Posts tagged ASD
Articles and news from the latest research reports.
New Study Shows Limited Motor Skills In Early Infancy May Be Trait of Autism
Researchers from Kennedy Krieger Institute in Baltimore, Md., announced findings that provide evidence for reduced grasping and fine motor activity among six-month-old infants with an increased familial risk for autism spectrum disorders (ASD). The research, which was published in Child Development, has important implications for our overall understanding of ASDs. Furthermore, the results suggest that subtle lags in object exploration-related motor skills in early infancy may present an ASD endophenotype - a heritable characteristic that may have genetic relation to ASD without predicting a full diagnosis- and further our understanding of the genes involved in the disorder.
“Among the infants with familial history of ASD, many were shown to have reduced fine motor skills regardless of eventual ASD diagnosis,” says Dr. Rebecca Landa, lead author and director of Kennedy Krieger’s Center for Autism and Related Disorders. “This means that reduced fine motor skills could be an ASD endophenotype without predicting full diagnosis. Identifying potential endophenotypes has important implications for future research and may improve our understanding of the neurobiology and genetics of ASDs.”
Researchers conducted two experiments examining the correlation of early motor development and object exploration in children with low risk (LR) or high risk (HR) of developing an ASD. Researchers measured key early learning skills, such as object manipulation and grasping activity, in infants at six months of age and again at 10 months. While all infants scored within the expected range and showed no difference in terms of their object manipulation, there were subtle signs that showed reduced grasping activity in HR infants as compared to their LR age-peers. These findings demonstrate that regardless of developmental outcomes, early motor skill differences in HR infants may represent an endophenotype that can be linked to ASD.
About Experiment 1
In experiment 1, participants included 129 infants, largely consisting of infant siblings of children with confirmed ASD diagnoses. During the testing period, most participants were six months old and were then followed longitudinally to the age of 36 months. Infants completed an assessment using the Mullen Scales of Early Learning (MSEL), which is a standardized assessment tool providing scores in five categories: Gross Motor (GM); Fine Motor (FM); Visual Reception (VR); Receptive Language (RL); and Expressive Language (EL). Based on the results of this assessment, infants were then divided into four groups : low-risk (LR) infants without ASD; high-risk (HR) infants without ASD, language, or social delays; HR infants showing language or social delays but not ASD; and HR infants with autism or ASD diagnosis. All children in the HR ASD group met DSM-IV diagnostic criteria for the disorder.
All four groups in Experiment 1 scored within the typical range on the MSEL subtests, meaning that none exhibited a clinical delay in their overall fine motor development at age six months. Subtle differences between HR and LR infants emerged even in HR infants who did not receive a diagnosis of ASD or other delays by age 36 months, which suggests that lower fine motor scores on the MSEL are characteristic of infants at high familial risk for ASD. In order to examine whether the HR infants would catch up to the LR infants in time, researchers conducted a second experiment with new participants.
About Experiment 2
Experiment 2 focused on a new group of six-month-old infants in both LR and HR categories and examined only their grasping behaviors in a naturalistic, free-play context, which was an important factor that emerged in Experiment 1. Participants included 42 infants who were siblings of children with ASD. The infants were observed in an unstructured play session.
The results of Experiment 2 showed reduced grasping and object exploration activity in six-month-old infants at HR for ASD. Overall, the MSEL FM T-score results observed in Experiment 2 show a similar pattern as in Experiment 1, but statistical results are somewhat weakened by an effect of gender in the LR sample. Unique to Experiment 2, was the sole focus on object manipulation-related items of the MSEL, which offered a consistent measure to identify differences between HR and LR infants. Reduced grasping activity in HR infants at age 6 months was also observed during an unstructured free-play task in Experiment 2, which provides additional evidence for the findings observed in Experiment 1. However, the HR infants caught up to the LR group in grasping, as measured in this study, by 10 months of age.
Future studies are needed to examine these preliminary findings more closely to specifically assess grasping ability in infants that receive an ASD diagnosis later in life.
(Image: Bigstock)
Environmental Influences May Cause Autism in Some Cases
Research by scientists at Albert Einstein College of Medicine of Yeshiva University may help explain how some cases of autism spectrum disorder (ASD) can result from environmental influences rather than gene mutations. The findings, published online today in PLOS Genetics, shed light on why older mothers are at increased risk for having children with ASD and could pave the way for more research into the role of environment on ASD.
The U.S. Centers for Disease Control and Prevention announced in March that one in 68 U.S. children has an ASD—a 30 percent rise from 1 in 88 two years ago. A significant number of people with an ASD have gene mutations that are responsible for their condition. But a number of studies—particularly those involving identical twins, in which one twin has ASD and the other does not—show that not all ASD cases arise from mutations.
In fact, a major study of more than 14,000 children with ASDs published earlier this month in the Journal of the American Medical Association concluded that gene abnormalities could explain only half the risk for developing ASD. The other half of the risk was attributable to “nongenetic influences,” meaning environmental factors that could include the conditions in the womb or a pregnant woman’s stress level or diet.
(Source: einstein.yu.edu)
Mice with ‘mohawks’ help scientists link autism to 2 biological pathways in brain
"Aha" moments are rare in medical research, scientists say. As rare, they add, as finding mice with Mohawk-like hairstyles.
But both events happened in a lab at NYU Langone Medical Center, months after an international team of neuroscientists bred hundreds of mice with a suspect genetic mutation tied to autism spectrum disorders.
Almost all the grown mice, the NYU Langone team observed, had sideways,”overgroomed” hair with a highly stylized center hairline between their ears and hardly a tuft elsewhere. Mice typically groom each other’s hair.
Researchers say they knew instantly they were on to something, as the telltale overgrooming — a repetitive motor behavior — had been linked in other experiments in mice to the brain condition that prevents children from developing normal social, behavioral, cognitive, and motor skills. People with autism, the researchers point out, exhibit noticeably dysfunctional behaviors, such as withdrawal, and stereotypical, repetitive movements, including constant hand-flapping, or rocking.
Now and for what NYU Langone researchers believe to be the first time, an autistic motor behavior has been traced to specific biological pathways that are genetically determined.
The findings, says senior study investigator Gordon Fishell, PhD, the Julius Raynes Professor of Neuroscience and Physiology at NYU Langone, could with additional testing in humans lead to new treatments for some autism, assuming the pathways’ effects as seen in mice are reversible.
In the study, to be published in the journal Nature online May 25, researchers knocked out production in mice of a protein called Cntnap4. This protein had been found in earlier studies in specialized brain cells, known as interneurons, in people with a history of autism.
Researchers found that knocking out Cntnap4 affected two highly specialized chemical messengers in the brain, GABA and dopamine. Both are so-called neurotransmitters, chemical signals released from one nerve cell to the next to stimulate similar sensations throughout the body. GABA, short for gamma-aminobutyric acid, is the main inhibitory neurotransmitter in the brain. It not only helps control brain impulses, but also helps regulate muscle tone. Dopamine is a well-known hormonal stimulant, highly touted for producing soothing, pleasing sensations.
Among the researchers’ key findings was that in Mohawk-coiffed mice, reduced Cntnap4 production led to depressed GABA signaling and overstimulation with dopamine. Researchers say the lost protein had opposite effects on the neurotransmitters because GABA is fast acting and quickly released, so interfering with its action decreases signaling, while dopamine’s signaling is longer-acting, so impairing its action increases its release.
"Our study tells us that to design better tools for treating a disease like autism, you have to get to the underlying genetic roots of its dysfunctional behaviors, whether it is overgrooming in mice or repetitive motor behaviors in humans," says Dr. Fishell. "There have been many candidate genes implicated in contributing to autism, but animal and human studies to identify their action have so far not led to any therapies. Our research suggests that reversing the disease’s effects in signaling pathways like GABA and dopamine are potential treatment options."
The U.S. Centers for Disease Control and Prevention estimate that one in 68 American children under age 8 has some form of autism, with five times as many boys as girls suffering from the spectrum of disorders.
As part of their study, researchers performed dozens of genetic, behavioral, and neural tests with growing mice to isolate and pinpoint where Cntnap4 acted in their brains, and how it affected chemical signaling among specific interneuron brain cells, which help relay and filter chemical signals between neurons in localized areas of the brain.
They found that Cntnap4 in mature interneurons strengthened GABA signaling, but did not do so in younger interneurons. When researchers traced where Cntnap4 acted in immature brain cells, Dr. Fishell says tests showed that it stimulated “a big bolus of dopamine.”
As part of testing to confirm the hereditary link among Cntnap4, the two pathways, and grooming behaviors, researchers exposed young mice with normal levels of Cntnap4, who did not groom each other, to mature mice with and without Cntnap4. Only mature mice deficient in Cntnap4 preened the hairstyle on other mice. Further tests in young mice without Cntnap4 showed that other, mature mice with normal amounts of Cntnap4 largely let them be, without any particular grooming or hairstyle.
Dr. Fishell and his team plan further analyses of how GABA and dopamine production changes as brain cells mature, and precisely what cellular mechanisms are involved in autism. Their goal is to control and rebalance any biological systems that go awry, as a possible future therapy for the disease.
Screening for Autism: There’s an App for That
Most schools across the United States provide simple vision tests to their students—not to prescribe glasses, but to identify potential problems and recommend a trip to the optometrist. Researchers are now on the cusp of providing the same kind of service for autism.
Researchers at Duke University have developed software that tracks and records infants’ activity during videotaped autism screening tests. Their results show that the program is as good at spotting behavioral markers of autism as experts giving the test themselves, and better than non-expert medical clinicians and students in training.
The results appear online in the journal Autism Research and Treatment.
“We’re not trying to replace the experts,” said Jordan Hashemi, a graduate student in computer and electrical engineering at Duke. “We’re trying to transfer the knowledge of the relatively few autism experts available into classrooms and homes across the country. We want to give people tools they don’t currently have, because research has shown that early intervention can greatly impact the severity of the symptoms common in autism spectrum disorders.”
The study focused on three behavioral tests that can help identify autism in very young children.
In one test, an infant’s attention is drawn to a toy being shaken on the left side and then redirected to a toy being shaken on the right side. Clinicians count how long it takes for the child’s attention to shift in response to the changing stimulus. The second test passes a toy across the infant’s field of view and looks for any delay in the child tracking its motion. In the last test, a clinician rolls a ball to a child and looks for eye contact afterward—a sign of the child’s engagement with their play partner.
In all of the tests, the person administering them isn’t just controlling the stimulus, he or she is also counting how long it takes for the child to react—an imprecise science at best. The new program allows testers to forget about taking measurements while also providing more accuracy, recording reaction times down to tenths of a second.
“The great benefit of the video and software is for general practitioners who do not have the trained eye to look for subtle early warning signs of autism,” said Amy Esler, an assistant professor of pediatrics and autism researcher at the University of Minnesota, who participated in some of the trials highlighted in the paper.
“The software has the potential to automatically analyze a child’s eye gaze, walking patterns or motor behaviors for signs that are distinct from typical development,” Esler said. “These signs would signal to doctors that they need to refer a family to a specialist for a more detailed evaluation.”
According to Hashemi and his adviser, Guillermo Sapiro, professor of electrical and computer engineering and biomedical engineering at Duke, because the program is non-invasive, it could be useful immediately in homes and clinics. Neither, however, expects it to become widely used—not because clinicians, teachers and parents aren’t willing, but because the researchers are working on an even more practical solution.
Later this year, the Duke team (which includes students and faculty from engineering and psychiatry) plans to test a new tablet application that could do away with the need for a person to administer any tests at all. The program would watch for physical and facial responses to visual cues played on the screen, analyze the data and automatically report any potential red flags. Any parent, teacher or clinician would simply need to download the app and sit their child down in front of it for a few minutes.
The efforts are part of the Information Initiative at Duke, which connects researchers from disparate fields to experts in computer programming to help analyze large data sets.
“We’re currently working with autism experts at Duke Medicine to determine what sorts of easy tests could be used on just a computer or tablet screen to spot any potential concerns,” said Sapiro. “The goal is to mimic the same sorts of social interactions that the tests with the toys and balls measure, but without the toys and balls. The research has shown that the earlier autism can be spotted, the more beneficial intervention can be. And we want to provide everyone in the world with the ability to spot those signs as early as possible.”
(Source: pratt.duke.edu)
Can Chemicals Produced by Gut Microbiota Affect Children with Autism?
Children with autism spectrum disorders (ASD) have significantly different concentrations of certain bacterial-produced chemicals, called metabolites, in their feces compared to children without ASD. This research, presented at the annual meeting of the American Society for Microbiology, provides further evidence that bacteria in the gut may be linked to autism.
“Most gut bacteria are beneficial, aiding food digestion, producing vitamins, and protecting against harmful bacteria. If left unchecked, however, harmful bacteria can excrete dangerous metabolites or disturb a balance in metabolites that can affect the gut and the rest of the body, including the brain,” says Dae-Wook Kang of the Biodesign Institute of Arizona State University, an author on the study.
Increasing evidence suggests that children with ASD have altered gut bacteria. In order to identify possible microbial metabolites associated with ASD Kang and his colleagues looked for and compared the compounds in fecal samples from children with and without ASD. They found that children with ASD had significantly different concentrations of seven of the 50 compounds they identified.
“Most of the seven metabolites could play a role in the brain, working as neurotransmitters or controlling neurotransmitter biosynthesis,” says Kang. “We suspect that gut microbes may alter levels of neurotransmitter-related metabolites affecting gut-to-brain communication and/or altering brain function.”
Children with ASD had significantly lower levels of the metabolites homovanillate and N,N-dimethylglycine. Homovanillate is the breakdown product of dopamine (a major neurotransmitter), indicating an imbalance in dopamine catabolism (the breaking down in living organisms of more complex substances into simpler ones with the release of energy). N,N-dimethylglycine is a building block for proteins and neurotransmitters, and has been used to reduce symptoms of ASD and epileptic seizures.
The glutamine/glutamate ratio was significantly higher in children with ASD. Glutamine and glutamate are further metabolized to gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter. An imbalance between glutamate and GABA transmission has been associated with ASD-like behaviors such as hyper-excitation.
Using next-generation sequencing technology, the researchers also were able to detect hundreds of unique bacterial species and confirmed that children with ASD harbored distinct and less diverse gut bacterial composition.
“Correlations between gut bacteria and neurotransmitter-related metabolites are stepping stones for a better understanding of the crosstalk between gut bacteria and autism, which may provide potential targets for diagnosis or treatment of neurological symptoms in children with ASD,” says Kang.
(Image: Thinkstock)
Environmental factors as important as genes in understanding autism
Environmental factors are more important than previously thought in understanding the causes of autism, and equally as important as genes, according to the largest study to date to look at how autism runs in families.
The study also shows that children with a brother or sister with autism are 10 times more likely to develop autism; 3 times if they have a half-brother or sister; and 2 if they have a cousin with autism, providing much needed information for parents and clinicians for assessing individual risk.
The study, which looked at over 2 million people, was led by researchers at King’s College London, Karolinska Institutet in Sweden and Mount Sinai in the US, and is published in JAMA today.
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder defined by impairments in social interaction and communication and the presence of restrictive and repetitive behaviours. The exact causes are unknown but evidence has shown it is likely to include a range of genetic and environmental risk factors.
Using Swedish national health registers, the researchers analysed anonymous data from all 2 million children born in Sweden in between 1982 and 2006, 14,516 of which had a diagnosis of ASD. The researchers analysed pairs of family members: identical and non-identical twins, siblings, maternal and paternal half-siblings and cousins.
The study involved two separate measures of autism risk – heritability, which is the proportion of risk in the population that can be attributed to genetic factors; and Relative Recurrent Risk which measures individual risk for people who have a relative with autism.
Most previous studies have suggested that heritability of autism may be as high as 80-90%, but one study has hinted at a lower estimate. The new study is the largest and most comprehensive to date and estimates heritability of autism to be 50%, with the other 50% explained by non-heritable or environmental factors.
Environmental factors are split into ‘shared environments’ which are shared between family members (such as family socio-economic status), and ‘non-shared environments’ which are unique to the individual (such as birth complications or maternal infections or medication during the pre and perinatal period). In this study, factors which are unique to the individual, or ‘non-shared environments’ were the major source of environmental risk.
Professor Avi Reichenberg, author of the study from Mount Sinai Seaver Center for Autism Research, who led the study whilst at King’s College London, says: “Heritability is a population measure, so whilst it does not tell us much about risk at an individual level, it does tell us where to look for causes. We were surprised by our findings as we did not expect the importance of environmental factors in autism to be so strong. Recent research efforts have tended to focus on genes, but it’s now clear that we need much more research to focus on identifying what these environmental factors are. In the same way that there are multiple genetic factors to consider, there will likely be many different environmental factors contributing to the development of autism.”
In the other part of the study, the researchers looked at individual risk. In the general population, autism affects approximately 1 in 100 children. The researchers found that children with a brother or sister with autism were 10.3 times more likely to develop autism; 3.3-2.9 times if they had a half-brother or sister with autism; and 2.0 times if they had a cousin with autism. There were no differences in relative risk between genders. This is the first study to provide such a comprehensive and far reaching analysis of individual risk extended as far as cousins.
Dr Sven Sandin, author of the study from King’s College London and Karolinska, says: “Our study was prompted by a very basic question which parents often ask: ‘if I have a child with autism, what is the risk my next child will too?’ Our study shows that at an individual level, the risk of autism increases according to how close you are genetically to other relatives with autism. We can now provide accurate information about autism risk which can comfort and guide parents and clinicians in their decisions.”
(Source: eurekalert.org)
Scientists Find Connection Between Gene Mutation, Key Symptoms of Autism
Scientists have known that abnormal brain growth is associated with autism spectrum disorder. However, the relationship between the two has not been well understood.
(Image: Thinkstock)
Now, scientists from the Florida campus of The Scripps Research Institute (TSRI) have shown that mutations in a specific gene that is disrupted in some individuals with autism results in too much growth throughout the brain, and yet surprisingly specific problems in social interactions, at least in mouse models that mimic this risk factor in humans.
“What was striking is that these were basically normal animals in terms of behavior, but there were consistent deficits in tests of social interaction and recognition—which approximate a major symptom of autism,” said Damon Page, a TSRI biologist who led the study. “This suggests that when most parts of the brain are overgrown, the brain somehow adapts to it with minimal effects on behavior in general. However, brain circuits relevant to social behavior are more vulnerable or less able to tolerate this overgrowth.”
The study, which focuses on the gene phosphatase and tensin homolog (PTEN), was recently published online ahead of print by the journal Human Molecular Genetics.
Autism spectrum disorder is a neurodevelopmental disorder involving a range of symptoms and disabilities involving social deficits and communication difficulties, repetitive behaviors and interests, and sometimes cognitive delays. The disorder affects in approximately one percent of the population; some 80 percent of those diagnosed are male.
In a previous study, Page and colleagues found that mutations in Pten causes increased brain size and social deficits, with both symptoms being exacerbated by a second “hit” to a gene that regulates levels of the neurotransmitter serotonin in the brain. In the new study, the TSRI team set out to explore whether mutations in Pten result in widespread or localized overgrowth within the brain, and whether changes in brain growth are associated with broad or selective deficits in tests of autism-relevant behaviors in genetically altered mice. The team tested mice for autism spectrum disorder-related behaviors including mood, anxiety, intellectual, and circadian rhythm and/or sleep abnormalities.
The researchers found that Pten mutant mice showed altered social behavior, but few other changes—a more subtle change than would have been predicted given broad expression and critical cellular function of the gene.
Intriguingly, some of the more subtle impairments were sex-specific. In addition to social impairments, males with the mutated gene showed abnormalities related to repetitive behavior and mood/anxiety, while females exhibited additional circadian activity and emotional learning problems.
The results raise the question of how mutations in PTEN, a general regulator of growth, can have relatively selective effects on behavior and cognitive development. One idea is that PTEN mutations may desynchronize the normal pattern of growth in key cell types—the study points to dopamine neurons—that are relevant for social behavior.
“Timing is everything,” Page said. “Connections have to form in the right place at the right time for circuits to develop normally. Circuitry involved in social behavior may turn out to be particularly vulnerable to the effects of poorly coordinated growth.”
(Source: scripps.edu)
Researchers Find Association Between SSRI Use During Pregnancy and Autism and Developmental Delays in Boys
In a study of nearly 1,000 mother-child pairs, researchers from the Bloomberg School of Public health found that prenatal exposure to selective serotonin reuptake inhibitors (SSRIs), a frequently prescribed treatment for depression, anxiety and other disorders, was associated with autism spectrum disorder (ASD) and developmental delays (DD) in boys. The study, published in the online edition of Pediatrics, analyzed data from large samples of ASD and DD cases, and population-based controls, where a uniform protocol was implemented to confirm ASD and DD diagnoses by trained clinicians using validated standardized instruments.
The study included 966 mother-child pairs from the Childhood Autism Risks from Genetics and the Environment (CHARGE) Study, a population-based case-control study based at the University of California at Davis’ MIND Institute. The researchers broke the data into three groups: Those diagnosed with autism spectrum disorder (ASD), those with developmental delays (DD) and those with typical development (TD). The children ranged in ages two to five. A majority of the children were boys – 82.5% in the ASD group were boys, 65.6% in the DD group were boys and 85.6% in the TD were boys. While the study included girls, the substantially stronger effect in boys alone suggests possible gender difference in the effect of prenatal SSRI exposure.
“We found prenatal SSRI exposure was nearly 3 times as likely in boys with ASD relative to typical development, with the greatest risk when exposure took place during the first trimester,” said Li-Ching Lee, Ph.D., Sc.M., psychiatric epidemiologist in the Bloomberg School’s Department of Epidemiology. “SSRI was also elevated among boys with DD, with the strongest exposure effect in the third trimester.”
The data analysis was completed by Rebecca Harrington, Ph.D., M.P.H, in conjunction with her doctoral dissertation at the Bloomberg School. Dr. Lee was one of her advisors.
Serotonin is critical to early brain development; exposure during pregnancy to anything that influences serotonin levels can have potential effect on birth and developmental outcomes. The prevalence of ADS continues to rise. According to the Centers for Disease Control and Prevention, an estimated 1 in 68 children in the U.S. is identified with ADS, and it is almost five times more common among boys than girls. One may question whether the increased use of SSRI in recent years is a contributor to the dramatic rise of ASD prevalence.
"This study provides further evidence that in some children, prenatal exposure to SSRIs may influence their risk for developing an autism spectrum disorder,” said Irva Hertz-Picciotto, Ph.D., M.P.H., chief of the Division of Environmental and Occupational Health in the UC Davis Department of Public Health Sciences and a researcher at the UC Davis MIND Institute. “This research also highlights the challenge for women and their physicians to balance the risks versus the benefits of taking these medications, given that a mother’s underlying mental-health conditions also may pose a risk, both to herself and her child.”
Regarding treatment, the authors note that maternal depression itself carries risks for the fetus, and the benefits of using SSRI during pregnancy should be considered carefully against the potential harm. The researchers also note that large sample studies are needed to investigate the effects in girls with ASD. Limitations of the study acknowledged include the difficulty in isolating SSRI effects from those of their indications for use, lack of information on SSRI dosage precluded dose-response analyses, and the relatively small sample of DD children resulted in imprecise estimates of association, which should be viewed with caution.
(Source: jhsph.edu)
Key Brain ‘Networks’ May Differ in Autism
Differences in brain connectivity may help explain the social impairments common in those who have autism spectrum disorders, new research suggests.
The small study compared the brains of 25 teens with an autism spectrum disorder to those of 25 typically developing teens, all aged 11 to 18. The researchers found key differences between the two groups in brain “networks” that help people to figure out what others are thinking, and to understand others’ actions and emotions.
"It is generally agreed that the way the networks are organized is not typical [in those with autism]," explained study lead researcher Inna Fishman, assistant research professor of psychology at San Diego State University.
The prevailing idea until now, she said, has been that these neurological networks are under-connected in people with autism. However, “we found they were over-connected — they talk to each other way more than expected at that age.”
The study is published in the April 16 online edition of JAMA Psychiatry.
Autism rates have skyrocketed in recent years, according to recent data from the Centers for Disease Control. Much of that has to do with our growing awareness of the disorder. But despite what we are learning about the possible origins and causes of autism, which has no cure, it continues to frustrate and perplex.
In honor of Autism Awareness Month, we’ve compiled a list of longform journalism pieces that give glimpses into the world of those diagnosed with the disorder, and the struggle of those who love and care for them. In one, a father figures out the secret to connecting with his autistic son. In another, we meet the first person ever diagnosed with the disorder. Bookmark these four deep dives into the world of autism, and take your time to read them throughout the month.
“Reaching My Autistic Son Through Disney,” The New York Times Magazine
“Catch Me If You Can,” Outside
“Navigating Love and Autism,” The New York Times
“Autism’s First Child,” The Atlantic