1. Mild cognitive impairment, Alzheimer’s diagnoses trigger lower self-ratings of quality of life

    August 20, 2017 by Ashley

    From the University of Pennsylvania School of Medicine press release:

    Researchers at Penn Medicine have discovered that a patient’s awareness of a diagnosis of cognitive impairment may diminish their self-assessment of quality of life. In a study published this month in the Journal of Gerontology: Psychological Sciences the researchers report that older adults who were aware of their diagnosis — either Mild Cognitive Impairment or mild stage Alzheimer’s disease dementia — reported greater depression, higher stress, and lower quality of life than those who were unaware. They also found that older adults who had an expectation that their disease would worsen over time reported lower overall satisfaction with daily life.

    “These findings suggest that a patient’s quality of life could be impacted by a diagnostic label and their expectations for the prognosis. So, when a clinician discloses the diagnosis and prognosis of Mild Cognitive Impairment or mild stage Alzheimer’s disease, a patient may experience additional symptoms, like anxiety or depression,” said the study’s lead author, Shana Stites, PsyD, MA, MS, a clinical psychologist in the Penn Memory Center, senior research investigator for the Penn Project on Precision Medicine for the Brain (P3MB).

    For many years, a diagnosis of Alzheimer’s disease was often not made until a patient had substantial memory and cognitive problems — by which time patients themselves were often unaware of their diagnosis. Advances in awareness, as well in diagnostic methods, mean doctors are diagnosing Alzheimer’s disease earlier, and in the future, routine diagnosis may occur before symptoms even begin. According to Stites, early diagnosis holds the promise for opportunities to prevent cognitive and functional losses and to plan for these losses. But study results show that an early diagnosis of Alzheimer’s disease can also bring challenges.

    The Penn Researchers studied how awareness of diagnosis impacts on self-ratings of quality of life in people with one of two disorders, Mild Cognitive Impairment — a disorder defined by slight but noticeable declines in cognitive abilities — or mild stage Alzheimer’s disease dementia. They compared these ratings to a group of adults above the age of 65 with normal cognition. Study participants completed measures of multiple domains of quality of life including cognitive problems, activities of daily living, physical functioning, mental wellbeing, and perceptions of one’s daily life. The researchers compared the measure of quality of life by cognitive performance, diagnosis awareness, and diagnostic group.

    The findings help to identify psychological processes underlying relationships between cognitive decline and quality of life. According to Stites, the study has practical implications for current and future clinical practice.

    “It’s not just an issue of to tell or not to tell, it’s an issue of how you tell and what you tell because when you give someone a diagnosis you’re also communicating, either directly or indirectly, a lot of information that can affect the activities people do in daily life, their planning for employment and lifestyle, emotional wellbeing, and social relationships with close friends and family members. These issues need to be explicitly addressed with patients,” Stites said. “Maybe at this point we can’t prevent cognitive decline, but we certainly have effective interventions for treating depression and for managing other symptoms.”

    The researchers note that further study is needed to understand what drives the impact of awareness of diagnosis and prognosis on quality of life. Future studies might include pre-clinical research that is being done in Alzheimer’s disease, where clinicians are working to diagnose people who are at risk of developing the disease based on genes and biomarkers to determine how diagnosis awareness might affect an individual’s sense of identity and functioning in the world if they learn that they have a high probability of developing Alzheimer’s disease in the future.

    A diagnosis of Alzheimer’s disease can evoke assumptions, stereotypes, feelings, and attitudes that can affect a person’s quality of life, how they view themselves and how they are treated by others. This study is part of the research team’s ongoing efforts to understand how early diagnosis can impact a person’s quality of life and wellbeing. The results add to what they’ve been learning about the stigma of Alzheimer’s disease.


  2. Lutein, found in leafy greens, may counter cognitive aging

    August 19, 2017 by Ashley

    From the University of Illinois at Urbana-Champaign press release:

    Spinach and kale are favorites of those looking to stay physically fit, but they also could keep consumers cognitively fit, according to a new study from University of Illinois researchers.

    The study, which included 60 adults aged 25 to 45, found that middle-aged participants with higher levels of lutein — a nutrient found in green leafy vegetables such as spinach and kale, as well as avocados and eggs — had neural responses that were more on par with younger individuals than with their peers. The findings were published in the journal Frontiers in Aging Neuroscience.

    “Now there’s an additional reason to eat nutrient-rich foods such as green leafy vegetables, eggs and avocados,” said Naiman Khan, a professor of kinesiology and community health at Illinois. “We know these foods are related to other health benefits, but these data indicate that there may be cognitive benefits as well.”

    Most other studies have focused on older adults, after there has already been a period of decline. The Illinois researchers chose to focus on young to middle-aged adults to see whether there was a notable difference between those with higher and lower lutein levels.

    “As people get older, they experience typical decline. However, research has shown that this process can start earlier than expected. You can even start to see some differences in the 30s,” said Anne Walk, a postdoctoral scholar and first author of the paper. “We want to understand how diet impacts cognition throughout the lifespan. If lutein can protect against decline, we should encourage people to consume lutein-rich foods at a point in their lives when it has maximum benefit.”

    Lutein is a nutrient that the body can’t make on its own, so it must be acquired through diet. Lutein accumulates in brain tissues, but also accumulates in the eye, which allows researchers to measure levels without relying on invasive techniques.

    The Illinois researchers measured lutein in the study participants’ eyes by having participants look into a scope and respond to a flickering light. Then, using electrodes on the scalp, the researchers measured neural activity in the brain while the participants performed a task that tested attention.

    “The neuro-electrical signature of older participants with higher levels of lutein looked much more like their younger counterparts than their peers with less lutein,” Walk said. “Lutein appears to have some protective role, since the data suggest that those with more lutein were able to engage more cognitive resources to complete the task.”

    Next, Khan’s group is running intervention trials, aiming to understand how increased dietary consumption of lutein may increase lutein in the eye, and how closely the levels relate to changes in cognitive performance.

    “In this study we focused on attention, but we also would like to understand the effects of lutein on learning and memory. There’s a lot we are very curious about,” Khan said.


  3. Newly discovered biomarkers may lead to promising diagnostic tool for Alzheimer’s

    by Ashley

    From the Ohio State University press release:

    Diagnosing Alzheimer’s disease and determining a patient’s prognosis is an inexact business, and that stands in the way of better personalized care and advances in treatment.

    A new study from The Ohio State University has identified a potential new way of confirming the disease and predicting a patient’s outlook.

    First, the team of researchers discovered new physical biomarkers that could help pinpoint a diagnosis — changes to proteins found in the spinal fluid and blood of patients. In particular, as Alzheimer’s severity increased, the proteins were longer, more rigid and more clustered, said lead researcher Mingjun Zhang, a professor of biomedical engineering at Ohio State.

    After finding these new clues to the disease, the research team entered information about the biomarkers and several other factors — including scores from cognitive assessments of patients — into an algorithm designed to rate the severity of illness.

    The researchers found that the equation could identify disease stages and progression.

    “With a tool like this you may predict how fast this disease will go, and currently we can’t do that — we just know everyone is different,” Zhang said. “Looking at multiple indicators of the disease all at once increases the reliability of the diagnosis and prognosis.”

    The research appears in the journal Science Advances.

    The information used in the study came from a database of medical information — and samples of spinal fluid and blood — from patients seen by study co-author Douglas Scharre, a professor of clinical neurology and psychiatry in the Neurological Institute at Ohio State’s Wexner Medical Center.

    The experimental tools aren’t ready for clinical use yet, but could lead to improvements in treatment in multiple ways, Scharre said.

    “It was fairly easy to see changes between normal aging and different stages of Alzheimer’s disease using these biomarkers, and to see significant changes,” he said.

    Currently available medications treat only symptoms of the disease and work best with an early diagnosis. Improved diagnostic tools could help doctors sort out more quickly which patients have Alzheimer’s disease and which are experiencing cognitive decline for other reasons, Scharre said.

    Early evidence from tests of experimental drugs designed to alter the disease indicate that they would work best in the early stages as well, he said.

    And, ideally, these biomarkers and algorithm — or something similar — could speed up discovery of new treatments to improve the outlook for those with later stages of Alzheimer’s disease. Having an easily observable biomarker that changes quickly over time would be a powerful tool for those trying to monitor the impact of their experimental treatments, Scharre said.

    “A biomarker that shows that in three months, or three weeks even, that this drug is not doing a darn thing or is slowing down the disease will help us to not waste time in finding better treatments,” he said.

    Zhang said doctors treating patients with Alzheimer’s disease already try to take a number of factors about a given patient to estimate disease stage and to predict how quickly the disease will move.

    “We’ve taken what they do and converted it to a computational model with different weights for different factors,” Zhang said. “We’re using engineering techniques to look at a human disease process, a dynamic process.”

    Looking for physical changes in proteins is a growing area of interest for those seeking disease biomarkers, said Jeff Kuret, a study co-author and professor of biological chemistry and pharmacology at Ohio State.

    “The goal is to have a sensitive test that could be applied at the early stages of Alzheimer’s disease and would not be too expensive,” Kuret said.

    The study authors said it’s too soon to estimate how much tools such as this would cost if they were developed for routine use, but said that identifying a blood test — rather than one that relies on spinal fluid — would be key to minimizing risks and costs.

    Kuret said this kind of test is especially promising for Alzheimer’s because it’s a relatively slow-moving illness and one in which the ability to determine stages of disease could lead to better, more personalized treatments down the road.

    “To be able to follow individual patients from pre-symptomatic through all stages of Alzheimer’s progression would be incredibly helpful,” he said.


  4. Dementia: BACE inhibitor improves brain function

    August 18, 2017 by Ashley

    From the Technical University of Munich (TUM) press release:

    The protein amyloid beta is believed to be the major cause of Alzheimer’s disease. Substances that reduce the production of amyloid beta, such as BACE inhibitors, are therefore promising candidates for new drug treatments. A team at the Technical University of Munich (TUM) has recently demonstrated that one such BACE inhibitor reduces the amount of amyloid beta in the brain. By doing so, it can restore the normal function of nerve cells and significantly improve memory performance.

    Around 50 million people worldwide suffer from dementia. To date, no effective drug is available that is able to halt or cure the disease. Moreover, the exact causes of the disease have yet to be definitively explained. However, there is a greater accumulation of the protein amyloid beta in Alzheimer’s patients than in healthy people. As a result, the protein clumps together and damages nerve cells.

    Affected cells can become hyperactive. They then constantly send false signals to neighboring cells. In addition, certain brain waves such as slow oscillations spin out of control. These waves play a key role in the formation of memories by transferring learned information into long-term memory.

    Brain functions restored in mice

    “A successful treatment must take effect as early in the course of the disease as possible. In our experiments, we have therefore blocked the enzyme beta secretase BACE, which produces amyloid beta,” explains Dr Marc Aurel Busche, young investigator group leader at the Institute for Neuroscience of the TUM and psychiatrist in the Department of Psychiatry and Psychotherapy of the TUM university hospital rechts der Isar.

    The researchers tested a substance that inhibits beta secretase in a mouse model of Alzheimer’s. The mice produce large amounts of amyloid beta, which, as in humans, leads to the formation of amyloid beta plaques in the brain and causes memory loss. During the study, the mice were given the inhibitor in their food for up to eight weeks, after which they were examined. For this purpose, the researchers used a special imaging technique known as two-photon microscopy, which allowed them to observe individual nerve cells in the brain.

    As expected, the mice had less amyloid beta in their brain after this period, since its production was inhibited. However, the effect of the substance was much more far-reaching: the animals’ brain functions actually normalized. There were fewer hyperactive nerve cells, and the slow-wave brain patterns once again resembled those in healthy mice. A key finding for the scientists was the observation that the animals’ memory also improved. The mice were able to locate a hidden platform in a water-filled maze as quickly as their healthy counterparts.

    Clinical trial planned

    “What really impressed and amazed us was the reversibility of the symptoms. Before the treatment, the mice had a marked clinical picture with amyloid beta plaques in their brain. Nevertheless, the substance was able to restore important brain functions and abilities,” explains Aylin Keskin, lead author of the publication. Moreover, the researchers’ study showed yet another benefit: “We were also able to demonstrate which neural deficits really are caused by amyloid beta. That was not fully understood with regard to hyperactive nerve cells, for example,” Keskin says.

    The scientists’ findings will soon find its way into clinical practice: A large-scale clinical trial is planned with around 1000 participants to test a slightly modified form of the BACE inhibitor. “Needless to say, we very much hope that the promising discoveries in the animal model will translate to humans,” Busche says.


  5. Protein involved in Alzheimer’s disease may also be implicated in cognitive abilities

    August 17, 2017 by Ashley

    From the IOS Press press release:

    Rare mutations in the amyloid precursor protein (APP) have previously been shown to be strongly associated with Alzheimer’s disease (AD). Common genetic variants in this protein may also be linked to intelligence (IQ) in children, according to recent research performed at the University of Bergen, Norway.

    Results of the research were published online in the Journal of Alzheimer’s Disease. Senior author Dr. Tetyana Zayats is a researcher at the KGJebsen Centre for Neuropsychiatric Disorders at the University of Bergen.

    The study analyzed genetic markers and IQ collected from 5,165 children in the Avon Longitudinal Study of Parents and Children. The genetic findings were followed up in the genetic data from two adult datasets (1) 17,008 cases with AD and 37,154 controls, and (2) 112,151 individuals assessed for general cognitive functioning. The function of the genetic markers was analysed using reporter assays in cells.

    Brain cells communicate via synapses containing hundreds of specialized proteins. Mutations in some of these proteins lead to dysfunctional synapses and brain diseases such as epilepsy, intellectual disability, autism or AD. Dr. Zayats and co-workers at the University of Bergen examined a subgroup of these proteins that have been implicated in synaptic plasticity and learning (the ARC complex). They found that a variation in DNA sequence within the gene encoding a member of this group of proteins, amyloid beta precursor protein (APP) was associated with non-verbal (fluid) intelligence in children, which reflects our capacity to reason and solve problems. In adults, this variation revealed association with AD, while the overall genetic variation within the APP gene itself appeared to be correlated with the efficiency of information processing (reaction time).

    “This study has potential implications for our understanding of the normal function of these synaptic proteins as well as their involvement in disease” said Dr. Zayats.

    APP encodes the amyloid-? precursor protein that forms amyloid-? — containing neuritic plaques, the accumulation of which is one of the key pathological hallmarks in AD brains. However, it is unclear how these plaques affect brain functions and whether they lead to AD.

    “Our understanding of biological processes underlying synaptic functioning could be expanded by examining human genetics throughout the lifespan as genetic influences may be the driving force behind the stability of our cognitive functioning,” Dr. Zayats commented.

    Genetic correlation between intelligence and AD has also been found in large-scale genome-wide analyses on general cognitive ability in adults. Several genes involved in general intelligence have previously reported to be associated with AD or related dementias. Such overlap has also been noted for the APP gene, where a coding variant was shown to be protective against both AD and cognitive decline in elderly.

    “While this is only an exploratory study, in-depth functional and association follow up examinations are needed,” Dr. Zayats noted. “Examining genetic overlap between cognitive functioning and AD in children — not only adults — presents us with a new avenue to further our understanding of the role of synaptic plasticity in cognitive functioning and disease.”


  6. New, noninvasive diagnostic may help differentiate between Alzheimer’s and frontotemporal dementia

    August 13, 2017 by Ashley

    From the American Academy of Neurology press release:

    A new method may help determine whether a person has Alzheimer’s disease or frontotemporal dementia, two different types of dementia that often have similar symptoms, according to a preliminary study published in the July 26, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology.

    “Making the correct diagnosis can be difficult,” said study author Barbara Borroni, MD, of the University of Brescia in Brescia, Italy. “Current methods can be expensive brain scans or invasive lumbar punctures involving a needle inserted in the spine, so it’s exciting that we may be able to make the diagnosis quickly and easily with this non-invasive procedure.”

    For the technique, called transcranial magnetic stimulation (TMS), a large electromagnetic coil is placed against the scalp. It creates electrical currents that stimulate nerve cells.

    Once thought to be rare, frontotemporal dementia is now believed to make up 10 to 15 percent of dementia cases. It is often initially misdiagnosed as a psychiatric problem, Alzheimer’s disease or Parkinson’s disease because of its wide range of symptoms. The disease generally affects people in their mid-40s to mid-60s and is characterized by severe behavior changes and language problems. While there is no cure for frontotemporal dementia, it is important to accurately identify the disease so that doctors can help patients manage their symptoms and avoid unnecessary treatment.

    For the study, researchers looked at 79 people with probable Alzheimer’s disease, 61 people with probable frontotemporal dementia, and 32 people of the same age who did not have any signs of dementia.

    Using TMS, researchers were able to measure the brain’s ability to conduct electrical signals among various circuits in the brain. They found that people with Alzheimer’s disease mainly had problems with one type of circuit, while people with frontotemporal dementia had problems with another type of circuit.

    Researchers were then able to accurately distinguish frontotemporal dementia from Alzheimer’s disease with 90 percent accuracy, Alzheimer’s disease from healthy brains with 87 percent accuracy and frontotemporal dementia from healthy brains with 86 percent accuracy. The results were almost as good when researchers tested only people with mild forms of the disease. The accuracy of the results for a comparison of the two patient groups was comparable to tests with positron emission tomography (PET) brain scans or through testing spinal fluid through lumbar punctures, Borroni said.

    Limitations of the study include that those operating the stimulation device were aware when they were conducting the procedure on a healthy person, but they did not know whether the other participants had Alzheimer’s disease or frontotemporal dementia. In addition, the dementia diagnoses were not confirmed by autopsy after death.

    “If our results can be replicated with larger studies, this will be very exciting,” Borroni said. “Doctors might soon be able to quickly and easily diagnose frontotemporal dementia with this non-invasive procedure. This disease unfortunately can’t be cured, but it can be managed — especially if it is caught early.”


  7. Mediterranean-style diets linked to better brain function in older adults

    August 12, 2017 by Ashley

    From the American Geriatrics Society press release:

    Eating foods included in two healthy diets — the Mediterranean or the MIND diet — is linked to a lower risk for memory difficulties in older adults, according to a study published in the Journal of the American Geriatrics Society.

    The Mediterranean diet is rich in fruits, vegetables, whole grains, beans, potatoes, nuts, olive oil and fish. Processed foods, fried and fast foods, snack foods, red meat, poultry and whole-fat dairy foods are infrequently eaten on the Mediterranean diet.

    The MIND diet is a version of the Mediterranean diet that includes 15 types of foods. Ten are considered “brain-healthy:” green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, seafood, poultry, olive oil, and wine. Five are considered unhealthy: red meat, butter and stick margarine, cheese, pastries, sweets and fried/fast foods.

    Researchers examined information from 5,907 older adults who participated in the Health and Retirement Study. The participants filled out questionnaires about their eating habits. Researchers then measured the participants’ cognitive abilities — mostly on their memory and attention skills.

    The researchers compared the diets of participants to their performance on the cognitive tests. They found that older people who ate Mediterranean and MIND-style diets scored significantly better on the cognitive function tests than those who ate less healthy diets. In fact, older people who ate a Mediterranean-style diet had 35% lower risk of scoring poorly on cognitive tests. Even those who ate a moderate Mediterranean-style diet had 15% lower risk of doing poorly on cognitive tests. The researchers noted similar results for people who ate MIND-style diets.

    This study suggests that eating Mediterranean and MIND-style diets is linked to better overall cognitive function in older adults, said the researchers. What’s more, older adults who followed these healthy diets had lower risks for having cognitive impairment in later life, noted the researchers.


  8. Increased risk of dementia in patients who experience delirium after surgery

    August 11, 2017 by Ashley

    From the Oxford University Press USA press release:

    Delirium is common in elderly hospitalized patients, affecting an estimated 14 — 56% of patients. It frequently manifests as a sudden change in behavior, with patients suffering acute confusion, inattention, disorganized thinking and fluctuating mental status.

    Pre-existing cognitive impairment or dementia in patients undergoing surgery are widely recognized as risk factors for postoperative delirium, increasing its likelihood and severity.

    However, little previous research has focused on whether delirium itself portends or even accelerates a decline into dementia in patients who showed no previous signs of cognitive impairment.

    Research published today in the British Journal of Anaesthesiafocuses on patients over the age of 65 who were assessed as cognitively normal prior to surgery. This study, led by Professor Juraj Sprung of the Mayo Clinic in Minnesota, finds those who developed postoperative delirium were three times more likely to suffer permanent cognitive impairment or dementia.

    Over a ten year period, patients over the age of 65 enrolled at the Mayo Clinic Study of Ageing in Olmsted County Minnesota who were exposed to general anesthesia were included in an investigation involving over two 2000 patients. Their cognitive status was evaluated in regular 15 month periods before and after surgery by neuropsychologic testing and clinical assessment. Out of 2014 patients, 1667 were deemed to be cognitively normal before surgery. Of the 1152 patients who returned for follow-up cognitive evaluation, 109 (9.5%) had developed mild cognitive impairment (pre-dementia) or dementia, and those who had suffered postoperative delirium were three times more likely to be subsequently diagnosed with permanent cognitive decline or dementia. This research is the first to focus on the association between delirium and long-term cognitive decline in patients with normal mental capacity before surgery.

    While previous studies have highlighted cognitive decline in the elderly following postoperative delirium, no others have involved such a detailed neuro-cognitive assessment identifying those with normal pre-operative cognitive abilities who go on to develop dementia. In conclusion, researchers believe that postoperative delirium could be a warning sign of future permanent cognitive impairment (dementia) in patients who at the time of surgery were still just above the threshold for registering cognitive decline. Alternatively, postoperative delirium could itself produce injury, which per se accelerates the trajectory of decline into dementia.

    “Our research shows that delirium after surgery is not only distressing for patients and their families, but also may be a warning that patients could later develop dementia, said Sprung. “We don’t yet know whether taking steps to prevent postoperative delirium could also help prevent dementia — but we need to find out.”

    British Journal of Anaesthesia Editor-in-Chief Professor Hugh Hemmings said: “This important research identifies a significant risk factor for developing dementia postoperatively, and highlights the need for more research in preventing, identifying and treating postoperative delirium.”


  9. Risk for bipolar disorder associated with faster aging

    August 10, 2017 by Ashley

    From the King’s College London press release:

    New King’s College London research suggests that people with a family history of bipolar disorder may ‘age’ more rapidly than those without a history of the disease.

    The study, published in Neuropsychopharmacology, also shows that bipolar patients treated with lithium — the main medication for the illness — have longer telomeres (a sign of slower biological aging) compared to bipolar disorder patients not treated with lithium. This suggests that the drug may mask the aging effects associated with bipolar disorder, or even help to reverse it.

    Faster aging at the biological level could explain why rates of aging-related diseases such as cardiovascular disease, type-2 diabetes and obesity are higher amongst bipolar disorder patients. However, more research is needed in the relatives of bipolar disorder patients to better understand if they are also at a higher risk for aging-related diseases.

    Unaffected first-degree relatives represent a group of individuals at risk for bipolar disorder who have not been treated with medications, so studying them may represent a truer reflection of the relationship between aging and bipolar disorder. To measure biological aging, the researchers studied a feature of chromosomes called telomeres in 63 patients with bipolar disorder, 74 first-degree relatives and 80 unrelated healthy people.

    Telomeres sit on the end of our chromosomes and act like ‘caps’, protecting the strands of DNA stored inside each of our cells as we age. Telomeres shorten each time a cell divides to make new cells, until they are so short that they are totally degraded and cells are no longer able to replicate. Telomere length therefore acts as a marker of biological age, with shortened telomeres representing older cells, and commonly older individuals.

    The rate at which telomeres shorten across our lifespan can vary, based on a range of environmental and genetic factors. This means that two unrelated people of the same chronological age may not be the same age biologically.

    The researchers from King’s College London and the Icahn School of Medicine at Mount Sinai found that healthy relatives of bipolar patients had shorter telomeres compared to healthy controls (who had no risk for the disorder running in their family). This suggests that genetic or environmental factors associated with family risk for bipolar disorder are also linked to faster biological aging.

    They also conducted MRI (magnetic resonance imaging) scans to explore the relationship between telomere length and brain structure, particularly in the hippocampus, an area of the brain involved in the regulation of mood. They discovered that higher rates of biological aging (i.e. shorter telomeres) were associated with having a smaller hippocampus.

    The study authors suggest that a reduction in telomere length may be associated with a reduced ability of new brain cells to grow in the hippocampus, which can reduce the size of the hippocampus and consequently increase risk for mood disorders such as bipolar disorder.

    Dr Timothy Powell, first author of the study, from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, said: ‘Our study provides the first evidence that familial risk for bipolar disorder is associated with shorter telomeres, which may explain why bipolar disorder patients are also at a greater risk for aging-related diseases.

    ‘We still need to dissect the environmental and genetic contributions to shortened telomeres in those at high risk for bipolar disorder. For instance, do those at risk for bipolar disorder carry genes predisposing them to faster biological aging, or are they more likely to partake in environmental factors which promote aging (e.g. smoking, poor diet)? Identifying modifiable risk factors to prevent advanced aging would be a really important next step.’

    Dr Sophia Frangou, co-senior author of the study, from the Icahn School of Medicine at Mount Sinai, said: ‘Our study shows that telomere length is a promising biomarker of biological aging and susceptibility to disease in the context of bipolar disorder. Moreover, it suggests that proteins which protect against telomere shortening may provide novel treatment targets for people with bipolar disorder and those predisposed to it.’

    Dr Gerome Breen, co-senior author, also at IoPPN, said: ‘Up to now it has been unclear whether or not bipolar disorder patients are at risk of accelerated aging. This study shows that they are at greater risk of faster aging and drugs commonly used to treat the disorder may actually mask or reverse this effect.’


  10. Sleep disorders may increase cognitive problems particularly in those at risk for Alzheimer’s

    August 8, 2017 by Ashley

    From the American Thoracic Society press release:

    People who carry a genetic susceptibility to Alzheimer’s disease appear to be at greater risk of diminished cognition from sleep-disordered breathing than those without the susceptibility, according to new research published online, ahead of print in the Annals of the American Thoracic Society.

    In “Greater Cognitive Deficits with Sleep-Disordered Breathing among Individuals with Genetic Susceptibility to Alzheimer’s Disease: The Multi-Ethnic Study of Atherosclerosis,” researchers report that study participants carrying the apolipoprotein ?-4 (APOE-?4) allele showed greater cognitive deficits with the various indices of sleep-disordered breathing compared to those without the allele.

    APOE is a major cholesterol carrier that supports injury repair in the brain. Other studies have shown that those carrying the alternate form of the gene, ?4 allele, are at increased risk of Alzheimer’s disease. Estimates are that 20 percent of the population carries the ?4 allele.

    “Previous studies have shown inconsistent findings between sleep-disordered breathing and cognition, which may be due to the different tests used,” said lead study author Dayna A. Johnson, PhD, MPH, MS, MSW, instructor of medicine at Brigham and Women’s Hospital and Harvard Medical School.

    Dr. Johnson and colleagues investigated the association in a diverse sample using several indicators of sleep-disordered breathing and cognition. They also evaluated whether the presence of the APOE-?4 allele, which is known to increase risk of Alzheimer’s disease, influenced the link between sleep-disordered breathing and cognition.

    The authors analyzed data from 1,752 participants (average age 68) in the Multi-Ethnic Study of Atherosclerosis (MESA) who underwent an in-home polysomnography (sleep) study, completed standardized sleep questions, and a battery of tests to measure their cognition. The authors defined sleep-disordered breathing as an apnea-hypopnea index (AHI), which measures the number of stopped or shallow breaths per hour, as AHI > 15, and sleep apnea syndrome as AHI > 5 (below 5 is normal) plus self-reported sleepiness (based on a standardized scale).

    The study found:

    • Increased overnight hypoxemia (oxygen saturation below 90 percent) or increased daytime sleepiness was associated with poorer attention and memory.
    • More daytime sleepiness was also associated with slower cognitive processing speed.
    • Sleep apnea syndrome was associated with poorer attention and processing speed.
    • These associations were strongest in APOE-?4 carriers.

    The researchers adjusted for race, age, body mass index, education level, smoking status, hypertension, diabetes, benzodiazepine use, and depressive symptoms.

    Dr. Johnson said that, overall, the effects of the various sleep factors they measured on cognition were small, but in the range previously reported for several other lifestyle and health risk factors for dementia. Screening and treating sleep-disordered breathing, she added, may help reduce a person’s risk of dementia, especially if that individual carries APOE-?4.

    “Our study provides further evidence that sleep-disordered breathing negatively affects attention, processing speed and memory, which are robust predictors of cognitive decline,” said senior study author Susan Redline, MD, MPH, Peter C. Farrell Professor of Sleep Medicine, Harvard Medical School.

    “Given the lack of effective treatment for Alzheimer’s disease, our results support the potential for sleep-disordered breathing screening and treatment as part of a strategy to reduce dementia risk.”

    Find the report online at: http://www.thoracic.org/about/newsroom/press-releases/resources/sleep-disordered-breathing-ad-cognition.pdf