At WIRED Health 2025, Orchid CEO Noor Siddiqui and genomics pioneer George Church laid out their view of the future of genetic screening.
NASA announced a trailblazing experiment that aims to take personalized medicine to new heights. The experiment is part of a strategic plan to gather valuable scientific data during the Artemis II mission, enabling NASA to “know before we go” back to the lunar surface and on to Mars.
The AVATAR (A Virtual Astronaut Tissue Analog Response) investigation will use organ-on-a-chip devices, or organ chips, to study the effects of deep space radiation and microgravity on human health. The chips will contain cells from Artemis II astronauts and fly side-by-side with crew on their approximately 10-day journey around the Moon. This research, combined with other studies on the health and performance of Artemis II astronauts, will give NASA insight into how to best protect astronauts as exploration expands to the surface of the Moon, Mars, and beyond.
Researchers at Oregon Health and Sciences University’s Vollum Institute have revealed the molecular structure of the serotonin transporter (SERT), providing new insight into the mechanism of antidepressant action of two widely prescribed selective serotonin reuptake inhibitors (SSRIs) commonly used to treat depression. In their Nature paper, authors Jonathan Coleman, Evan Green, and Eric Gouaux describe their use of X-ray crystallography to capture images of human SERT structures. They collected data at the Beamline 5.0.2 in the Berkeley Center for Structural Biology and used the Phenix software suite to build models and refine the structures. The resulting structures show antidepressants citalopram and paroxetine lock SERT in an outward-open conformation, directly blocking serotonin binding.
Deep-brain structures like the basal ganglia or the thalamus wield major influence on our behavior. If something goes awry, dysregulation in the deep brain may trigger neurological conditions like Parkinson’s disease or depression.
Despite the clear importance of these structures, our knowledge about them remains limited by their location, making them difficult to study and treat.
In a new study, researchers unveil a device that might offer an alternative to invasive procedures. Featuring a novel ultrasound helmet, it not only modulates deep-brain circuits without surgery, but reportedly can do so with unrivaled precision.
I’ve just hopped on a video call with the CEO of Retro Biosciences, the Sam Altman-backed longevity company, when I mention it’s quite hot.
Joe Betts-LaCroix takes my passing comment as a cue to muse on the wonders of air conditioning, and how energy and heat were once synonymous — until they weren’t.
As a multi-hyphenate scientist, entrepreneur, and once-inventor of the world’s smallest computer, Betts-LaCroix is excited by paradigm change.
At the helm of what is essentially Altman’s playground for experimenting with pushing the limits of the human lifespan, Betts-LaCroix is hoping to engineer the same shift that air conditioning brought to hot summer days for your brain and body. Ideally, one day, decouple aging from decline and disease.
The experimental memory pill works by clearing out “gunk in the cells” linked to Alzheimer’s and Parkinson’s, Betts-LaCroix said. If the pill works, it will restart stalled autophagy processes in the body, cleaning up damage, “especially in the brain cells,” he said.
In contrast, other new Alzheimer’s drugs, like Eisai’s Leqembi and Eli Lilly’s Kisunla, slow down cognitive decline by flushing out sticky amyloid plaques that are a hallmark of the disease.
One fundamental feature of neurodegenerative diseases is a breakdown in communication. Even before brain cells die, the delicate machinery that keeps neurons in touch—by clearing away protein waste at the synapses—starts to fail.
When the cleanup falters, the connections between brain cells are impaired and the flow of signals responsible for reasoning, language, memory, and even basic bodily functions are progressively disrupted.
Now, a new study identifies a novel strategy for preventing unwanted proteins from clogging synapses and ultimately congealing into protein plaques.
In a new study, University of California, Irvine chemical and biomolecular engineering researchers report the creation of biomolecules that can help grow light-sensitive heart muscle cells in the laboratory. The development enables a biotechnology that could deliver light-triggered signals to the heart, improving its function, without requiring genetic modifications or invasive procedures.
“We show for the first time that light can be converted into cardiac stimulatory cues, with synthetic materials made of biomolecules,” said Herdeline Ann Ardoña, assistant professor of chemical and biomolecular engineering. “This can be beneficial for downstream medical applications, such as in cardiac pacemaking technologies, or helping direct therapeutic patient-derived stem cells to better mimic adult heart cell features.”
The findings are reported in the Proceedings of the National Academy of Sciences. The paper’s co-first authors are recent Ph.D. graduate Sujeung Lim, and Ze-Fan Yao, previous postdoctoral scholar in the Ardoña Research Group.
Endogenous bioelectrical patterns are an important regulator of anatomical pattern during embryogenesis, regeneration, and cancer. While there are three known classes of instructive bioelectric patterns: directly encoding, indirectly encoding, and binary trigger, it is not known how these design principles could be exploited by evolution and what their relative advantages might be. To better understand the evolutionary role of bioelectricity in anatomical homeostasis, we developed a neural cellular automaton (NCA). We used evolutionary algorithms to optimize these models to achieve reliable morphogenetic patterns driven by the different ways in which tissues can interpret their bioelectrical pattern for downstream anatomical outcomes. We found that: All three types of bioelectrical codes allow the reaching of target morphologies; Resetting of the bioelectrical pattern and the change in duration of the binary trigger alter morphogenesis; Direct pattern organisms show an emergent robustness to changes in initial anatomical configurations; Indirect pattern organisms show an emergent robustness to bioelectrical perturbation; Direct and indirect pattern organisms show a emergent generalizability competency to new (rotated) bioelectrical patterns; Direct pattern organisms show an emergent repatterning competency in post-developmental-phase. Because our simulation was fundamentally a homeostatic system seeking to achieve specific goals in anatomical state space (the space of possible morphologies), we sought to determine how the system would react when we abrogated the incentive loop driving anatomical homeostasis. To abrogate the stress/reward system that drives error minimization, we used anxiolytic neuromodulators. Simulating the effects of selective serotonin reuptake inhibitors diminished the ability of artificial embryos to reduce error between anatomical state and bioelectric prepattern, leading to higher variance of developmental outcomes, global morphological degradation, and induced in some organisms a bistability with respect to possible anatomical outcomes. These computational findings were validated by data collected from in vivo experiments in SSRI exposure in planarian flatworm regeneration.