion in indirect costs to the U.S. health system in 2010 alone.

    According to the researchers the relationship between TBI and long-term cognitive trajectories remains poorly understood due to limitations of previous studies, including small sample sizes, short follow-up periods, biased samples, high attrition rates, limited or no reports of exposure to repetitive head impacts (such as those received through contact sports), and very brief cognitive test batteries.

    In an effort to examine this possible connection, researchers compared performance on cognitive tests over time for 706 participants (432 with normal cognition; 274 AD dementia) from the National Alzheimer’s Coordinating Center database. Normal and AD dementia participants with a history of TBI with loss of consciousness were matched to an equal number of demographically and clinically similar participants without a TBI history. The researchers also examined the possible role of genetics in the relationship between TBI and cognitive decline by studying a gene known to increase risk for AD dementia, the APOE ?4 gene.

    “Although we expected the rates of cognitive change to differ significantly between those with a history of TBI compared to those with no history of TBI, we found no significant difference between the groups, regardless of their APOE genotype,” explained corresponding author Robert Stern, PhD, Director of the Clinical Core of the Boston University Alzheimer’s Disease Center (BU ADC) and professor of neurology, neurosurgery and anatomy and neurobiology at Boston University School of Medicine.

    The study’s first author Yorghos Tripodis, PhD, Associate Director of the Data Management and Biostatistics Core of the BU ADC and associate professor of Biostatistics at Boston University School of Public Health, cautioned, “Our findings should still be interpreted cautiously due to the crude and limited assessment of TBI history available through the NACC database.” The researchers recommended that future studies should collect information on the number of past TBIs (including mild TBIs, as well as exposure to sub-concussive trauma through contact sports and other activities) along with time since TBI, which may play a significant role in cognitive change.


  7. Study examines link between sleep disruptions and Alzheimer’s

    July 23, 2017 by Ashley

    From the Washington University in St. Louis press release:

    A good night’s sleep refreshes body and mind, but a poor night’s sleep can do just the opposite. A study from Washington University School of Medicine in St. Louis, Radboud University Medical Centre in the Netherlands, and Stanford University has shown that disrupting just one night of sleep in healthy, middle-aged adults causes an increase in amyloid beta, a brain protein associated with Alzheimer’s disease. And a week of tossing and turning leads to an increase in another brain protein, tau, which has been linked to brain damage in Alzheimer’s and other neurological diseases.

    “We showed that poor sleep is associated with higher levels of two Alzheimer’s-associated proteins,” said David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor, head of the Department of Neurology and the study’s senior author. “We think that perhaps chronic poor sleep during middle age may increase the risk of Alzheimer’s later in life.”

    These findings, published July 10 in the journal Brain, may help explain why poor sleep has been associated with the development of dementias such as Alzheimer’s.

    More than 5 million Americans are living with Alzheimer’s disease, which is characterized by gradual memory loss and cognitive decline. The brains of people with Alzheimer’s are dotted with plaques of amyloid beta protein and tangles of tau protein, which together cause brain tissue to atrophy and die. There are no therapies that have been proven to prevent, slow or reverse the course of the disease.

    Previous studies by Holtzman, co-first author Yo-El Ju, MD, an assistant professor of neurology, and others have shown that poor sleep increases the risk of cognitive problems. People with sleep apnea, for example, a condition in which people repeatedly stop breathing at night, are at risk for developing mild cognitive impairment an average of 10 years earlier than people without the sleep disorder. Mild cognitive impairment is an early warning sign for Alzheimer’s disease.

    But it wasn’t clear how poor sleep damages the brain. To find out, the researchers — Holtzman; Ju; co-first author and graduate student Sharon Ooms of Radboud; Jurgen Claassen, MD, PhD, of Radboud; Emmanuel Mignot, MD, PhD, of Stanford; and colleagues — studied 17 healthy adults ages 35 to 65 with no sleep problems or cognitive impairments. Each participant wore an activity monitor on the wrist for up to two weeks that measured how much time they spent sleeping each night.

    After five or more successive nights of wearing the monitor, each participant came to the School of Medicine to spend a night in a specially designed sleep room. The room is dark, soundproof, climate-controlled and just big enough for one; a perfect place for sleeping, even as the participants wore headphones over the ears and electrodes on the scalp to monitor brain waves.

    Half the participants were randomly assigned to have their sleep disrupted during the night they spent in the sleep room. Every time their brain signals settled into the slow-wave pattern characteristic of deep, dreamless sleep, the researchers sent a series of beeps through the headphones, gradually getting louder, until the participants’ slow-wave patterns dissipated and they entered shallower sleep.

    The next morning, the participants who had been beeped out of slow-wave sleep reported feeling tired and unrefreshed, even though they had slept just as long as usual and rarely recalled being awakened during the night. Each underwent a spinal tap so the researchers could measure the levels of amyloid beta and tau in the fluid surrounding the brain and spinal cord.

    A month or more later, the process was repeated, except that those who had their sleep disrupted the first time were allowed to sleep through the night undisturbed, and those who had slept uninterrupted the first time were disturbed by beeps when they began to enter slow-wave sleep.

    The researchers compared each participant’s amyloid beta and tau levels after the disrupted night to the levels after the uninterrupted night, and found a 10 percent increase in amyloid beta levels after a single night of interrupted sleep, but no corresponding increase in tau levels. However, participants whose activity monitors showed they had slept poorly at home for the week before the spinal tap showed a spike in levels of tau.

    “We were not surprised to find that tau levels didn’t budge after just one night of disrupted sleep while amyloid levels did, because amyloid levels normally change more quickly than tau levels,” Ju said. “But we could see, when the participants had several bad nights in a row at home, that their tau levels had risen.”

    Slow-wave sleep is the deep sleep that people need to wake up feeling rested. Sleep apnea disrupts slow-wave sleep, so people with the disorder often wake up feeling unrefreshed, even after a full eight hours of shut-eye.

    Slow-wave sleep is also the time when neurons rest and the brain clears away the molecular byproducts of mental activity that accumulate during the day, when the brain is busily thinking and working.

    Ju thinks it is unlikely that a single night or even a week of poor sleep, miserable though it may be, has much effect on overall risk of developing Alzheimer’s disease. Amyloid beta and tau levels probably go back down the next time the person has a good night’s sleep, she said.

    “The main concern is people who have chronic sleep problems,” Ju said. “I think that may lead to chronically elevated amyloid levels, which animal studies have shown lead to increased risk of amyloid plaques and Alzheimer’s.”

    Ju emphasized that her study was not designed to determine whether sleeping more or sleeping better reduce risk of Alzheimer’s but, she said, neither can hurt.

    “Many, many Americans are chronically sleep-deprived, and it negatively affects their health in many ways,” Ju said. “At this point, we can’t say whether improving sleep will reduce your risk of developing Alzheimer’s. All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer’s disease. But a good night’s sleep is something you want to be striving for anyway.”


  8. Sleep problems may be early sign of Alzheimer’s

    July 22, 2017 by Ashley

    From the American Academy of Neurology press release:

    Poor sleep may be a sign that people who are otherwise healthy may be more at risk of developing Alzheimer’s disease later in life than people who do not have sleep problems, according to a study published in the July 5, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. Researchers have found a link between sleep disturbances and biological markers for Alzheimer’s disease found in the spinal fluid.

    “Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways,” said study author Barbara B. Bendlin, PhD, of the University of Wisconsin-Madison. “For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well.”

    Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer’s disease.

    For the study, researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer’s, either having a parent with the disease or being a carrier of a gene that increases the risk for Alzheimer’s disease called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer’s disease.

    Researchers found that people who reported worse sleep quality, more sleep problems and daytime sleepiness had more biological markers for Alzheimer’s disease in their spinal fluid than people who did not have sleep problems. Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.

    “It’s important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save $367 billion in health care spending,” said Bendlin.

    While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea.

    The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.

    “It’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep,” said Bendlin. “More research is needed to further define the relationship between sleep and these biomarkers.”

    Bendlin added, “There are already many effective ways to improve sleep. It may be possible that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”

    One limitation of the study was that sleep problems were self-reported. Monitoring of sleep patterns by health professionals may be beneficial in future studies.


  9. Some patients with dementia may experience delayed-onset PTSD

    July 21, 2017 by Ashley

    From the Wiley press release:

    Delayed-onset post-traumatic symptoms in the elderly may be misdiagnosed as falling under the umbrella of behavioural and psychological symptoms of dementia (BPSD), according to a recent review.

    The review describes three cases where post-traumatic stress disorder (PTSD) symptoms are experienced by patients suffering with dementia long after the original traumatic event.

    Considering PTSD in individuals with dementia is important because PTSD is usually associated with working-age adults and is infrequently diagnosed in the elderly. In the early stages of dementia, recognising early life trauma may enable patients to access psychological therapy prior to significant cognitive decline. In patients with more advanced dementias, an awareness of earlier trauma exposure can help clinicians differentiate between delayed PTSD and BPSD in patients suffering with emotional and behavioural disturbances.

    “Every patient with dementia has a unique narrative, which if captured in the earlier stages of the disease, enables clinicians and their families to understand the origin of their distress. Therefore, it is important to look for a history of previous trauma in patients with BPSD as this could be due to delayed onset PTSD,” said Dr. Tarun Kuruvilla, senior author of the Progress in Neurology & Psychiatry review.


  10. Study suggests hippocampus underlies the link between slowed walking and mental decline

    July 19, 2017 by Ashley

    From the Health Sciences at the University of Pittsburgh press release:

    The connection between slowed walking speed and declining mental acuity appears to arise in the right hippocampus, a finger-shaped region buried deep in the brain at ear-level, according to a 14-year study conducted by scientists at the University of Pittsburgh Graduate School of Public Health.

    The finding, published today in Neurology, the medical journal of the American Academy of Neurology, indicates that older patients may benefit if their doctors regularly measure their walking speed and watch for changes over time, which could be early signs of cognitive decline and warrant referral to a specialist for diagnostic testing.

    “Prevention and early treatment may hold the key to reducing the global burden of dementia, but the current screening approaches are too invasive and costly to be widely used,” said lead author Andrea Rosso, Ph.D., M.P.H., assistant professor in Pitt Public Health’s Department of Epidemiology. “Our study required only a stopwatch, tape and an 18-foot-long hallway, along with about five minutes of time once every year or so.”

    Rosso and her colleagues assessed 175 older adults ages 70 to 79 when they enrolled in the Health, Aging and Body Composition (Health ABC) study in Pittsburgh or Memphis, Tennessee. At the beginning of the study, the participants were all in good mental health and had normal brain scans. Multiple times over 14 years, the participants walked an 18-foot stretch of hallway at what they deemed a normal walking pace while a research assistant timed them. At the conclusion of the study, the participants were tested again for their mental acuity and received brain scans.

    As previous studies have shown, slowing in the participants’ gait, or walking speed, was associated with cognitive impairment. However, Rosso’s research determined that participants with a slowing gait and cognitive decline also experienced shrinkage of their right hippocampus, an area of the brain important to both memory and spatial orientation. It was the only area of the brain where the researchers found a shrinking volume to be related to both gait slowing and cognitive impairment.

    Rosso’s study also found gait slowing over an extended period of time to be a stronger predictor of cognitive decline than simply slowing at a single time point, which is what other, similar research evaluated. All the participants slowed over time, but those who slowed by 0.1 seconds more per year than their peers were 47 percent more likely to develop cognitive impairment. The finding held even when the researchers took into account slowing due to muscle weakness, knee pain and diseases, including diabetes, heart disease and hypertension.

    “A fraction of a second is subtle, but over 14 years, or even less, you would notice,” said Rosso, also an assistant professor in Pitt’s Clinical and Translational Science Institute. “People should not just write off these changes in walking speed. It may not just be that grandma’s getting slow — it could be an early indicator of something more serious.”

    While the team noted that slowing gait speed is not a sensitive enough measure to diagnose a cognitive issue, they argue that it should be included in regular geriatric evaluations to determine if there’s a need for further testing. If cognitive decline can be detected early, there are therapies that can delay its onset, and the extra time could allow patients and families to plan for the eventual need for assisted care.

    “Typically when physicians notice a slowing gait in their patients, they’ll consider it a mechanical issue and refer the patient to physical therapy,” said Rosso. “What we’re finding is that physicians also should consider that there may be a brain pathology driving the slowing gait and refer the patient for a cognitive evaluation.”