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Fundamental constraints to the logic of living systems

Excellent review in which Solé et al. explore how physical/mathematical constraints may determine what subset of biological systems could theoretically evolve in the universe. Lots of fascinating ideas applying concepts like Turing machines, cellular automata, McCulloch-Pitts networks, energy minimization, and phase transitions to multiscale biological and evolutionary phenomena!

I found the description of how parasites almost inevitably emerge and drive increased biodiversity in computational models of evolution particularly fascinating. Interestingly, I recall this idea was featured in the Hyperion Cantos novels during an explanation of the history of artificial intelligence in their fictional universe!

Abstract. It has been argued that the historical nature of evolution makes it a highly path-dependent process. Under this view, the outcome of evolutionary dynamics could have resulted in organisms with different forms and functions. At the same time, there is ample evidence that convergence and constraints strongly limit the domain of the potential design principles that evolution can achieve. Are these limitations relevant in shaping the fabric of the possible? Here, we argue that fundamental constraints are associated with the logic of living matter. We illustrate this idea by considering the thermodynamic properties of living systems, the linear nature of molecular information, the cellular nature of the building blocks of life, multicellularity and development, the threshold nature of computations in cognitive systems and the discrete nature of the architecture of ecosystems. In all these examples, we present available evidence and suggest potential avenues towards a well-defined theoretical formulation.

Competitive interactions shape mammalian brain network dynamics and computation

Brain network architecture may balance cooperation and competition across circuits. Here the authors use computational whole-brain modeling across three species to show that models with competition are more realistic, more personalized and perform better.

The Abstraction Fallacy: Why AI Can Simulate But Not Instantiate Consciousness

The core issue: computation isn’t an intrinsic physical process; it’s an extrinsic, descriptive map. It logically requires an active, experiencing cognitive agent, a “mapmaker”, to alphabetize continuous physics into meaningful, discrete symbols.

Computational functionalism dominates current debates on AI consciousness. This is the hypothesis that subjective experience emerges entirely from abstract causal topology, regardless of the underlying physical substrate. We argue this view fundamentally mischaracterizes how physics relates to information. We call this mistake the Abstraction Fallacy. Tracing the causal origins of abstraction reveals that symbolic computation is not an intrinsic physical process. Instead, it is a mapmaker-dependent description. It requires an active, experiencing cognitive agent to alphabetize continuous physics into a finite set of meaningful states. Consequently, we do not need a complete, finalized theory of consciousness to assess AI sentience—a demand that simply pushes the question beyond near-term resolution and deepens the AI welfare trap. What we actually need is a rigorous ontology of computation. The framework proposed here explicitly separates simulation (behavioral mimicry driven by vehicle causality) from instantiation (intrinsic physical constitution driven by content causality). Establishing this ontological boundary shows why algorithmic symbol manipulation is structurally incapable of instantiating experience. Crucially, this argument does not rely on biological exclusivity. If an artificial system were ever conscious, it would be because of its specific physical constitution, never its syntactic architecture. Ultimately, this framework offers a physically grounded refutation of computational functionalism to resolve the current uncertainty surrounding AI consciousness.

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Oligodendrocyte molecular perturbations associated with tau in Alzheimer’s

The findings suggest that in AD, part of what happens in the brain may involve changes in DNA tagging that affect the function of oligodendrocytes, particularly in relation to the buildup of the toxic protein tau.

Oligodendrocytes are the brain cells that make myelin, the insulation that helps nerve cells communicate. Scientists have theorized that disrupting neuron communication contributes to symptoms for people with AD. Researchers in this study found that nearly all significant methylation changes — small chemical tags added to DNA that help control when genes are turned on or off — were linked to the tau protein. This supports the idea that this protein plays a key role in brain cell changes tied to AD.

“Our team has previously shown that oligodendrocytes are affected in Alzheimer’s and another tau-related disease, progressive supranuclear palsy (PSP),” says the author. “These new results further highlight that problems in oligodendrocytes and myelin are central to AD. They also point to specific molecular pathways, particularly epigenetic changes, that could be targeted in future therapies.”

The study results identified new genes that may play a role in AD, including one called LDB3, and confirmed many findings across multiple independent datasets, showing its reliability. The identification of specific genes provides potential targets for future research — for example, scientists might investigate whether interventions that reverse methylation or support oligodendrocyte health can slow or modify disease progression for patients with AD. ScienceMission sciencenewshighlights.

In a study published in Nature Communications, the researchers have identified specific DNA-level changes in the brains of people with Alzheimer’s disease (AD). Using advanced biological analysis, the team mapped alterations in the brain’s regulatory landscape that may help explain why Alzheimer’s presents and progresses differently from person to person. The findings could also open new avenues for understanding other neurodegenerative diseases.

Alzheimer’s disease is the most common cause of dementia. Biologically, the disease begins with the formation of protein deposits, known as amyloid plaques, and neurofibrillary tangles in the brain. This causes brain cells to die over time and the brain to shrink. About 6.9 million people in the U.S. age 65 and older live with Alzheimer’s disease. There is no cure, and in advanced stages, complications can result in a significant decline in quality of life and death.

Continue reading “Oligodendrocyte molecular perturbations associated with tau in Alzheimer’s” | >

A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway

High-altitude survival gene in mammals may help reverse nerve damage from conditions like multiple sclerosis.

Neuron.

Li et al. report that a gain-of-function Retsat variant, associated with high-altitude adaptation, promotes myelination by boosting neuronal synthesis of the signaling metabolite ATDRA. This molecule activates RXR-γ in oligodendrocyte progenitors. Administration of the prodrug ATDR promotes remyelination in models of myelin disease.

Stress-induced nucleolar rejuvenation via chaperone-mediated segregation in a filamentous fungus

Audra M. Rogers, Martin J. Egan et al. @UArkansas demonstrate that heat stress triggers nucleolar remodeling in filamentous fungi, enabling segregation of damaged material and selective inheritance of a new nucleolar compartment. This reveals a chaperone-mediated quality control mechanism that preserves nuclear function in highly polarized, multinucleate cells.

Model for nucleolar remodeling, partitioning, and quality control following heat shock. Schematic illustration of nucleolar remodeling in M. oryzae during recovery from heat stress. Heat shock damages the existing nucleolus. (2–3) A new nucleolar bud emerges from the old (preexisting) nucleolus and expands through de novo synthesis. Partial nuclear envelope breakdown permits entry of the molecular chaperones such as Hsp104 and Hsp70. The old nucleolar compartment accumulates SUMO-modified material and selectively recruits Hsp70 and Hsp104, mediating the partitioning of old and new nucleolar material. The newly formed nucleolus disassembles at mitotic onset and is preferentially inherited by daughter nuclei, while the old nucleolus is extruded and diminishes.

Figure 5.

How the brain can selectively focus attention on one voice among others in a noisy environment

MIT neuroscientists have figured out how the brain is able to focus on a single voice among a cacophony of many voices, shedding light on a longstanding neuroscientific phenomenon known as the “cocktail party problem.”

This attentional focus becomes necessary when you’re in any crowded environment, such as a cocktail party, with many conversations going on at once. Somehow, your brain is able to follow the voice of the person you’re talking to, despite all the other voices that you’re hearing in the background.

Using a computational model of the auditory system, the MIT team found that amplifying the activity of the neural processing units that respond to features of a target voice, such as its pitch, allows that voice to be boosted to the forefront of attention.

Stress rewires brain control networks, boosting pain tolerance in ice test

Stress resilience isn’t a flatline. It’s a flex, according to new research from Florida International University. Marcelo Bigliassi, assistant professor of psychophysiology, and Ph.D. student Dayanne Antonio thrive in creating stressful environments.

They set out to explore how the brain’s internal wiring and a person’s subjective experience of stress interact to determine how they respond to stressful situations. The findings were published in the Journal of Applied Physiology.

Study participants plunged one hand into a bucket of ice-cold water. Frigidly cold water. As the seconds ticked by, the body’s stress systems revved up, and their skin began to sweat.

Enhancer dynamics and cellular architecture in the human spinal cord

Human spinal cord enhancer dynamics and cellular architecture.

The researchers present an innovative framework redefining human spinal cord cellular diversity through epigenetic configuration and spatial organization.

They identify unseen enhancer classes that define both stable cell-type identity and transitions between cells undergoing differentiation.

The authors also identify gene regulatory networks in glial cells that reorganize along the rostrocaudal axis, demonstrating anatomical differences in gene regulation.

The researchers demonstrate spatial organization of cells into distinct cellular networks and address the functional significance of this observation in the context of paracrine signaling. sciencenewshighlights ScienceMission https://sciencemission.com/Enhancer-dynamics

Kandror et al. present an innovative framework redefining human spinal cord cellular diversity through epigenetic configuration and spatial organization. They identify unseen enhancer classes, show cell-type-specific reconfiguration of gene regulatory networks along the rostrocaudal axis, and uncover cellular networks mediated by discrete paracrine signaling, challenging conventional definitions of cellular state.

Continue reading “Enhancer dynamics and cellular architecture in the human spinal cord” | >

Abstract: Tumor-intrinsic chromatin programs enforce immune evasion in glioblastoma:

Rongze Olivia Lu & colleagues provide a Commentary on Xinchun Zhang et al.: https://doi.org/10.1172/JCI195556

Address correspondence to: Rongze Olivia Lu, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, 1,450 3rd St., Helen Diller Cancer Building, San Francisco, California 94,158, USA. Email: [email protected].

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