Can genetics predict bothersome hot flashes?

Can genetics predict bothersome hot flashes?

New study suggests that some of the same genetic variants that help to predict reproductive aging are associated with frequency and severity of hot flashes

CLEVELAND, Ohio (April 28, 2021)–Hot flashes are a hallmark of the menopause transition. Yet, they don’t strike with the same frequency or severity for all women. A new study suggests that some of the same genetic factors that affect a woman’s reproductive life cycle may also help predict her likelihood of having bothersome hot flashes. Study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).

Despite multiple studies on the subject, questions still remain as to why some women are more affected than others by hot flashes and night sweats during the menopause transition. Genetics may be one reason, because black women have more problems with hot flashes than white women do, and Chinese and Japanese women seem to suffer the least with symptoms. Prior studies have also attempted to address why some women experience hot flashes much earlier in the menopause transition than other women who have more frequent hot flashes postmenopause. Still there are others who consistently experience hot flashes for more than a decade.

In this study involving more than 1,200 women of various ethnicities, researchers concluded that some of the same genetic factors that predict reproductive aging may also be associated with hot flashes, thus suggesting that genetics may play a role in predicting the severity and frequency of a woman’s hot flashes.

Factors shown to affect reproductive aging and likely to influence a woman’s experience with hot flashes include the age at menarche and the age at menopause. Some studies have also previously suggested an association between body mass index and the frequency and severity of hot flashes, although this relationship is described as complex and dependent on the stage of reproductive aging. Lower estrogen levels have also been associated with more prevalent and frequent hot flashes. Although a number of these studies provided evidence of some overlap in genes associated with age at menarche and age at natural menopause, no prior studies focused on how these factors affected hot flashes.

Researchers believe that understanding the effect of genetic variants is critical to identifying future treatments for managing bothersome hot flashes. They created a video highlighting their results that can be found at https://links.lww.com/MENO/A761.

Results are published in the article “Genetic variants predictive of reproductive aging are associated with vasomotor symptoms in a multiracial/ethnic cohort.”

“This study found that genetic factors associated with aging of the reproductive system may be linked to vasomotor symptoms during the menopause transition and differ across racial/ethnic groups. These findings move us one step closer to being able to predict a woman’s experience with menopause symptoms and, subsequently, to provide management recommendations based, in part, on her genetics. In addition, researchers may be able to use these specific genetic variations as targets for the development of new drugs to alleviate vasomotor symptoms,” says Dr. Stephanie Faubion, NAMS medical director.

Source:  EurekAlert

Lupus treatments

Lupus treatments can be tailored to patient’s individual cells, study shows

Lupus treatments can be tailored to patient's individual cells, study shows

The kidneys of patients living with systemic lupus erythematosus (SLE) are often under assault, and not all those living with the disease will respond to standard treatment. A new report published in the journal Nature Immunology online May 20 shows how tissue samples from these patients can accurately predict those more likely than not to respond to therapy. SLE is a disease marked by the attack on joints, skin, and kidneys by the body’s immune system.

“Our latest research redefines how a kidney biopsy can be used to tailor drug therapy in lupus patients,” says study co-senior investigator Jill Buyon, MD, the Sir Deryck and Lady Va Maughan Professor of Rheumatology at NYU School of Medicine. “Moreover, our results point to simple skin biopsy as a potential tool to track the progression of kidney damage from the disease and to tell whether treatments are working as intended or need to be changed.”

Researchers say treating lupus, which afflicts an estimated 1 million Americans, predominantly women, is difficult because its onset, symptoms, and progression vary significantly from patient to patient over time. The disorder’s origins remain unknown, although many suspect that genetic factors passed down from parents to their children as well as environmental triggers, such as sun exposure and infection, are likely responsible.

Multiple organs, including the brain and linings of the heart and lungs can be involved, the researchers add, making it harder to detect where the disease started or to predict which tissues will be affected. Existing therapies focus on immune-suppressing drugs designed to check any attack. However, these treatments are not cures and only relieve SLE signs and symptoms, such as joint pain, difficulty breathing, and low blood cell counts in some patients.

For the new study, researchers analyzed the cellular profile and genetic activity of kidney and skin tissue samples from 21 SLE patients in the New York area. Most were women between the ages of 16 and 53, and of all races. Study participants were at the time of biopsy also among the half of all SLE patients who experience lupus nephritis, a form of kidney inflammation that can cause lasting damage to the organ.

Researchers used a gene-mapping tool called scRNA-Seq that allowed them to track the action of more than 4,000 specific cells. The cell-specific biopsy profiles from patients having lupus-related kidney “flares” were then compared with biopsy results from three women who did not have lupus or any other known disease.

Specifically, the study showed similar immune system signaling and scar-forming gene activity in kidney tubular cells affected by lupus and skin keratinocyte cells from the same patients.

Gene activity from exposure to an immune cell signaling protein, type 1 interferon (IFN), in both cell types from SLE patients increased 3.8 times and 2.5 times, respectively, when compared with biopsies from healthy women. Moreover, the increase in scar-forming gene activity in the kidney cells of SLE patients was observed in those who did not respond to therapy.

Researchers say finding similarities between cell activation in the kidney and skin is important because the skin can be more easily and repeatedly biopsied than the kidney. And since cellular changes observed in the skin closely mirrored changes involved in SLE kidney damage, sampling skin could, they say, offer clues as to what, if any, malfunction is about to occur in the kidney.

Buyon says IFN typically shows up in cells as part of the immune system response to infection and for decades has been linked to lupus. The latest study reinforces its role, as yet unexplained, in the disease.

While researchers have plans to determine the source of the IFN affecting both types of cells, they say their immediate next step is to analyze results from 160 additional patients’ kidney biopsies and as many as 400,000 different cells. They also plan to test additional skin cells, with assistance from the NYU Colton Center for Autoimmunity, for differences between lupus patients with and without nephritis.

“If confirmed in further experiments, our findings could personalize lupus therapy based on what an individual patient’s cells are telling us about immune activity,” says Buyon, director of rheumatology in the Department of Medicine at NYU Langone Health, where she also serves as director of its Lupus Center. “Moreover, this research should help shed light on the underlying biological pathways behind organ injury in lupus, the interrelated roles of kidney and skin cells, and how type 1 interferon propels this disease.”

Source: EurekaAlert

factors may trigger lupus

Environmental factors may trigger lupus onset and progression

Environmental factors may trigger lupus onset and progression

While genetics play a role in the development of Lupus, a systemic autoimmune disease that can attack any organ system in the human body, so do environmental triggers, such as particulates in air pollution and ultraviolet light, explains Gaurav Gulati, MD, a physician-researcher at the University of Cincinnati (UC) College of Medicine.

“The tough part about Lupus is that treatment options remain limited and the understanding of the disease in terms of its onset and progression is also limited,” says Gulati, an assistant professor in the UC Division of Immunology, Allergy and Rheumatology and a UC Health physician. “The disease has a wide spectrum in terms of age distribution so it can also affect children or young adults who can have more severe manifestation and long-term damage from disease as it progresses over time.”

Lupus affects 1.5 million people in the United States and occurs in both men and women, though 90 percent of those diagnosed are women, with African-Americans disproportionately impacted by the disease, according to the Lupus Foundation of America. It can cause inflammation, swelling and damage to joints, skin, kidneys, blood, the heart and lungs and in severe cases Lupus can be fatal.

Gulati recently conducted a literary review of more than 100 research articles on Lupus and concludes that while there is a genetic predisposition for the disease, it is not the sole cause. His findings are available online in the scholarly journal Seminars in Arthritis and Rheumatism.

Researchers studying Lupus have identified a triad relationship of one’s genome or genetic background; epigenome or how genetic material is modified over a lifetime; and exposome, which refers to the environmental factors individuals are exposed to over time, says Gulati.

Gulati says a study looking at Lupus occurrence in identical twins found that clinical manifestation of the disease occurred in both siblings only 24 percent of cases. It’s more likely that genetic risk factors along with environmental influence play a pivotal role in Lupus development. Ultraviolet radiation from sunlight exerts toxic effects on the skin triggering flare-ups in Lupus symptoms, while particulate air pollution, especially from diesel vehicular exhaust, can also potentially worsen the condition.

“This is of particular interest in Cincinnati,” says Gulati. “We live in a city that is surrounded by many major roads and highways. There are several in our city and there is a huge amount of truck traffic which slows down allowing exposure to particulate air pollution even more.”

Gulati says trace elements–especially heavy metals–prevalent in the environment that can be triggers for Lupus. He says research in animal models indicates that many, including uranium, lead and cadmium, are capable of inducing autoimmunity.

It has been demonstrated that elements like mercury, nickel and gold have potentiate delayed hypersensitivity reactions in patients with connective tissue disease, notes Gulati in his manuscript. The resultant enhanced inflammation has been considered a pathogenic factor in exacerbations of autoimmune and inflammatory diseases including Lupus, which occurs in significantly higher rates among dental workers and others exposed to mercury.

Reproductive-age women are disproportionately impacted by Lupus, says Gulati, who cited a study in the United Kingdom that found an increased risk of Lupus in women using oral contraceptives. The hormonal influence in Lupus is also seen in exposure to xenoestrogens, natural or chemical components that imitate estrogen. Bisphenol A, (BPA) an environmental pollutant, is among the class of xenoestrogens that could be triggers for Lupus, says Gulati. It is used to make polycarbonate plastic and epoxy resins and is a common contaminant of many packaged foods and beverages.

Gulati offers some suggestions for Lupus patients to lessen some of the environmental factors that can trigger Lupus symptoms.

  • Regular follow-up with your rheumatologist for diagnosis and management of Lupus is vital to make early diagnosis and avoid long-term damage.
  • Avoid direct sunlight when possible. UV radiation can cause cells in the skin to die and cause Lupus flare-ups.
  • Always use sunscreen whenever there is a risk of being exposed to ultraviolet radiation. Using sunscreen even on cloudy days will lessen your risk of exposure.
  • Stop smoking. Cigarette smoking contains multiple triggers, including cadmium and polycyclic hydrocarbons, and can worsen Lupus symptoms.

Source: EurekAlert

Mental Health

May is Mental Health Awareness Day

May is Mental Health Awareness Day

 

In the United States, millions of Americans struggle with some kinds of mental health illness. 1 in 5 Americans experience some kind of mental illness and face several challenges over the course of their lifetime.
Around 70-90% of patients that seek proper treatment for mental illness see a reduction in their symptoms. This May join us in the movement to raise mental health awareness and #BeKindToYourMind.

 

*Depression is one of the leading causes of mental illness

* 18% of US adults live with a mental illness

* Anxiety is one of the most common illnesses in America

* 2.6% of Americans live with bipolar disorder

 

Source: MHA America, NAMI

COVID viruses are losing parts of their genome

Why it matters that COVID viruses are losing parts of their genome

Why it matters that COVID viruses are losing parts of their genome

Again and again, the new coronavirus has sloughed off small chunks of its genome, leading to changes in a viral protein that is frequently targeted by antibodies.

When evolution snips out a stretch of an organism’s genome, the change is called a deletion. Kevin McCarthy and Paul Duprex at the University of Pittsburgh School of Medicine in Pennsylvania and their colleagues searched a database of SARS-CoV-2 genome sequences and identified more than 1,000 viruses with deletions in the genomic region that encodes a protein called spike (K. R. McCarthy et alScience https://doi.org/10.1126/science.abf6950; 2021). The virus uses the spike protein to invade cells.

Further analysis showed that the deletions tended to crop up at a few distinct sites in the genomic region coding for spike. Some of the deletions have arisen independently multiple times, and some show evidence of spread from one person to another.

A powerful antibody against SARS-CoV-2 could not latch onto spike proteins harboring some of the deletions that the team identified. But antibody mixtures collected from people who had recovered from COVID-19 could disable viral variants that had deletions.

Source: Nature.com

Pediatric Minority Patients

Pediatric Minority Patients Less Likely to Undergo ED Imaging

Pediatric Minority Patients Less Likely to Undergo ED Imaging

Significant racial and ethnic differences in diagnostic imaging rates exist among children receiving care in pediatric EDs across the United States, Jennifer R. Marin, MD, of the University of Pittsburgh Medical Center Children’s Hospital of Pittsburgh, and associates reported.

Specifically, visits with non-Hispanic Black and Hispanic patients less frequently included radiography, CT, ultrasonography, and MRI than those of non-Hispanic White patients. The findings persisted across most diagnostic groups, even when stratified according to insurance type, Marin and colleagues reported in a multicenter cross-sectional study in JAMA Network Open.

The authors collected administrative data from the Pediatric Health Information System on 44 tertiary care children’s hospitals in 17 major metropolitan areas across the United States. They evaluated a total of 13,087,522 ED visits by 6,230,911 patients that occurred between Jan. 1, 2016, and Dec. 31, 2019. Of these, 28.2% included at least one imaging study. Altogether, 33.5% were performed on non-Hispanic White children, compared with just 24.1% of non-Hispanic Black children (adjusted odds ratio, 0.82) and 26.1% of Hispanic children (aOR, 0.87). After adjusting for relevant confounding factors, non-Hispanic Black and Hispanic children were less likely to have any imaging at all during their visits.

“Our findings suggest that a child’s race and ethnicity may be independently associated with the decision to perform imaging during ED visits,” Marin and associates said, adding that “the differential use of diagnostic imaging by race/ethnicity may reflect underuse of imaging in non-Hispanic Black and Hispanic children, or alternatively, overuse in non-Hispanic White children.”

Overuse vs Underuse: Racial Bias or Parental Anxiety?

Overuse of imaging carries its own risks, but underuse can lead to misdiagnosis, the need for additional care, and possibly worse outcomes in the long run, Marin and colleagues explained. “Although we were unable to discern underuse from overuse using an administrative database, it is likely that much of the imaging in White children is unnecessary.”

Higher parental anxiety was just one of the explanations the authors offered for excessive imaging in White children. Especially in cases of diagnostic imaging for head trauma, one survey of adult ED patients showed that the peace of mind CT offers with its more definitive diagnosis was worth the additional possible risk of radiation.

Language barriers in non–English-speaking patients may also affect likelihood of testing as part of an ED visit.

Implicit physician racial bias, which can be amplified under the stress of working in an ED, can affect patient interactions, treatment decisions and adherence, and ultimately overall health outcomes, the authors noted. The goal in ensuring parity is to routinely follow clinical guidelines and use objective scoring tools that minimize subjectivity. At the institutional level, internal quality assurance evaluations go a long way toward understanding and limiting bias.

Historically, White patients are more likely than minority patients to have a medical home, which can influence whether ED physicians order imaging studies and whether imaging of White patients may have been triggered by a primary care physician referral, Marin and associates said.

Source: Medscape.com

influenza vaccine

Intranasal influenza vaccine spurs strong immune response in Phase 1 study

Intranasal influenza vaccine spurs strong immune response in Phase 1 study

What

An experimental single-dose, intranasal influenza vaccine was safe and produced a durable immune response when tested in a Phase 1 study published in the Journal of Clinical Investigation. The investigational vaccine, called Ad4-H5-VTN, is a recombinant, replicating adenovirus vaccine designed to spur antibodies to hemagglutinin, a protein found on the surface of influenza viruses that attaches to human cells.

The investigational vaccine was developed by Emergent Biosolutions Inc., (Gaithersburg, Maryland). It was administered intranasally (28 study participants), as an oral capsule (10 participants) and via a tonsillar swab (25 participants) to healthy men and non-pregnant women ages 18 to 49 years.

The participants who received the vaccine intranasally or via tonsillar swab showed significantly higher H5-specific neutralizing antibody levels compared to the group receiving the vaccine capsule orally. The participants who received the intranasal vaccine shed viral DNA for two-to-four weeks, but virus could be cultured for a median of only one day. Participants had evidence of H5-specific CD4+ and CD8+ T-cell responses. Additionally, volunteers who received the intranasal vaccine had high levels of serum neutralizing antibodies at 26 weeks after vaccination, and this level was unchanged at three to five years after a single intranasal dose of the vaccine. The duration of viral shedding correlated with a high magnitude of neutralizing antibody response at week 26. In addition, the intranasal vaccine induced a mucosal antibody response in the nose, mouth, and rectum.

The study authors speculate that replication-competent vector vaccines may have advantages over other types of vaccines because they can express viral proteins at higher levels and for longer durations. Additionally, this type of vaccine induces a mucosal immune response that is critical for limiting transmission of viruses that infect mucosal tissues.

The vaccine platform could be highly adaptable for use against other viruses including HIV and SARS-CoV-2, according to the authors.

Article

K Matsuda et al. A Replication Competent Adenovirus-Vectored Influenza Vaccine Induces Durable Systemic and Mucosal Immunity. Journal of Clinical Investigation DOI: doi.org/10.1172/JCI140794.

Who

Mark Connors, M.D., chief of the HIV-specific Immunity Section in NIAID’s Laboratory of Immunoregulation and principal investigator for the Phase 1 study, is available for interviews. 

NIAID conducts and supports research — at NIH, throughout the United States, and worldwide — to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

Source: NIH.gov

Sleep Problems in Autism

Study Links Gene to Sleep Problems in Autism

Study Links Gene to Sleep Problems in Autism

Up to 80 percent of children with autism spectrum disorder (ASD) experience sleep problems. The source of these problems has been as much of a mystery as the exact causes of ASD, which scientists are still working to unravel. A new study led by a team of neuroscientists at Washington State University has brought scientists closer to identifying the causes of disturbed sleep in autism, which could open the door to future treatment that would bring relief to children with autism and their caregivers.

“Poor sleep is not only a problem for individuals with autism but is also one of the top concerns among caregivers,” said Lucia Peixoto, an assistant professor in the WSU Elson S. Floyd College of Medicine and the principal investigator and senior author on the study. “In addition, there is a clear link between sleep problems and severity of core autism symptoms such as social and communication challenges and repetitive behaviors. If we can get to the root of these sleep issues, this could potentially help ease other autism symptoms as well.”

Published in the open access journal eLife, the team’s findings suggest that sleep problems in patients with autism spectrum disorder may be linked to a mutation in the gene SHANK3 that in turn regulates the genes of the body’s 24-hour day and night cycle. Their study showed that people who were missing the SHANK3 gene and mice that lacked part of the gene had difficulty falling asleep. Their study in mice also strongly supported one possible explanation as to why individuals with autism have trouble falling asleep: It’s not that they are not sleepy. They are sleepy, but they simply cannot fall asleep.

Peixoto and her colleagues took a multistep approach to their study. First, they analyzed sleep data from patients with Phelan-McDermid syndrome (PMS), a genetic disorder that often goes hand in hand with autism and is thought to be related to the SHANK3 gene. They found that PMS patients who are missing the SHANK3 gene have trouble falling asleep and wake up multiple times during the night, starting at age five.

“Many kids with Phelan-McDermid syndrome sleep less than six hours a night, and their sleep is really poor across their lifespan so it’s an ongoing source of difficulty for them,” said postdoctoral research associate and co-first author Hannah Schoch.

Schoch along with co-first author and postdoctoral research associate Ashley Ingiosi did much of the hands-on work for the study. For the next step, Ingiosi studied sleep in a mouse model of PMS, which used mice that are missing a part of the Shank3 gene and wild-type control mice.

When kept on a light-dark cycle of 12 hours each and allowed to sleep normally, mice with the Shank3 mutation spent more time awake at the end of the dark period, when nocturnal mice would normally take a nap. The data also suggested that the quality of their deep sleep was reduced.

In a subsequent sleep deprivation experiment, all mice were kept awake for the first five hours of their main sleep phase.

“What we found is that the Shank3 mutant mice were able to build up a need for sleep to the same extent as wild-type mice, which tells us that they were sleepy,” Ingiosi said. “But it actually took them twice as long to fall asleep.”

A gene expression analysis of these mice showed decreased activity in a group of genes related to the body’s circadian clock, which helps to maintain a 24-hour day/night rhythm. Sleep deprivation made this worse–the team found that the number of genes that didn’t turn on correctly was twice as high in sleep deprived mutant mice. This suggests that sleep deprivation exaggerates the genetic differences between Shank3 mutants and wild-type mice, Peixoto said, which may translate to a worsening of symptoms in people who have conditions associated with SHANK3 mutations, such as PMS and autism.

The final experiment looked at how changes in circadian clock genes affected daily activity patterns in Shank3 mutant mice. They showed that the decrease in circadian clock gene activity did not change the timing of daily rest-activity rhythms in the mice, but–surprisingly–did make them less active.

Follow-up studies to be conducted by the research team will delve deeper into two questions: whether the sleep issues in mice with Shank3 mutations are present at birth or develop over time and what the mechanism is by which SHANK3 mutations cause sleep issues.

“If we are able to understand the molecular mechanisms underlying the sleep problem in Shank3 mutant mice, we expect that this will also strongly relate to sleep problems in autism in general,” Peixoto said. “And that would suggest novel points of intervention.”

 

Source: Drug, Discovery & Development

autism diagnoses

A new biomarker panel could accelerate autism diagnoses

New biomarker panel could accelerate autism diagnoses

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut elit tellus, luctus nec ullamcorper mattis, pulvinar dapibus leo.Investigators at the UC Davis MIND Institute and NeuroPointDX, a division of Stemina Biomarker Discovery, have identified a group of blood metabolites that could help detect some children with autism spectrum disorder (ASD). Part of the Children’s Autism Metabolome Project (CAMP), the largest metabolomic ASD study ever attempted, these findings are a key step toward developing an ASD biomarker test. The research was published September 6 in the journal Biological Psychiatry.

“With this panel of alterations in amino acid metabolism, we can detect about 17 percent of kids with ASD,” said David G. Amaral, founding director of research at the MIND Institute and senior author on the paper. “This is the first of hopefully many panels that will identify other subsets of kids with autism.”

No biomarker tests for ASD currently exist. Children are diagnosed based on their altered behaviors, which may not become evident until children are 2-4 years old. Families often must wait over a year or more for an appointment with a specialist, delaying diagnosis even further.

CAMP researchers believe the answer lies in the metabolome – the molecules that remain after larger molecules have been broken down (metabolized). Metabolomics has the advantage of monitoring both genetic and environmental contributions to the development of autism.

“By the time you’re getting to metabolomics, you’re looking at how the body is working, not just the genes it has,” said Amaral, a professor of Psychiatry and Behavioral Sciences.

The team hopes to use these and other CAMP findings to accelerate diagnosis and move kids into intensive behavioral therapy at an earlier age, which has proven quite effective. The multisite study has collected blood samples from 1,100 children – about two-thirds having been diagnosed with ASD – between 18 months and 4 years old. This is the first publication from the CAMP effort.

“One of the major goals of the MIND Institute is the development of early biological markers for detecting the risk of autism spectrum disorder,” Amaral said. “It would have been difficult for the MIND Institute to carry out the CAMP study on its own.”

Amaral added that CAMP is an excellent example of an academic/corporate partnership that has the promise of benefitting the autism community.

“It is unlikely that a single marker will detect all autism,” he said. “This paper demonstrates that alterations in metabolic profiles can detect sizable subsets of individuals with autism. The hope is that we will be able to generate a panel of biomarkers that will detect a large proportion of people at risk. Moreover, this approach highlights metabolic pathways that may be targets of intervention.”

In their work the research team compared blood metabolites – specifically, amino acids – in 516 kids with ASD and 164 children showing typical development. They found that 17 percent of the ASD children had unique concentrations of specific amino acids (metabotypes) in their blood. Though a 17 percent subgroup may seem small, it is actually quite significant. ASD encompasses a complex array of symptoms, and no one expected to find a single group of markers that would diagnose all subsets. Rather, the researchers hope to create a number of metabolomic assays that cover all variations.

“The long-term vision is, once we’ve been able to analyze all the data from CAMP, we would have a series of panels,” said Amaral. “Each of these would be able to detect a subset of kids with autism. Ultimately, metabolomics may be able to identify most children with autism.”

In addition to enabling earlier diagnosis, this work also could help generate targeted interventions for specific ASD groups. Amaral points to phenylketonuria (PKU) as a possible template. PKU is a rare disease in which the amino acid phenylalanine builds up, causing brain damage. However, relatively small dietary adjustments can make a big difference.

“With just a simple dietary modification, a child can move from being profoundly disabled to one who lives a reasonably normal life,” said Amaral. “That’s the hope with autism as well.”

The CAMP researchers will continue to validate these results while simultaneously investigating other metabotypes.

“I’m optimistic this is not a one-off,” said Amaral. “There are going to be other panels that can detect other groups of kids with ASD.”

###

Other researchers included Alan M. Smith, Joseph J. King, Paul R. West, Michael A. Ludwig, Elizabeth L. R. Donley and Robert E. Burrier at Stemina.

This work was supported by the National Institutes of Health (NIH 5 R44 MH107124-03 and 1R01MH103371), the Nancy Lurie Marks Family Foundation and The Robert E. and Donna Landreth Family Fund.

David G. Amaral receives research funding from Stemina and is on the Scientific Advisory Boards of Stemina Biomarker Discovery, Inc. and Axial Therapeutics

Source: EurekAlert.com 

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World Autism Awareness Day

World Autism Awareness Day

Autism spectrum disorder (ASD) is a developmental condition that can affect social, communication, and behavioral challenges. Autism affects the nervous system and affects how someone interacts, communicates or behaves. Early detection and educational therapies may reduce symptoms and support development. People with ASD might have trouble communicating and repeat certain behaviors. Most signs of Autism begin at an early age and may last a lifetime. Join us on Friday, April 2nd for World Autism Awareness Day.

  • ASD affects 1 in 68 children
  • Boys are nearly 5 times more likely than girls to be diagnosed with ASD
  • Autism generally appears before the age of 3
  • There is no current cure for Autism
  • ASD is not degenerative and diagnosed individuals can continuously improve
  • Up to 1/3 of people with ASD also develop seizures disorders
  • Hyperlexia commonly accompanies ASD

#AutismAwarenessDay

Source: CDC, Autism Speaks, Mayo Clinic