1. Using omega 3 fatty acids to treat Alzheimer’s and other diseases?

    August 3, 2017 by Ashley

    From the Louisiana State University Health Sciences Center press release:

    Understanding how dietary essential fatty acids work may lead to effective treatments for diseases and conditions such as stroke, Alzheimer’s disease, age-related macular degeneration, Parkinson’s disease and other retinal and neurodegenerative diseases. The key is to be able to intervene during the early stages of the disease. That is the conclusion of a Minireview by Nicolas Bazan, MD, PhD, Boyd Professor and Director, and Aram Asatryan, PhD, postdoctoral researcher, at the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine published in the Journal of Biological Chemistry‘s Thematic Minireview Series: Inflammatory transcription confronts homeostatic disruptions.

    Docosahexaenoic acid (DHA), a key essential Omega-3 fatty acid, produces signaling molecules called docosanoids in response to disruptions in the state of equilibrium within cells caused by injury or disease. Neuroprotectin D1 (NDP1) is a docosanoid that the Bazan lab discovered and found protects neurons by controlling which and how certain genes in the retina and brain respond.

    Research shows that the preclinical events in Alzheimer’s disease including neuroinflammation, damage to dendritic spines — small doorknob-shaped protrusions that help transmit electrical signals to the cell — and problems with cell-to-cell communication coincide with decreased DHA content in the brain. The neuroprotective bioactivity of NPD1 includes inflammatory modulating properties as well as features that promote cell survival, both of which contribute to restoring a stable state of equilibrium, or homeostasis, within the cell.

    In experimental models of stroke, researchers at LSU Health New Orleans Neuroscience Center led by Bazan have shown that the administration of NPD1 reduces the size of stroke damage and also saves tissue in the rim surrounding the stroke core, which remains viable for a short time.

    Research has demonstrated that DHA from the liver is also retained and concentrated in photoreceptor cells and that retinal degeneration occurs when photoreceptor cells fail to capture DHA. When a gene that regulates the uptake of DHA is turned off, photoreceptor cells die and a single amino acid mutation in this receptor can cause retinitis pigmentosa.

    Cells die through a variety of mechanisms. Contributors include a family of reactive oxygen species — compounds formed continuously as by-products of aerobic metabolism such as from reactions to drugs and environmental toxins, or when the levels of antioxidants are diminished creating oxidative stress, as well as inflammation and the disease process. Cell death is considered to be reversible until a first “point of no return” checkpoint is passed. The authors describe how NPD1 acts to stop cells from passing that checkpoint in cell death activation pathways including apoptosis, necrosis, necroptosis, pyroptosis, and pyronecrosis, among others.

    The Minireview summarizes the effects of the essential fatty acid family member DHA and its bioactive derivative NPD1 in the context of a specific target of gene regulation. The authors also describe the mechanism of a pathway of regulation by a bioactive lipid that has a significant impact on cellular homeostasis — how NPD1 activates pro-survival genes and suppresses pro-death genes.

    “The organizational and functional complexity of the brain raises new questions regarding how the cellular events described here operate in response to disrupted homeostasis to attain neuroprotection in pathological conditions,” notes Bazan. “It is our hope that this knowledge will contribute to managing early stages of such devastating diseases as Alzheimer’s, stroke, traumatic brain injury, age-related macular degeneration, Parkinson’s and others.”


  2. Bacteria found in Alzheimer’s brains

    August 1, 2017 by Ashley

    From the Frontiers press release:

    Researchers in the UK have used DNA sequencing to examine bacteria in post-mortem brains from patients with Alzheimer’s disease. Their findings suggest increased bacterial populations and different proportions of specific bacteria in Alzheimer’s, compared with healthy brains. The findings may support evidence that bacterial infection and inflammation in the brain could contribute to Alzheimer’s disease.

    Alzheimer’s disease is a neurodegenerative disease that results in cognitive decline, and eventually death. In the brain, the disease causes neurons to die and break down, and involves high levels of a peptide called amyloid and aggregations of a protein called tau. However, scientists are coming to appreciate that inflammation may also play a role.

    “Alzheimer’s brains usually contain evidence of neuroinflammation, and researchers increasingly think that this could be a possible driver of the disease, by causing neurons in the brain to degenerate,” says David Emery, a researcher from the University of Bristol, and an author on the study, which was recently published in Frontiers in Aging Neuroscience.

    So, what’s causing this inflammation? Some genetic risk-factors for Alzheimer’s disease can have effects on the inflammatory response, but infection may also play a role. “Neuroinflammation in the brain may be a reaction to the presence of bacteria,” says Emery. The brain is normally sealed behind specialized blood vessels that make it very difficult for things like bacteria in the blood to enter. However, at least one of the genetic risk-factors for Alzheimer’s disease may cause these blood vessels to lose some of their integrity, which could allow bacteria to enter and colonize the brain.

    The research team set out to discover if there were any differences in the types of bacteria present in brains from Alzheimer’s disease patients and healthy brains. “Previous studies looking at bacteria in the Alzheimer’s brain have primarily investigated specific bacterial species,” explains Shelley Allen, another researcher involved in the study. “We wanted to use an unbiased method to obtain the fullest overview possible of the entire bacterial population in the Alzheimer’s brain, and compare these results with those from a healthy aged brain.”

    The researchers analyzed eight Alzheimer’s and six healthy brain samples from a brain bank, where people donate their brains after death for medical research. They used a technique called next generation sequencing (NGS) to detect specific bacterial genes. “NGS technology allows millions of these DNA molecules to be sequenced at the same time, providing an unbiased overview of a complex bacterial population,” explains Allen.

    They found that the Alzheimer’s brains contained different proportions of specific bacteria compared with the healthy brains. “Comparing the bacterial populations showed at least a tenfold higher ratio overall of Actinobacteria (mostly P. acnes) to Proteobacteria in the Alzheimer’s brain compared with the healthy brain,” says Emery.

    However, the researchers were surprised to find that there also appeared to be more bacteria in the Alzheimer’s brains. “Unexpectedly, Alzheimer’s brains gave on average an apparent 7-fold increase in bacterial sequences above that seen in the healthy brain,” says Allen. “The healthy brains yielded only low levels of bacterial sequences, consistent with either a background signal or normal levels present in the blood stream in brain tissue.”

    The team caution that the NGS method does not directly indicate actual bacterial numbers, and further work will be required to confirm that bacteria play an active role in Alzheimer’s disease. “We need quantitative studies on the bacterial presence in the brain,” says Allen. “Larger numbers of brain samples are required, and future studies should also investigate if bacteria are involved in other neurodegenerative diseases involving neuroinflammation.”


  3. Study links hospitalizations and cognitive decline in older adults

    July 31, 2017 by Ashley

    From the Rush University Medical Center press release:

    Emergency and urgent hospitalizations are associated with an increased rate of cognitive decline in older adults, report researchers at Rush University Medical Center. The results of their study suggest that hospitalization may be a more of a major risk factor for long-term cognitive decline in older adults than previously recognized.

    “We found that those who have non-elective (emergency or urgent) hospitalizations and who have not previously been diagnosed with dementia or Alzheimer’s disease had a rapid decline in cognitive function (i.e., thinking abilities) compared to the prehospital rates,” said Bryan James, PhD, an epidemiologist and in the Rush Alzheimer’s Disease Center and an assistant professor in the Rush Department of Internal Medicine. “By comparison, people who were never hospitalized and those who had elective hospitalizations did not experience the drastic decline in cognitive function.”

    James and colleagues presented the research data at the Alzheimer’s Association International Conference in London on July 17.

    Study compares hospitalization data and cognitive assessments for 930 older adults

    The data emerged from a study of 930 older adults (75 percent female, an average age of 81 years old) enrolled in the Rush Memory and Aging Project (MAP) in Chicago. The study involved annual cognitive assessments and clinical evaluations.

    Information on hospitalizations was acquired by linking records of 1999 to 2010 Medicare claims for these participants with their MAP data. All hospital admissions were designated as elective, emergency, or urgent (the latter two were combined as non-elective for analysis). Non-elective hospitalizations thus include emergencies and admissions for conditions that require immediate attention.

    Of the 930 participants, 613 were hospitalized at least once over an average of almost five years of observation. Of those who were hospitalized, 260 (28 percent) had at least one elective hospital admission, and 553 (60 percent) had at least one non-elective hospital admission. These groups included 200 participants (22 percent) who had both types of hospitalizations.

    Non-elective hospitalizations were associated with an approximately 60 percent acceleration in the rate of cognitive decline from before hospitalization. Elective hospitalizations, however, were not associated with acceleration in the rate of decline at all.

    ‘Elective admissions do not necessarily carry the same risk’

    “We saw a clear distinction: non-elective admissions drive the association between hospitalization and long-term changes in cognitive function in later life, while elective admissions do not necessarily carry the same risk of negative cognitive outcomes,” James said. “These findings have important implications for the medical decision making and care of older adults. While recognizing that all medical procedures carry some degree of risk, this study implies that planned hospital encounters may not be as dangerous to the cognitive health of older persons as emergency or urgent situations.”

    This work expands upon previous research which has shown that after being hospitalized, older adults are at high risk for memory and other cognitive problems, including both transient (temporary) delirium and long-term changes in cognition, including dementia. According to the Healthcare Cost and Utilization Project in October 2010, 40 percent of all hospitalized patients in U.S. are age 65 and older. Therefore, hospitalization may be an under-recognized risk factor for cognitive decline and dementia for a large number of older adults that deserves more attention.

    Detection of dementia at the earliest stages has become a worldwide priority, because drug treatments, prevention strategies and other interventions will likely be more effective very early in the disease process, before extensive brain damage has occurred. Research results reported at the Alzheimer’s Association International Conference provide clues about associations between cognitive status in older people and several behavior and lifestyle factors, including verbal skill, hearing, dental health, and hospitalization.

    “It is essential that we learn more about factors that impact risk for Alzheimer’s disease and other dementias, especially lifestyle factors that we can change or treat,” said Maria C. Carrillo, PhD, Alzheimer’s Association chief science officer.


  4. Study suggests natural plant compound may reduce mental effects of aging

    July 28, 2017 by Ashley

    From the Salk Institute press release:

    Salk scientists have found further evidence that a natural compound in strawberries reduces cognitive deficits and inflammation associated with aging in mice. The work, which appeared in the Journals of Gerontology Series A in June 2017, builds on the team’s previous research into the antioxidant fisetin, finding it could help treat age-related mental decline and conditions like Alzheimer’s or stroke.

    “Companies have put fisetin into various health products but there hasn’t been enough serious testing of the compound,” says Pamela Maher, a senior staff scientist in Salk’s Cellular Neurobiology Laboratory and senior author of the paper. “Based on our ongoing work, we think fisetin might be helpful as a preventative for many age-associated neurodegenerative diseases, not just Alzheimer’s, and we’d like to encourage more rigorous study of it.”

    Maher, who works in the lab of David Schubert, the head of Salk’s Cellular Neurobiology Lab, has been studying fisetin for over a decade. Previous research by the lab found that fisetin reduced memory loss related to Alzheimer’s in mice genetically modified to develop the disease. But that study focused on genetic (familial) AD, which accounts for only 1 to 3 percent of cases. By far the bigger risk factor for developing what is termed sporadic AD, as well as other neurodegenerative disorders, is simply age. For the current inquiry, Maher turned to a strain of laboratory mice that age prematurely to better study sporadic AD. By 10 months of age, these mice typically show signs of physical and cognitive decline not seen in normal mice until two years of age.

    The Salk team fed the 3-month-old prematurely aging mice a daily dose of fisetin with their food for 7 months. Another group of the prematurely aging mice was fed the same food without fisetin. During the study period, mice took various activity and memory tests. The team also examined levels of specific proteins in the mice related to brain function, responses to stress and inflammation.

    “At 10 months, the differences between these two groups were striking,” says Maher. Mice not treated with fisetin had difficulties with all the cognitive tests as well as elevated markers of stress and inflammation. Brain cells called astrocytes and microglia, which are normally anti-inflammatory, were now driving rampant inflammation. Mice treated with fisetin, on the other hand, were not noticeably different in behavior, cognitive ability or inflammatory markers at 10 months than a group of untreated 3-month-old mice with the same condition. Additionally, the team found no evidence of acute toxicity in the fisetin-treated mice, even at high doses of the compound.

    “Mice are not people, of course,” says Maher, “But there are enough similarities that we think fisetin warrants a closer look, not only for potentially treating sporadic AD but also for reducing some of the cognitive effects associated with aging, generally.”

    Next, Maher hopes to partner with another group or company in order to conduct clinical trials of fisetin with human subjects.


  5. 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.


  6. 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.


  7. 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.


  8. 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.”


  9. 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.


  10. 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.