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Is The Brain an Analog Computer? Consciousness as Dynamic Brainwave Organization | Earl Miller

Professor Earl Miller discusses, Mind-Body Solution podcast.

Earl K. Miller is the Picower Professor of Neuroscience at the Massachusetts Institute of Technology. He has faculty positions in The Picower Institute for Learning and Memory and the Department of Brain and Cognitive Sciences. He holds degrees from Kent State University (B.A.) and Princeton University (M.A., Ph.D.) as well as an honorary Doctor of Science from Kent State University.

For decades, neuroscience treated the brain like a digital machine — storing information in synaptic connections and sustaining activity like a switch flipped on. But what if that model is incomplete?

In this conversation, I sit down with Earl Miller, MIT professor and head of the Miller Lab, to explore a growing shift in cognitive neuroscience: the brain may compute using dynamic electrical waves.

We discuss how oscillations coordinate millions of neurons, how waves interact with spikes in a two-way system, why large-scale brain organization may depend on rhythmic patterns, and what this means for artificial intelligence.

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Abstract: Emily Gutierrez-Morton

Yanchang Wang and colleagues (Florida State University) show that in yeast, polo-like kinase Cdc5 promotes the phosphorylation of SUMO protease Ulp2, reducing its affinity for SUMO chains and thereby facilitating polySUMOylation.

Genetics CellCycle

1Infectious Diseases Division, Department of Medicine and.

2Division of Plastic and Reconstructive Surgery, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.

3Department of Mathematics, Dartmouth College, Hanover, New Hampshire, USA.

Abstract: Can we identify infections earlier in patients undergoing breast implant reconstruction?

Jeffrey P. Henderson use metabolomic profiling of postimplantation drain fluid, revealing an infection-associated molecular signature that, in longitudinal samples, substantially pre-dated clinical infection diagnosis.

1Infectious Diseases Division, Department of Medicine and.

2Division of Plastic and Reconstructive Surgery, Washington University in St. Louis School of Medicine, St. Louis, Missouri, USA.

3Department of Mathematics, Dartmouth College, Hanover, New Hampshire, USA.

Immune cells selectively pull DNA from dying nuclei, revealing a process dubbed nucleocytosis

Over the years, cell biology has built a detailed picture of how cells compartmentalize their internal functions. Central to this organization is the nucleus, which houses the genetic material and is separated from the cytoplasm by a robust nuclear envelope.

Traditionally, the nuclear membrane has been considered a strict barrier, maintaining nuclear integrity except during carefully controlled processes such as mitosis. As a result, the release of nuclear material has largely been associated with cellular damage or death.

However, recent work by a research team in Japan suggests that this view may be incomplete.

Spatiotemporal coordination of Slit-Robo repulsion and neurturin-Gfrα attraction guides multipolar migration during retinal lamination

Lehtimäki et al. reveal how repulsive Slit1b/2-Robo2 and attractive neurturin-Gfrα1/2-Ret signaling jointly coordinate multipolar migration of horizontal cells through crowded, scaffold-free environments of the vertebrate retina. This work was enabled by sophisticated transcriptomics analysis, targeted F0 CRISPR screening, and 3D fixed and live imaging.

Brain organoids can be trained to solve a goal-directed task

This research is the first rigorous academic demonstration of goal-directed learning in lab-grown brain organoids, and lays the foundation for adaptive organoid computation—exploring the capacity of lab-grown brain organoids to learn and solve tasks.

Using organoids derived from mouse stem cells and an electrophysiology system developed by industry partners Maxwell Biosciences, the researchers use electrical simulation to send and receive information to and from neurons. By using stronger or weaker signals, they communicate to the organoid the angle of the pole, which exists in a virtual environment, as it falls in one direction or the other. As this happens, the researchers observe as the organoid sends back signals of how to apply force to balance the pole, and they apply this force to the virtual pole.

For their pole-balancing experiments, the researchers observe as the organoid controls the pole until it drops, which is called an episode. Then, the pole is reset and a new episode begins. In essence, the organoid plays a video game in which the goal is to balance the pole upright for as long as possible.

The researchers observe the organoid’s progress in five-episode increments. If the organoid keeps the pole upright for longer on average in the past five episodes as compared to the past 20, it receives no training signal since it has been improving. If it does not improve the average time it keeps the pole upright, it receives a training signal.

Training feedback is not given to the organoid while it is balancing the pole—only at the end of an episode. An AI algorithm called reinforcement learning is used to select which neurons within the organoid get the training signal.

The results of this study prove that the reinforcement learning algorithm can guide the brain organoids toward improved performance at the cart-pole task—meaning organoids can learn to balance the pole for longer periods of time.

The researchers adopted a rigorous framework for success to make sure they were observing true improvement, and not just random success, including a threshold for the minimum time an organoid needs to balance the pole to “win” the game.

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Tumor-immune-neural circuit disrupts energy homeostasis in cancer cachexia

Tumor-immune-neural circuit in cancer cachexia.

The mechanisms involved in cancer-mediated cachexia and anorexia are not well understood.

The researchers in this study delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia.

The authors show thay loss of GDF15 protects against appetite loss, muscle wasting, and fat loss in pancreatic, lung, and skin cancers.

Disrupting this feedforward loop with GDF15-neutralizing antibody, anti-CSF1R antibody, or Rearranged during Transfection (RET) inhibitor alleviates cachexia and anorexia across cancer models. sciencenewshighlights ScienceMission https://sciencemission.com/Tumor-immune-neural-circuit

Shi et al. delineate an interplay among tumor cells, immune cells, and the nervous system that drives cancer cachexia and anorexia. Specifically, tumor-derived CSF1 induces macrophage GDF15, which signals through the GFRAL-RET neural axis to enhance β-adrenergic activity and systemic wasting. Disrupting this feedforward loop alleviates cachexia across cancer models.

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Mapping ADHD Heterogeneity and Biotypes by Topological Deviations in Morphometric Similarity Networks

Normative modeling of morphometric similarity networks in ADHD identified three distinct biotypes with unique clinical-neural profiles, supporting more neurobiologically informed stratification for ADHD management.

Question Can normative modeling of topological properties derived from brain morphometric similarity networks yield robust stratification biomarkers for pediatric populations with attention-deficit/hyperactivity disorder (ADHD)?

Findings This multisite case-control study included 1,154 participants, characterizing ADHD heterogeneity through hub-centric topological deviations derived from morphometric similarity networks. Three distinct biotypes emerged, each exhibiting unique clinical-neural profiles with characteristic neurochemical and functional correlates, validated in an independent transdiagnostic cohort of 554 ADHD cases.

Meaning The integration of normative modeling with heterogeneity through discriminative analysis (HYDRA) clustering yielded both dimensional and categorical insights into ADHD heterogeneity, thereby enhancing our understanding of the ADHD’s neurobiological complexity.

Nanoparticles for Targeted Drug Delivery to Cancer Stem Cells: A Review of Recent Advances

Cancer stem cells (CSCs) are a subpopulation of cells that can initiate, self-renew, and sustain tumor growth. CSCs are responsible for tumor metastasis, recurrence, and drug resistance in cancer therapy. CSCs reside within a niche maintained by multiple unique factors in the microenvironment. These factors include hypoxia, excessive levels of angiogenesis, a change of mitochondrial activity from aerobic aspiration to aerobic glycolysis, an upregulated expression of CSC biomarkers and stem cell signaling, and an elevated synthesis of the cytochromes P450 family of enzymes responsible for drug clearance. Antibodies and ligands targeting the unique factors that maintain the niche are utilized for the delivery of anticancer therapeutics to CSCs. In this regard, nanomaterials, specifically nanoparticles (NPs), are extremely useful as carriers for the delivery of anticancer agents to CSCs.

Signaling pathways in the regulation of cancer stem cells and associated targeted therapy

The concept of stem cells dates back to the 18th century when scientists tried to elucidate how lower organisms developed tissues and organs. 1 These stem cells produce daughter cells that later undergo different biological processes, either continuous self‐renewal division, or differentiation into specialized cells with a limited lifespan. Normal tissue stem cells provide a life‐long source of cells for self‐renewal of tissues, which leads us to speculate that whether stem cells are capable of deriving a malignant cell population, and this lies the foundation of cancer stem cells (CSCs) theory. CSCs are defined as a subpopulation of malignant tumor cells with selective capacities for tumor initiation, self‐renewal, metastasis, and unlimited growth into bulks. 2

Despite decades of research on cancer treatment, it has been proved extremely challenging to achieve complete remission (CR) in cancer patients. Tumor relapse may be explained by the fact that antitumor therapeutics mainly target proliferative cancer cells but remain ineffective in quiescent CSCs. The role of CSC in tumor initiation was first identified in acute myeloid leukemia (AML). Since its isolation from a number of solid tumors and hematological malignancies, the CSC is believed to form the clonogenic core of these tumors. 3 Growing evidence now suggests that CSCs are responsible for multiple progressive tumor phenotypes, including recurrence, metastasis, and treatment failure. 4, 5 The intrinsic treatment resistance of tumors has partially attributed to the presence of the CSC subpopulation, 6, 7 and may also be induced by extrinsic factors, such as treatments and environments. 8, 9

Major signaling pathways are involved in the maintenance of stem cell properties and survival of CSCs, such as the Notch, Wnt, and Hedgehog (HH) pathways. 10 There is also intricate interplay network between these signal cascades and other oncogenic pathways. 11, 12, 13 Thus, targeting pathway molecules that regulate CSCs provides a new option for the treatment of therapy‐resistant or ‐refractory tumors. This review aims to provide an overview of the regulating networks and their immune interactions involved in CSC development. We also summarized the update on the development of CSC‐directed therapeutics, with a special focus on those with application approval or under clinical evaluation.

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