Abstract Despite substantial progress in identifying neural correlates of consciousness, no unified quantitative framework currently derives a formally specified order parameter for conscious-state organisation from established neurophysiological principles, or links thalamocortical coordination dynamics to measurable state transitions across pharmacological, pathological, and perturbational conditions through a single computational formalism. We propose a neurocomputational theoretical framework in which conscious states are associated with metastable regimes of large-scale thalamocortical coordination operating near critical dynamical boundaries. The framework is formalised through a dynamic coordination functional Φ(t), defined as a surface integral over the thalamocortical interface and directly operationalisable from high-density EEG as a weighted combination of gamma-band power spectral density, thalamocortical coherence, and theta-gamma phase-amplitude coupling. The thalamic reticular nucleus (TRN) is identified as the anatomical implementation of the control parameter governing proximity to the critical point, grounded in a Wilson-Cowan model of TRN inhibitory gating whose bifurcation structure is characterised computationally. Numerical simulation of the linearised field equation on the thalamocortical boundary demonstrates internal consistency: the simulated system produces power-law recovery dynamics tau_rec proportional to | θ — θ _c|^v with nu consistent with model A universality class [0.5, 1.5], and a Kuramoto mean-field derivation establishes that Φ(t) emerges as the natural order parameter of coupled thalamocortical oscillators rather than being postulated. The joint (|Φ(t)|, Var[|Φ(t)|]) phase space correctly separates simulated waking, anaesthetic, ictal, and minimally conscious regimes without parameter fitting to empirical data. All simulation code is publicly available. Six quantitatively specific, independently falsifiable predictions are derived across five experimental domains: power-law Gamma Dip scaling in near-threshold EEG with a specific exponent range; causal disruption of thalamocortical coherence by selective TRN silencing; opposite EEG scaling exponent deviations in ASD versus schizophrenia; systematic Φ_est collapse under propofol anaesthesia correlated with PCI; Φ_est as a real-time consciousness biomarker in disorders of consciousness; and clinical validity of Φ_est in disorders of consciousness and ictal state discrimination by the metastability index. Each prediction is stated with quantitative thresholds and a pre-specified falsification criterion. The framework provides: the first anatomically specified and formally derived order parameter for conscious-state organisation directly operationalisable from passive EEG; a mechanistically grounded identification of the TRN as the dynamical control parameter, testable by a single optogenetic experiment; and a computationally validated, pre-registerable programme of six falsifiable predictions defining a tractable empirical agenda. Φ_est would constitute a candidate real-time consciousness biomarker if the framework’s predictions are confirmed in purpose-designed experiments.
Category: genetics – Page 6
Reading and writing neural activity with Neuropixels Opto probes
High-density electrophysiology devices allow neuroscientists to observe spikes from large populations of neurons, and optogenetics allows them to drive or suppress those spikes. We show that a single device can combine these two capabilities, providing a high-resolution means to both read and write neural activity in the living brain.
Proteins can be selectively controlled with radio waves
In a significant advance in biological quantum sensing, a research team led by the Technical University of Munich (TUM) has discovered and tested a new mechanism of action in which proteins can be controlled with radio waves. In doing so, they influence a sensitive quantum state known as spin and make it visible via light. In the future, such findings could help detect and even direct biochemical processes in cells simply from the outside using radio waves.
Until now, quantum sensing has primarily been known from solid-state materials such as diamonds with deliberately introduced tiny defects. The researchers are now transferring this principle to proteins —biological molecules that can be genetically produced and specifically tailored. In the future, this could allow quantum sensors to be built directly into cells or tissue.
These protein-based sensors are potentially particularly well suited for biosensing—that is, for imaging living cells, tissues, or organs. In theory, they sit directly where measurement is needed, making them suitable for studies in organisms—unlike bulky solid-state sensors.
A new origin story for multicellular life points to physics, not genes alone
How did life make the leap from single cells to coordinated, multicellular organisms? And how do genetically identical cells still perform a version of that feat every time an embryo begins to take shape?
In a new Perspective paper appearing in the journal Nature Biotechnology, Bren Professor of Biology and Biological Engineering Magdalena Zernicka-Goetz and collaborator Qi Chen of the University of Utah ask one of biology’s oldest questions in a new way. The paper is titled “Decoding the origins of cellular self-organization for engineered biology.”
Tiny brain probe reveals how deep-brain neurons can be measured and manipulated
A new breakthrough technology, co-developed by UCL scientists, that simultaneously records and manipulates neuron activity deep within the brain could transform our understanding of neural circuits and neurological conditions, such as Alzheimer’s disease and schizophrenia.
The device, known as Neuropixels Opto and researched in mice, integrates two powerful but traditionally separate techniques—electrophysiology (the study of the electrical activity of living cells) and optogenetics (combining genetics and optics to control cells). They form a single probe, enabling unprecedented insight into how individual neurons in the brain function and interact.
Published in Nature Methods, the system allows researchers to monitor the electrical activity of hundreds of neurons while also selectively activating or silencing specific cells using light.
Targeted therapy reduces risk of lung cancer recurrence by 83% in rare genetic subtype
A new study co-led by investigators at the UCLA Health Jonsson Comprehensive Cancer Center shows that the targeted cancer drug selpercatinib can significantly reduce the risk of lung cancer returning in patients with a rare genetic subtype of early-stage non-small cell lung cancer (NSCLC), potentially offering a new treatment option to help keep the disease from coming back after standard therapy.
The international phase 3 clinical trial, called LIBRETTO-432, found that after two years, 92% of patients with stage II–IIIA RET fusion-positive NSCLC who received selpercatinib after standard treatment were alive without their cancer returning—a measure known as event-free survival—compared with 61% of patients who received a placebo. Overall, the treatment reduced the risk of cancer recurrence or death by 83%.
The results were shared during the Plenary Session on May 31 at the American Society of Clinical Oncology Annual Meeting by Dr. Jonathan Goldman, Health Sciences Clinical Professor in the Department of Medicine at the David Geffen School of Medicine at UCLA. The paper was also published in the New England Journal of Medicine.
Scientists discover inherited traits that break Mendel’s Laws of genetics
A major mouse study found that some inherited traits are passed down through epigenetic changes that break the classic rules of genetics. Researchers discovered hundreds of cases where these chemical DNA marks behaved unexpectedly, including some that seemed to emerge out of nowhere. They also identified the first known naturally occurring paramutation in a mammal, hinting that environmental influences may play a larger role in inheritance than scientists realized.
Longevity-linked APOE2 gene variant helps neurons repair DNA and resist aging
People who carry the APOE2 version of the apolipoprotein E gene are more likely to live to advanced age and are partly protected against Alzheimer’s disease, but scientists have struggled to explain why. A new study from the Buck Institute for Research on Aging, now published in Aging Cell, offers a mechanistic answer: APOE2 helps human neurons keep their DNA intact and resist becoming senescent, a damaged, dysfunctional state that accumulates with age and contributes to neurodegeneration.
The findings shift attention away from APOE’s well-known role in cholesterol transport and toward a previously underappreciated function of the gene: shaping how brain cells maintain the integrity of their genome as they age.
“We’ve known for years that APOE2 carriers tend to live longer and have a lower risk of Alzheimer’s, but the protective mechanism has been a black box,” says senior author Lisa M. Ellerby, Ph.D., professor at the Buck Institute. “Our work shows that APOE2 neurons are better at preventing and repairing DNA damage, and they resist the cellular aging program that drives so much of late-life decline. Our findings point to entirely new therapeutic directions.”
