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.
David Sinclair plans to test whole-body rejuvenation drugs in the XPrize competition
The outspoken longevity scientist David Sinclair has predicted that, one day, you’ll go to the doctor and get a prescription that will make you 10 years younger. MIT Technology Review has learned of his latest step toward this: human tests of a “reprogramming” drug.
Sinclair, a biologist at Harvard Medical School, plans to launch the tests in a $101 million competition organized by the XPrize Foundation. The winners will “restore” a person to an earlier apparent age, as measured by improvements in immune, cognitive, and muscle function.
The grand prize goes to any team able to show a 10-year (or greater) relative improvement after one year of treatment.
At SXSW London last week, I gave a talk called “Five things you need to know about AI,” in which I shared what I think are the biggest themes in AI right now.
I pulled a few things from our first AI10 list, an annual guide to the top trends in this buzzy world, but I also veered off on several tangents. In my half-hour slot, I tried to cover the key talking points that I think help to make sense of what’s going on in tech—and thus the economy—today.
Five key thoughts emerged: AI is everywhere all at once, it’s getting scary, a backlash is growing, it’s becoming a big deal for science—and I didn’t even need to show up at the talk. Read the full story for all the details.
The must-reads
I’ve combed the internet to find you today’s most fun/important/scary/fascinating stories about technology.
1 OpenAI has confidentially filed for a US IPO The listing could come as early as September. (Reuters $) + OpenAI is targeting a valuation of up to $1 trillion. (Financial Times $) + The IPO will test investor appetite for AI companies. (WSJ $) + The move follows IPO filings from Anthropic and SpaceX. (CNN)
2 The US claims BYD, Baidu, Alibaba, and others are aiding China’s military The Pentagon added them to a list of military-linked companies. (WSJ $) + The designations limit their operations in the US. (BBC) + The new additions also include humanoid firm Unitree. (TechCrunch) + The Pentagon is adapting to China’s tech rise. (MIT Technology Review)
3 Apple’s long-awaited AI overhaul of Siri is finally here “Siri AI” promises to be a more conversational assistant. (NYT $) + It includes a standalone app and screen-reading features. (Reuters $) + And arrives after two years of repeated delays. (Axios)
4 The White House and Congress are working to limit state AI laws A new deal would curb state rules for federal legislation. (Axios) + AI regulation has divided US politicians. (MIT Technology Review)
5 Meta is launching a “workforce academy” for building data centers The five-week program is free of charge and guarantees a job. (WSJ $) + It arrives shortly after Meta laid off 8,000 employees. (NPR) 6 Taiwan is mulling curbs on AI chip exports to China The new controls would further align with US restrictions. (Bloomberg $) + Future AI chips could be built on glass. (MIT Technology Review)
7 Meta has quietly removed face-recognition code from its smart glasses app The code identified by investigators has disappeared. (Wired $)
8 Humanoid robots are edging towards the battlefield American and Chinese militaries are pursuing the tech. (BBC)
9 The world’s first wind-powered underwater data center has launched It uses less power and water than land-based equivalents. (Guardian)
10 You could get some benefits of sleep without having to nod off If new brain stimulation works as well on humans as on mice, that is. (New Scientist $)
Quote of the day
“You’re on the train, but you know that there’s no destination.”
—Clara Shih, a former top AI executive at Salesforce and Meta, tells the New York Times that AI training can’t keep up with the field’s advances.
One More Thing
ILLUSTRATIONS BY AMRITA MARINO
Inside the race to make human sex cells in the lab
An embryo forms when sperm meets egg. But what if we could start with other cells—if a blood sample or skin biopsy could be transformed into “artificial” sperm and eggs? What if those were all you needed to make a baby?
That’s the promise of a radical approach to reproduction. Scientists have already created artificial eggs and sperm from mouse cells and used them to create mouse pups. Artificial human sex cells are next.
The advances could herald the end of infertility, but they raise major scientific and ethical challenges.
A University of Bath-led research effort received £500,000 to develop an organ-on-chip device that replicates connections between the brain, gut, and pancreas. The GlucoBrain project is designed to allow researchers to track how signals move between the organs and uncover why diabetes may lead to changes in memory and cognition.
Collaborators include investigators from the University of Oxford and Johns Hopkins. Their findings could pave the way for new treatments to improve the lives of millions of people affected by diabetes, dementia, or both, notes the team.
Diabetes and Alzheimer’s disease are two of the world’s most pressing health problems, especially in aging societies. While diabetes is widely known to affect the heart, kidneys, and eyes, growing evidence suggests it is also linked with problems in memory, learning, and brain function. However, the biological mechanisms behind this link remain poorly understood.
“Our gut, pancreas, and brain are constantly communicating via a network of signals, helping us regulate hunger and blood sugar,” says Despina Moschou, PhD, project lead. “But we still don’t fully understand how these signals interact at a cellular level and why glucose levels are linked to cognitive decline. “By creating a connected system on a chip, we can study in real time how signals travel between organs, how diabetes may impair brain function, and how new drugs could help.”
Most current knowledge on the link between diabetes and dementia comes from animal studies, simple cell cultures, and patient studies. While these are useful, they don’t fully and accurately capture all the complex interactions between our organs, hormones, and cells, points out Moschou.
Organ-on-chip technology uses living human cells in miniature devices that mimic how organs work in the body. Unlike cell cultures grown in a petri dish, these devices allow cells to grow in three dimensions, receive a controlled supply of nutrients and interact more naturally. Researchers will also be able to isolate these individual organs and cell types to understand exactly how they communicate at a molecular level.
The three-year project starts in October, bringing together engineers, clinicians, biologists and computer scientists to model the complex disease interactions. The team will first develop individual chip models for the gut, pancreas, and brain, before connecting them into a multi-organ system. They will gradually increase complexity and measure how each organ responds to glucose, hormones and different drug treatments.
Researchers from the University of Oxford will provide core clinical expertise in diabetes and metabolic disease, ensuring models are physiologically accurate. The team from Johns Hopkins University brings specialist expertise in Alzheimer’s disease and brain organoids.
GlucoBrain is a pilot project established to help researchers understand exactly how diseases like diabetes and dementia work at a deeper, biological level. This early-stage research will build the foundations for even more advanced and realistic models, bringing together more organs and cell types, explain team members. By harnessing the power of artificial intelligence, the devices have the potential to reveal new insights into how diseases emerge and develop.
“Not only would these devices give us an unprecedented way to study diseases, but they could help speed up drug discovery and testing, reducing reliance on animal models and making results more relevant to humans,” continues Moschou. “In the long term, they could pave the way for personalized medicine, using a patient’s own cells to identify the most effective treatment.”
The project is funded by the Engineering and Physical Sciences Research Council (EPSRC) Health Technologies Connectivity Awards.
IntroductionGrowing evidence suggests a mechanistic link between type 2 diabetes mellitus and Parkinson’s disease (PD), with insulin-degrading enzyme (IDE) implicated in both insulin and amyloid-β metabolism, as well as α-synuclein degradation. However, the role of IDE in PD pathogenesis remains insufficiently defined. This study aimed to investigate the association of IDE gene polymorphisms and serum IDE levels with sporadic PD in a Chinese Han population.MethodsFourteen single nucleotide polymorphisms (SNPs) within the IDE gene were genotyped in 463 patients with sporadic PD and 576 age- and sex-matched healthy controls (HCs). An independent cohort of 100 PD patients and 100 HCs was used to quantify serum IDE concentrations. Correlations between IDE levels and clinical features were assessed. Logistic regression was employed to identify independent factors associated with PD.ResultsAmong the examined SNPs, rs11187007 showed a nominal allelic association with PD (P = 0.046), which did not survive the Bonferroni correction. Serum IDE concentrations were significantly higher in PD patients than in HCs (P = 0.015). Elevated IDE levels were negatively correlated with Mini-Mental State Examination scores (R = –0.230, P = 0.027) and positively associated with more severe symptoms. Logistic regression indicated that elevated serum IDE levels were associated with PD.ConclusionOur findings highlight that elevated serum IDE correlates with PD, suggesting a role for IDE in neurodegeneration, warranting further mechanistic and longitudinal studies to evaluate its potential as a therapeutic target in PD.
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<![CDATA[GLP-1 drugs like semaglutide may curb alcohol and opioid cravings, as trials expand, combos emerge, and interaction risks surface.]]>
Psychostimulant use disorder (PSUD) and nicotine use disorder (NUD) affect tens of millions of people worldwide, yet no clinically-approved medications exist for PSUD and existing NUD treatments have limited long-term efficacy. Recent preclinical evidence suggests that glucagon-like peptide-1 receptor (GLP-1R) agonists could be repurposed for treating PSUD and NUD. This review summarizes the current literature investigating the efficacy of GLP-1R agonists to reduce psychostimulant and nicotine-mediated behaviors in animal models of PSUD and NUD, respectively.
