Conner James Black, associate director of the Autism Center at the Child Mind Institute, encourages families to have two separate devices: one for communication and another for entertainment, rather than using one for both.
BackgroundThe Autism Diagnostic Observation Schedule, Second Edition (ADOS-2), is widely used in the diagnostic evaluation of autism spectrum disorder (ASD); however, its diagnostic performance in real-world clinical referral populations remains heterogeneous, particularly across modules and clinical contexts. This systematic review and meta-analysis evaluated the module-specific diagnostic accuracy of ADOS-2 using hierarchical meta-analytic modeling and examined sources of heterogeneity in updated evidence clinical studies.MethodsA systematic search of PubMed/MEDLINE, Scopus, and Web of Science was conducted from January 2021 to February 2026, with additional screening of reference lists. Studies were included if they evaluated ADOS-2 diagnostic accuracy in real-world clinical referral populations, used DSM- or ICD-based clinical best-estimate diagnosis as the reference standard, and reported extractable 2×2 data. Diagnostic accuracy was pooled using a hierarchical summary receiver operating characteristic (HSROC) model with a bivariate random-effects approach. Module-specific analyses (Toddler Module, Modules 1–2, Module 3, Module 4) and meta-regression were performed to examine heterogeneity.ResultsTen studies were included in the qualitative synthesis, and six provided extractable 2×2 data for quantitative pooling. Overall pooled sensitivity was 0.88 (95% CI: 0.83–0.92) and pooled specificity was 0.74 (95% CI: 0.68–0.80), with an HSROC AUC of 0.86. The Toddler Module showed the highest diagnostic performance (sensitivity 0.92; specificity 0.88; AUC 0.94), whereas specificity decreased in Modules 3 and 4. Meta-regression identified module level, psychiatric referral setting, and adult samples as significant contributors to reduced specificity. No significant publication bias was detected.ConclusionsADOS-2 demonstrates high overall sensitivity but variable specificity across modules in real-world clinical referral populations. Reduced specificity was more commonly observed in higher ADOS-2 modules, which are typically administered to verbally fluent adolescents and adults with greater psychiatric complexity.
This is today’s edition of The Download, our weekday newsletter that provides a daily dose of what’s going on in the world of technology.
Europe’s extreme heat is shutting down power plants
Europe is in the middle of a record-breaking heat wave, and the grid is being pushed to its limits as people turn to fans and air-conditioning to try to stay cool. But some power plants won’t be online to help handle the load.
The main source of stress is increased demand, largely driven by cooling. And the challenges are only expected to worsen as climate change brings more frequent and intense heat waves.
Grid planning in the age of climate change generally means that we need a lot more supply, and quickly. But one interesting facet to this challenge is that in some places, seasonal patterns are shifting, compounding the difficulty of meeting demand.
Europe has historically seen its grid peak in the winter when electric heating is widespread. So some planned outages happen in the spring and into the summer, which is affecting the supply right now. But a growing need for air-conditioning will alter the balance.
This story is from The Spark, our weekly newsletter giving you the inside track on all things climate. Sign up to receive it in your inbox every Wednesday.
IBM unveils chip technology that could help extend Moore’s Law another decade
IBM has built a new prototype chip with around 100 billion transistors on an area the size of a fingernail. That’s twice the density of the company’s previous state-of-the-art technology announced in 2021. And the design could pave the way for faster and more energy-efficient computers for years to come.
In the last fifteen years, transistors have been shrunk close to their limits. They can’t get smaller without their function deteriorating. IBM’s new chip resolves this with an approach familiar to urban planners: building up.
I’ve combed the internet to find you today’s most fun/important/scary/fascinating stories about technology.
1 Anthropic says Alibaba “illicitly” extracted Claude’s capabilities It claims the Chinese firm ran a “brazen” campaign to access the model. (BBC) + It says it’s the “largest known distillation attack” on the company. (CNBC) + The technique trains a weaker model on a stronger one’s outputs. (FT $) + Anthropic previously accused other Chinese rivals of using it. (CNN) + But it’s still feuding with the White House. (MIT Technology Review)
2 NASA has detected possible chemical signatures of ancient life on Mars The Perseverance rover spotted complex carbon on rocks. (New Scientist $) + The molecules are typically associated with dead organisms. (Guardian) + The US has lost its lead in the hunt for alien life. (MIT Technology Review)
3 The EU has joined a US pact to stop relying on Chinese AI Much of the rest of the world seems to still be a battleground for control. (FT $) + China is expanding its AI push in the Global South to counter the US. (The Wire China) + Chinese AI experts are freaking out about the AI arms race. (Wired $)
4 OpenAI and Broadcom have unveiled their first jointly designed AI chip Jalapeño is built to power large-scale AI systems like ChatGPT. (NYT $) + It’s part of OpenAI’s push to “build the full stack.” (CNBC)
5 A new report shows ICE has built a vast hi-tech surveillance system It includes facial recognition, drones, and data scraping.(Guardian) + Is the Pentagon allowed to surveil citizens with AI? (MIT Technology Review)
6 Electronics can now be printed onto living tissue Which could enable smart implants and ingestible diagnostics. (The Economist $)
7 The data center boom is sparking a third wave of inflation Demand for memory chips is pushing prices higher.(WSJ $)
8 Companies are scrambling to curb spending on AI token “chewing” Accenture data shows non-technical staff are draining budgets. (404 Media)
9 Claude Design is creating a bland wave of website uniformity The AI tool is homogenizing the internet’s aesthetic. (The New Yorker $)
10 Elon Musk has lost his trillionaire status Thanks to SpaceX stock coming back to Earth. (Business Insider)
Quote of the day
“Tom Brown is not being a weirdo like Dario and can actually engage.”
—A person directly familiar with calls between the Trump administration and Anthropic tells Wired that they’ve improved since cofounder Tom Brown replaced CEO Dario Amodei in the talks.
One More Thing
TONY LUONG
The quest to learn if our brain’s mutations affect mental health
For years, scientists searching for the roots of conditions like schizophrenia, autism, and Alzheimer’s have focused on single genes. But the real source may lie in a more complex genetic puzzle inside the brain.
Mike McConnell has spent decades exploring the idea that neurons do not all share identical DNA, and that these differences could help explain psychiatric disease. His work has contributed to evidence that brain cells can form a “genetic mosaic,” with mutations that vary across the brain.
A University of California, Riverside-led research team has developed a gene therapy that restored production of a missing brain protein, corrected abnormalities in brain circuitry, and improved behavior in a mouse model of Fragile X syndrome (FXS). The study, published in the journal Molecular Therapy Nucleic Acids, tested an adeno-associated virus (AAV)-based therapy carrying a normal human version of the FMR1 gene to produce the Fragile X messenger ribonucleoprotein (FMRP) and found that early treatment normalized several measures of brain activity while improving social behavior, exploratory behavior, and cognitive flexibility.
“In a typical brain, FMRP acts like a brake or a volume control,” said senior author Iryna Ethell, PhD, a professor of biomedical sciences at the UC Riverside School of Medicine. “Without it, neural circuits become overactive and less efficient, which contributes to many of the developmental and behavioral challenges associated with FXS.”
FXS is the most common single-gene cause of autism spectrum disorder. According to the researchers, the disorder typically manifests from expansion of CGG repeats in the 5′ untranslated region of FMR1. The mutation causes methylation and silencing of the gene, leading to a major reduction or complete loss of FMRP, an RNA-binding protein that regulates numerous messenger RNAs involved in synapse formation, maturation, and function. Loss of the protein can lead to abnormal synaptic activity and increased cortical hyperexcitability.
FXS can produce sensory hypersensitivity, seizures, anxiety, intellectual disability, developmental delays, repetitive behaviors, and social communication difficulty. Current treatments for this syndrome don’t seek to cure it, rather they are aimed at managing the associated symptoms of anxiety, hyperactivity, irritability, aggression, depression, and seizures.
The therapy developed by the research team was designed to replace missing FMRP rather than repair the original mutation. To do this, the researchers used an AAV9 viral vector to deliver human FMR1 isoform 7, one of the most abundant forms of the protein found in the brain. The therapy was tested in newborn mice lacking FMRP via intracerebroventricular injections at either a low or high doses.
The work built on earlier research that explored the potential of AAV-mediated restoration of FMRP in rodent models. These prior studies used a range of viral serotypes, promoters, delivery routes, and FMRP isoforms and showed they could partially or completely correct specific biochemical, physiological, and behavioral abnormalities. The researchers noted that studies involving mouse and rat FMRP homologs had shown that restoring the protein could improve a range of Fragile X-related deficits.
The current study showed that high-dose treatment produced the strongest positive effects in the mouse models. Electroencephalography showed normalization of baseline gamma power, improvements in responses to sound, reduced background neural activity, and improved habituation to repeated auditory stimuli. The therapy also restored abnormal patterns of brain-wave coupling that have been associated with Fragile X-related dysfunction.
Behavioral testing showed that these improvements persisted into adulthood. Mice receiving the higher dose displayed normalized exploratory behavior, improved social preference, and better performance in probabilistic reversal learning, a measure of cognitive flexibility that requires adapting when previously rewarded behaviors stop producing rewards.
“Fragile X mice tend to persist with an old solution even after the rules change,” Ethell said. “After treatment, they became much better at adapting, performing similarly to mice with normal FMR1 function.”
The researchers noted that their work showed the importance of delivering at therapy for FXS early in its development. They said that widespread distribution of the potential new gene therapy throughout the brain was necessary to achieve a therapeutic benefit. There was a clear relationship between the proportion of neurons expressing the therapeutic gene and the degree of functional recovery, which indicated that restoring FMRP in a sufficient number of cortical cells is critical for correcting any behavioral deficits.
While a promising step, the investigators said that the work was a preclinical study and that future research will now focus on developing delivery methods that can of have broad distribution across the human brain. The team also believes their approach could have broader applications.
“Beyond FXS, the findings may provide a roadmap for treating other genetic neurodevelopmental disorders caused by the loss of a single critical protein,” Ethell said. “Our study shows it may be possible to restore function across complex brain networks by replacing a missing gene. That gives us reason to be optimistic about the future of genetic medicine.”
The prevalence of autism spectrum disorder (ASD) is roughly one in 36 people, with a male-to-female ratio of 4:1. The disorder is known to be influenced by multiple factors, both genetic (gene mutations and copy number variations) and environmental, such as infections during pregnancy. However, the role of immunity in genetic ASD remains unclear.
One area of interest lies in lymphocytes—cells that are known to shape neurodevelopment and behavior. But their roles in neurodevelopmental disorders are not well defined.
Now, new research shows that a subset of T cells—γδ T cells—can infiltrate the brain and contribute to changes in social behavior in a genetic mouse model that mimics behavioral features of ASD. Depleting these cells from the brain increased sociability, suggesting that targeting abnormal immune function during neurodevelopment may offer interventions for ASD.
Infections during pregnancy can induce the release of interleukin-17A (IL-17A) from T helper 17 cells and γδ T cells. Prior research has linked this type of maternal immune activation to neurodevelopmental disorders, but there is a lack of evidence connecting IL-17A and social behaviors in genetic mouse models.
To investigate this further, a team of researchers from the Division of Allergy and Immunology in the Medical Institute of Bioregulation at Kyushu University, in Fukuoka, Japan, studied 15q11-13 duplication (15q dup) mice—a mouse model that mimics a chromosome duplication found in some humans with ASD. These mice also demonstrate reduced social interactions, behavioral inflexibility, and increased anxiety-like behaviors.
The team analyzed immune cell populations in the brains of the 15q dup mice. Their findings suggest an increase in γδ T cells in the developing brains when compared with wild-type mice.
Using single-cell RNA sequencing (scRNA-seq), the team uncovered that this was most likely due to microglia in the brain expressing the chemokine CXCL16, which promotes immune cell migration. CXCL16 was highly expressed in the brains of 15q dup mice and contributed to increased infiltration of γδ T cells.
In addition, experiments revealed that deleting IL-17A–producing γδ T cells or blocking them with antibodies after birth increased sociability and reduced anxiety-like behaviors in the15q dupmice.
Taken together, the authors note that these findings suggest that “immune dysregulation contributes to social behavior deficits in 15q dup mice, consistent with observations in maternal immune activation models, and may represent a potential target for interventions for ASD-associated differences in social behavior.”
Conditions: Asperger’s Disorder; Asperger Disorder; Autism Disorder; Autism; ADHD – Attention Deficit Disorder With Hyperactivity; ADHD; ASD; Alcohol Abuse/Dependence; Alcohol Addiction; Alcohol and Other Drug Use Disorders; Alcohol and Other Substance Use Prevention; Gambling Addiction; Gambling Disorder; Sex Abuse; Sex Behavior; Sex Crimes; Sex Disorder; Sex Disorders; Gender Dysphoria, Adult; Eating Behavior Disorders; Narcotic-Related Disorders; Narcotic Addiction; Narcissism; Psychiatric Disorder; Psychedelic Effects in Healthy Volunteers; Psychedelic Experiences; Psychedelic Drug Dependence; Marijuana Use Disorder; Marijuana Abuse and Dependence; Smoking (Tobacco) Addiction; Smoking Among Youth; Smoking Abstinence; Abstinence, Sex; Opiate Substitution Treatment; Opioid Abuse (Disorder); Opioid Abuse and Addiction; Cocaine Abuse; MDMA (‘Ecstasy’); Addiction Disorders; Homeless and Low Incomes People, Refugees; Homelessness; Reliability and Validity; Anger Problems; Child Abuse, Sexual
Interventions: Behavioral: AI City Hall Project (AIhealth4u – Public Health Central); Behavioral: AI City Hall Project (QAIAx Microcity A – AI Public Health Central)
Sponsors: Veterans Recovery Network Inc.; U.S. Special Operations Command; Central Virginia VA Health Care System; AI-119 Vulcan Project Research & Educational Technology Company (fka Henry Nanpei Academy Project)
