Small Risk of Autism Seen in Babies Born Preterm and Post-Term

FRIDAY, Sept. 25, 2020 — There may be a slightly increased risk of autism for each week a child is born before or after 40 weeks of gestation, according to a new study.

Researchers are still trying to pinpoint the causes of autism, but both genetic and environmental factors are believed to play a role.

Some previous studies have suggested that being born before or after full term (40 weeks) may be associated with an increased risk of autism. But many of those studies were limited in scope and didn’t account for sex and birth weight.

In this study, researchers analyzed data on more than 3.5 million children born in Sweden, Finland and Norway between 1995 and 2015. Of those, 1.44% were diagnosed with autism, and 4.7% were born preterm (before 37 weeks of gestation).

The overall risk of autism was low, especially for girls born after 42 weeks of gestation, but the risk increased for each week of gestational age before or after 40 weeks.

Of the children born at term (37 to 42 weeks), 0.83% were diagnosed with autism. The autism rates were 1.67% for those born at 22 to 31 weeks; 1.08% for those born at 32 to 36 weeks; and 1.74% for those born at 43 to 44 weeks.

These differences in risk were independent of sex and birth weight for gestational age, the researchers said. Dr. Martina Persson, an adjunct senior lecturer at the Karolinska Institute in Stockholm, Sweden, led the study.

The findings were published Sept. 22 in the journal PLOS Medicine.

In a journal news release, Persson and her colleagues said the study offers new information about the potential link between autism risk and gestational age at birth — a factor that’s potentially modifiable.

They also said further research is needed to learn more about these possible links and whether they could point to ways to reduce autism risk by addressing preterm birth.

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Insomnia, sleeping less than six hours may increase risk of cognitive impairment

Middle-aged adults who report symptoms of insomnia and are sleeping less than six hours a night may be at increased risk of cognitive impairment, according to a study by Penn State College of Medicine researchers. The results may help health care professionals understand which patients who report insomnia are at increased risk for developing dementia.

Insomnia is characterized by reports of difficulty falling asleep, difficulty staying asleep, or waking up too early and not being able to get back to sleep. When these symptoms occur at least three nights a week and for at least three months, it is considered a chronic disorder. Researchers found that adults who reported insomnia and obtained less than six hours of measured sleep in the laboratory were two times more likely to have cognitive impairment than people with the same insomnia complaints who got six or more hours of sleep in the lab. The study results were published in the journal Sleep on Sept. 24.

According to Julio Fernandez-Mendoza, associate professor of psychiatry and behavioral health and sleep specialist at Penn State Health Sleep Research and Treatment Center, about 25% of the adult general population reports insomnia symptoms and another 10% suffers from chronic insomnia. He said that being able to distinguish which of these individuals are at risk for further adverse health conditions is critical.

“This study reinforces the need to objectively measure the sleep of adults who complain of insomnia,” Fernandez-Mendoza said. In previous research, the team found that adults with insomnia who obtained less than six hours of sleep were at risk for various cardiometabolic conditions, including hypertension, diabetes, heart disease or stroke and mental health problems, such as depression.

“These new results demonstrate that these middle-aged adults also have an increased risk of cognitive impairment, which can be an early indicator of future dementia in a significant proportion of them,” Fernandez-Mendoza said.

Researchers examined data from the Penn State Adult Cohort, a randomly-selected, population-based sample of 1,741 adults who had one measured night of sleep. Before having their sleep measured in a sound, light and temperature-controlled room, participants completed a clinical history, physical exam and questionnaire to identify self-reported sleep disorders, physical health conditions, mental health problems and substance use. They also were evaluated for cognitive impairment before sleeping in the laboratory, including receiving tests that assessed attention, memory, language and other measures.

Fernandez-Mendoza and colleagues found that adults who reported insomnia symptoms or chronic insomnia and slept less than six hours in the lab were two times more likely to have cognitive impairment when compared to good sleepers. They also found that this association was particularly strong for adults with coexisting cardiometabolic conditions and cognitive impairment, which may be an indicator of vascular cognitive impairment—a condition where poor cardiovascular health results in impaired brain function.

Adults who reported insomnia but who slept six or more hours in the lab were not at risk of cognitive impairment when compared to good sleepers. The research team accounted for potential differences in sociodemographic factors—including age, sex, race, ethnicity, years of education—and the presence of physical and mental health problems, including sleep apnea, as well as substance use, such as smoking and alcohol intake.

Fernandez-Mendoza said that only having one measured night of sleep limited the study’s conclusion to in-lab sleep studies and cautioned that these data do not prove causality. Nevertheless, they further show that insomnia, cognitive impairment and cardiometabolic conditions, like high blood pressure, diabetes and heart disease, often tend to co-occur in adults who get less than six hours of sleep in the lab but not in those who can sleep six hours or more, he highlighted.

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Study shows that rheumatoid arthritis is associated with a 23% increased risk of developing diabetes

A new study presented at this year’s annual meeting of the European Association for the Study of Diabetes (EASD), held online this year, shows that rheumatoid arthritis (RA) is associated with a 23% increased risk of type 2 diabetes (T2D), and may indicate that both diseases are linked to the body’s inflammatory response. The research was conducted by Zixing Tian and Dr. Adrian Heald, University of Manchester, UK, and colleagues.

Inflammation has emerged as a key factor in the onset and progression of T2D, and RA is an autoimmune and inflammatory disease. The team suggest that the systemic inflammation associated with RA might therefore contribute to the risk of an individual developing diabetes in the future.

The team conducted a comprehensive search of a range of medical and scientific databases up to 10 March 2020, for cohort studies comparing the incidence of T2D among people with RA to the diabetes risk within the general population. Statistical analyses were performed to calculate the relative risks, as well as to test for possible publication bias (in which the outcome of research influences the decision whether to publish it or not). The eligible studies identified comprised a total of 1,629,854 participants. Most of the studies were population-based and one was hospital-based, while no evidence was found for publication bias in any of them.

The authors found that having RA was associated with a 23% higher chance of developing T2D, compared to the diabetes risk within the general population. They conclude that: “This finding supports the notion that inflammatory pathways are involved in the pathogenesis of diabetes.”

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Risk gene for Alzheimer’s has early effects on the brain

A genetic predisposition to late-onset Alzheimer’s disease affects how the brains of young adults cope with certain memory tasks. Researchers from the German Center for Neurodegenerative Diseases (DZNE) and the Ruhr-Universität Bochum report on this in the scientific journal Current Biology. Their findings are based on studies with magnetic resonance imaging in individuals at the age of about 20 years. The scientists suspect that the observed effects could be related to very early disease processes.

The causes for Alzheimer’s in old age are only poorly understood. It is believed that the disease is caused by an unfavorable interaction of lifestyle, external factors and genetic risks. The greatest genetic risk factor for late-onset Alzheimer’s disease stems from inherited mutations affecting “Apolipoprotein E” (ApoE), a protein relevant for fat metabolism and neurons. Three variants of the ApoE gene are known. The most common form is associated with an average risk for Alzheimer’s. One of the two rarer variants stands for an increased risk, and the other for a reduced risk.

“We were interested in finding out whether and how the different gene variants affect brain function. That is why we examined the brains of young adults in the scanner while they had to solve a task that challenged their memory,” explained Dr. Hweeling Lee, who led the current study at the DZNE in Bonn.

Distinguishing similar events

The group of study participants comprised of 82 young men and women. They were on average 20 years old, and all of them were university students considered to be cognitively healthy. According to their genotype for ApoE, 33 of them had an average, 34 an increased and 15 a reduced risk of developing Alzheimer’s disease at a late age. During the study in the brain scanner, all individuals were presented with more than 150 successive images displayed on a monitor. These were everyday objects such as a hammer, a pineapple or a cat. Some pictures were repeated after a while, but sometimes the position of the displayed objects on the screen had changed. The study participants had to identify whether an object was “new” or had been shown before—and if so, whether its position had shifted.

“We tested the ability to distinguish similar events from one another. This is called pattern separation,” said Hweeling Lee. “In everyday life, for example, it’s a matter of remembering whether a key has been placed in the left or right drawer of a dresser, or where the car was parked in a parking garage. We simulated such situations in a simplified way by changing the position of the depicted objects.”

High-resolution through modern technology

Simultaneously to this experiment, the brain activity of the volunteers was recorded using a technique called “functional magnetic resonance imaging”. Focus was on the hippocampus, an area only a few cubic centimeters in size, which can be found once in each brain hemisphere. The hippocampus is considered the switchboard of memory. It also belongs to those sections of the brain in which first damages occur in Alzheimer’s disease.

When measuring brain activity, the scanner was able to show its full potential: It was an “ultra-high field tomograph” with a magnetic field strength of seven Tesla. Such devices can achieve a better resolution than brain scanners usually used in medical examinations. This enabled the researchers to record brain activity in various sub-fields of the hippocampus with high precision. “Up to now, there were no comparable studies with such level of detail in ApoE genotyped participants. This is a unique feature of our research,” said Hweeling Lee.

No differences in memory performance

There were no differences between the three groups of subjects with regard to their ability for pattern separation. “All study participants performed similarly well in the memory test. It did not matter whether they had an increased, reduced or average risk for Alzheimer’s disease. Such results are certainly to be expected in young healthy people,” said Nikolai Axmacher, Professor of Neuropsychology at the Ruhr-Universität Bochum, who was also involved in the current study. “However, there were differences in brain activity. The different groups of study participants activated the various subfields of the hippocampus in different ways and to varying degrees. Their brains thus reacted differently to the memory task. In fact, we saw differences in brain activation not only between people with average and increased risk, but also between individuals with average and reduced risk.”

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COVID-19 data shows triple the number of suspected cases and twice the risk for ethnic minorities

There were three times as many suspected COVID-19 cases presented to GPs during the peak of the pandemic than shown in official COVID-19 test results, according to research led by Queen Mary University of London.

The study, published in the British Journal of General Practice, also shows that black, Asian, and minority ethnic (BAME) groups were twice as likely to present with COVID-19, and this is not explained by other factors such as other health conditions, obesity and social deprivation.

Lead author Dr. Sally Hull from Queen Mary University of London said: “Our results suggest that COVID-19 prevalence during the peak of the epidemic was higher than previously thought. The official COVID-19 test statistics are likely to have underrepresented the extent of the epidemic, as many people with COVID-19 would not have been tested, including those with milder symptoms or those who could not access testing centers. Much of the COVID-19 epidemic is being managed in primary care which has had to adjust rapidly to online consultations. We need timely reporting of COVID-19 test results to practices, and diagnostic information from NHS 111, so that practices can provide continuing care to patients with more severe episodes. It’s going to be very important how GPs record and manage cases in their community, as this can provide an early warning system if cases are rising again in an area and if we’re about to see a second wave of infection.”

Attention on COVID-19 initially focused on hospital presentations and intensive care, but little was known about the pattern of early presentations at GP surgeries. Community testing ceased in England on 12 March 2020, hence the extent of asymptomatic and milder symptomatic cases in community settings remains unknown.

The researchers studied anonymised data from the primary care records of approximately 1.2 million adults registered with 157 practices in four east London clinical commissioning groups (Newham, Tower Hamlets, City and Hackney, and Waltham Forest) during the peak of the London epidemic during March and April. Three of the four boroughs had death rates in the top five for London boroughs and 55 percent of the population are from ethnic minorities, hence the area is well placed to examine the over-representation of black and South Asian populations in suspected COVID-19.

The study found that:

  • GPs recorded 8,985 suspected COVID-19 cases between 14 February and 30 April 2020—triple the number who tested positive at government test centers over that period.
  • There was a two-fold increase in the odds of suspected COVID-19 for South Asian and black adults compared with white adults. This risk remains even after accounting for other factors, such as multiple health conditions, obesity and social deprivation, which are also strongly associated with increased risk of a suspected COVID-19 diagnosis.
  • The odds of suspected COVID-19 increased with social deprivation, numbers of long-term conditions and BMI.
  • There was a seven-fold increase in risk of suspected COVID-19 for those with dementia, which may reflect the excess risks to older people living in care homes.
  • In contrast with other studies, the current study did not find an excess of male cases, but found that females had a slight increase in risk of suspected COVID-19, which suggest that the known higher risks for men emerge later in the disease trajectory.
  • There was a sharp seasonal decline in upper and lower respiratory infections during the period that saw a rise in suspected COVID-19 cases, which may have been magnified by social distancing.

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Changes in gut microbiota can greatly impact alcohol-related liver disease and cancer risk

The importance of gut microbiota in alcohol-related liver disease and liver cancer has been demonstrated in two studies presented at the Digital International Liver Congress 2020. The key role of microbial biodiversity in the gut was highlighted in a study of fecal microbial transplantation. The technique shows promise as an intervention to improve some aspects of alcohol-related liver disease. A second study used a mouse model to associate changes in gut microbiota with the action of key signaling molecules, mediating the risk of hepatocarcinogenesis.

In recent years, imbalances in gut microbiota, or dysbiosis, have been implicated as contributing to alcoholic liver disease. In cases of chronic alcohol use, reactive oxygen species produced by alcohol metabolism can lead to chronic intestinal inflammation, which in turn can increase gut permeability and alter microbiota composition. This includes expansion of inflammation-associated bacteria such as Proteobacteria, and reduction of protective species such as Faecalibacterium. Increased gut permeability is believed to lead to translocation of gut bacterial DNA and endotoxins to the liver. The latter, in particular, are thought to induce pro-inflammatory toll-like receptor 4 (TLR4) signaling pathways that are associated with hepatocarcinogenesis.

The importance of gut microbiota raises the possibility manipulating it to improve patient outcomes. The first study tested whether fecal microbial transplant (FMT), the transfer of fecal bacteria from a healthy individual to a patient, could reduce cravings for alcohol as the first step for use in subsequent larger trials. In a double-blind, placebo-controlled, randomized pilot clinical trial, 20 patients with alcohol use disorder (AUD) and liver cirrhosis, all of whom had tried several options to quit alcohol unsuccessfully, were given FMT or placebo, with FMT shown to reduce alcohol cravings as well as total and psychosocial sickness impact profile at day 15 post-treatment. A corresponding significant increase in microbiota diversity was seen in FMT patients compared with baseline (p=0.02), including a higher relative abundance of Odoribacter. Alistipes and Roseburia were also more abundant in patients given FMT compared with placebo at day 15.

“FMT was safe and is shown to have an impact on reducing short-term alcohol cravings and improving psychosocial quality of life in patients with cirrhosis and AUD,” said study presenter Dr. Jasmohan S Bajaj of McGuire VA Medical Center, U.S. “The relative abundance of short-chain-fatty-acid-producing bacteria identified in patients with higher diversity after FMT demonstrates that altering the gut-brain axis is a potential avenue to alleviating AUD in those with cirrhosis.”

A second study explored how gut microbiota may affect the process of developing hepatocellular carcinoma. The study used mice genetically engineered to develop steatohepatitis (NEMO-hepa mice). By crossing these mice with others with inactivated genes involved in the inflammatory response to bacteria, and then altering the gut microbial balance with broad-spectrum antibiotics, the research team showed that knocking out the NLRP6 receptor (a key mediator of colonic homeostasis that can cause intestinal dysbiosis if deficient) leads to more severe steatohepatitis and a higher tumor burden. The degree of intestinal barrier permeability was highly correlated with tumor burden as well as several indicators of inflammation in the liver. Crucially, this immune phenotype could be transferred to other mice by FMT, provided they had functional TLR4 signaling, and could be reversed if the transplanted microbiota were depleted with broad-spectrum antibiotics.

“Strikingly, we also found that replacing depleted Akkermansia muciniphila bacteria in the guts of these mice helped ameliorate their inflammation and steatohepatitis,” said Dr. Kai Markus Schneider of University Hospital RWTH Aachen, Germany. “This knowledge of how short-term changes to microbiota reshape the hepatic tumor microenvironment has the potential to reveal new therapeutic options for cancer prevention and therapy.”

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Depressed or anxious teens risk heart attacks in middle age

Depression or anxiety in adolescence is linked with a 20% greater likelihood of having a heart attack mid-life, according to research released today at ESC Congress 2020.

In a warning to parents, study author Dr. Cecilia Bergh of Örebro University in Sweden, said: “Be vigilant and look for signs of stress, depression or anxiety that is beyond the normal teenage angst: seek help if there seems to be a persistent problem (telephone helplines may be particularly helpful during the COVID-19 pandemic). If a healthy lifestyle is encouraged as early as possible in childhood and adolescence it is more likely to persist into adulthood and improve long-term health.”

There are indications that mental well-being is declining in young people. This study investigated whether conditions like depression in adolescence (age 18 or 19) are associated with a higher risk of cardiovascular disease in adulthood. The researchers also examined the possible role of stress resilience (ability to cope with stress in everyday life) in helping to explain any associations.

The study included 238,013 men born between 1952 and 1956 who underwent extensive examinations in late adolescence (as part of their assessment for compulsory military service) and were then followed into middle age (up to the age of 58 years). The assessments at the age of 18 or 19 years included medical, psychiatric, and physical examinations by physicians and psychologists.

Stress resilience was measured by an interview with a psychologist and a questionnaire, and based on familial, medical, social, behavioural and personality characteristics.

A total of 34,503 men were diagnosed with a non-psychotic mental disorder (such as depression or anxiety) at conscription. Follow-up for cardiovascular disease was through hospital medical records.

The study found that a mental disorder in adolescence was associated with the risk of having a myocardial infarction (heart attack) by middle age. Compared to men without a mental illness in adolescence, the risk of myocardial infarction was 20% higher among men with a diagnosis—even after taking into account other characteristics in adolescence such as blood pressure, body mass index, general health, and parental socioeconomic status.

The association between mental illness and heart attack was partly—but not completely—explained by poorer stress resilience and lower physical fitness in teenagers with a mental illness. “We already knew that men who were physically fit in adolescence seem less likely to maintain fitness in later years if they have low stress resilience,” said Dr. Bergh. “Our previous research has also shown that low stress resilience is also coupled with a greater tendency towards addictive behaviour, signalled by higher risks of smoking, alcohol consumption and other drug use.”

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Adults with Alzheimer’s risk factors show subtle alterations in brain networks despite normal cognition

Researchers at McGill University and the Douglas Mental Health University Institute, in collaboration with the StoP-AD Center, have published a new paper in the Journal of Alzheimer’s Disease, examining how a known genetic risk factor for late-onset Alzheimer’s disease (AD) influences memory and brain function in cognitively intact older adults with a family history of AD.

For their study, the researchers looked at a specific gene, called apolipoprotein E (APOE), which has three allelic variants: e2, e3 and e4. Of these genetic variants, previous studies have shown adults with a single APOE e4 (+APOEe4) gene are at higher risk of developing AD. In this study, Drs. Sheida Rabipour, Maria Natasha Rajah and collaborators used functional magnetic resonance imaging (fMRI) to explore whether having a +APOEe4 genotype altered brain activity during memory task performance in older adults who may be at risk of developing AD.

“It turns out that the +APOEe4 variant, most strongly associated with AD development, doesn’t directly affect memory performance or brain activity in cognitively intact older adults,” explains Dr. Rabipour, a postdoctoral researcher in the lab of Dr. Rajah, and the study’s first author. “Rather, +APOEe4 seems to influence the brain regions and systems that older at-risk adults activate to support successfully remembering past events.”

Specifically, older adults with +APOEe4 use different brain regions, such as the parietal cortex, to support successful memory encoding, compared to adults without this genetic risk factor. In contrast, older adults without the APOEe4 genetic risk for AD use traditional memory-related brain regions, such as the medial temporal lobes and prefrontal cortex, to support successful memory encoding. The findings suggest that the role of +APOEe4, when examined over and above the influence of family history, is subtle, and affects the correlation between brain activity and memory performance.

Drawing on existing cohort for data

To complete their study, the researchers examined the influence of +APOEe4 in 165 healthy older adults from the PREVENT-AD cohort, factoring out age and family history, which are also important risk factors for AD. The team used a powerful multivariate analytical approach, enabling them to objectively disentangle people’s general sense of familiarity from specific recollection of an event and its associated context.

“We used a robust data-driven method that does not focus on any particular brain region, but rather examines the whole brain patterns of activity across the different stages and processes required to complete the memory task we designed,” says Dr. Rabipour.

The team was able to identify a distinct relationship between performance and brain activity patterns for recognition memory, even in cognitively normal older adults, based on +APOEe4 genotype. “In other words, even though all our participants were cognitively normal and performed well on the memory task, we were still able to detect a difference in the brain systems supporting memory function based on having a copy of +APOEe4,” notes Dr. Rabipour.

Moving forward

The findings of the study show that there are differences in the relationships between recognition and associated brain activity patterns based on genetic risk for AD and that these differences are measurable even in cognitively normal older adults, when accounting for family history of AD. Additionally they show that the tasks used to measure memory performance are important to consider when examining the nuances between different types of memory and how they may be affected by AD risk factors. Finally, the results suggest that family history and APOE genotype should be considered separately when examining AD risk.

“Understanding the ways in which different genotypes influence—or don’t influence—behavior and brain activity has important implications on the way we design treatments for AD-related memory impairments as well as our approach to preventing and delaying AD development,” explains Dr. Rabipour. “Using our task, we were also able to support a leading theory that memory systems for general familiarity are distinct from those that underlie detailed recollection of a past event. This could imply different approaches to diagnosing and treating conditions that impact one memory system compared to the other and may also help develop tools or strategies to enhance these types of memory as we age.”

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Vascular development may be at risk in autism

A Canadian collaboration led by Dr. Baptiste Lacoste has undertaken the first ever in-depth study of vasculature in the autistic brain. The product of four years of work, a paper published today in Nature Neuroscience lays out several lines of novel evidence that strongly implicate defects in endothelial cells—the lining of blood vessels—in autism.

Dr. Lacoste, a scientist at The Ottawa Hospital and an assistant professor in the University of Ottawa’s Faculty of Medicine and Brain and Mind Research institute, heads a lab that specializes in neurovascular interactions in health and disease. In collaboration with researchers at McGill University, Laval University, and the National Research Council of Canada, Dr. Lacoste’s team used a mouse model with one of the most common genetic mutations found in autism spectrum disorder—16p11.2 deletion, or “16p” for short.

The team, in which Dr. Lacoste’s graduate student Julie Ouellette and research associate Dr. Xavier Toussay played prominent roles, also used cells derived from the tissue of human autistic adults who carry the 16p mutation.

Nerves and blood vessels not in synch

“If you imagine you have a luxury car—a Ferrari—and it’s beautiful, sitting in your garage. But if you don’t put gas in the tank, the car won’t drive,” says Dr. Lacoste. “It’s exactly the same with the brain. It’s the most complex organ, but if you don’t have blood supply, the brain just doesn’t work properly.”

Normally, when brain cells light up, blood rushes to the active brain region, a phenomenon called ‘neurovascular coupling’. But when neurons of mice with the 16p deletion are stimulated, this study found that vascular responses in those brain regions were delayed and weaker.

This disconnect—or ‘neurovascular uncoupling’—was shown to originate in the blood vessels themselves: Arteries isolated from these mice and kept alive in a medium also showed a weak and sluggish response to chemicals that induce dilation of blood vessels. The team further isolated the source of the deficit in the endothelium, as opposed to the other cell types, such as muscle cells, that surround blood vessels.

Difficulties in development

Dr. Lacoste’s work further shows that problems with blood vessels begin very early in life for those who carry the 16p deletion. In a petri dish, both human-derived and mouse endothelial cells with the mutation were unable to sprout the extensions that normally connect blood vessels to each other, allowing the vascular network to expand and grow. Endothelial cells in the brains of newborn autistic mice had the same problem.

By adolescence, the mice still showed reduced vascular density in their brains. Interestingly, in contrast to the problems in the circulatory system, the researchers found that the neurons in the brains of these young mice appeared to be surprisingly well organized.

As the mice grew, other cells in the brain compensated for their dysfunctional endothelial cells, so that by adulthood they had developed a full network of blood vessels. However, as the researchers’ previous experiments showed, these blood vessels remained dysfunctional in adult mice.

“It’s a bit like if a plumber comes to your house and does a bad job installing the pipes,” says Dr. Lacoste. “You will have trouble getting the right water pressure in your sink from then on.”

Blood vessels and autistic behavior

When a person or mouse carries a 16p mutation, that genetic difference is replicated in every cell in their body. This makes it harder to pin down the cause of systemic developmental differences.

To address this difficulty, Dr. Lacoste’s team generated mice that only expressed the mutation in their endothelial cells—so-called “conditional mutants”. These mice showed similar deficits in their vascular development as whole-body mutants.

Remarkably, although every other cell in their brain and body was genetically normal, these conditional mutants displayed some behavioral signs of autism: hyperactivity, stereotypic movements, and motor learning impairment.

This indicated that the problems in the blood vessels contributed to neuronal dysfunction, which in turn led to the outward signs and symptoms of autism.

Further avenues of inquiry

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Study links increased exercise with lower sleep apnea risk

A study published online as an accepted paper in the Journal of Clinical Sleep Medicine found that increased physical activity is associated with a lower risk of obstructive sleep apnea, a common sleep-related breathing disorder. The study is the largest to date focused on the relationship between sleep apnea and levels of physical activity in the general community.

Researchers reviewed lifestyle, medical, socio-demographic and sleep health data collected from more than 155,000 adults participating in the Ontario Health Study. Based on the physical activity of participants with and without sleep apnea, the investigators determined that a modest increase in physical activity, including walking, is associated with a 10 percent reduction in the risk of developing sleep apnea.

“Our results highlight the importance of physical activity as a preventive measure against developing sleep apnea,” said senior author Lyle Palmer, who is professor of genetic epidemiology at the University of Adelaide in Australia. “One surprising finding was that not only vigorous physical activity but also just walking alone was associated with a decreased risk of sleep apnea.”

The authors found that adding 20 minutes to a daily walk and increasing vigorous daily activity by eight minutes would be enough to achieve a lower sleep apnea risk. The finding is independent of other known risk factors for sleep apnea such as sex, age, ethnicity and obesity.

It is estimated that more than 29 million American adults have sleep apnea, many of them undiagnosed. Untreated sleep apnea is associated with an increased risk of heart disease, stroke, high blood pressure and other potentially serious conditions.

“The rates of sleep apnea in children and adults are continuing to rise. Therefore, understanding the role of modifiable protective factors for sleep apnea is important,” said Palmer. “Exercise is one such protective factor and has many other positive effects on general health. Sleep health care professionals should be trying to get their patients to exercise more.”

The cross-sectional, population-based study analyzed baseline questionnaire data from 155,448 adult residents of Ontario, Canada (60% women and 40% men). Their mean age was 46 years, and about 75% were white. About 6.9% of participants reported being told by a doctor that they have sleep apnea. Those with sleep apnea were more sedentary, sitting for a median of 4.4 more hours per week than those without sleep apnea.

Due to the cross-sectional nature of the study, the authors were unable to make temporal inferences on the observed associations between physical activity and sleep apnea. However, they report that previous studies also have suggested that physical activity can reduce the severity of sleep apnea.

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