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In February 2023, Frontiers in Science published an article titled “Organoid Intelligence (OI): The New Frontier in Biocomputing and Intelligence-in-a-Dish.” Since its publication, this research has sparked significant scientific interest and gained coverage in Forbes, Financial Times, Wall Street Journal, BBC, CNN and many others.

So, what is organoid intelligence and why has this article gathered such attention?

Continue reading “Brain in a dish — the potential of organoid intelligence and biological computing” »

About 170 billion cells are in the brain, and as they go about their regular tasks, they produce waste — a lot of it.

The brain appears to rely on synchronized waves to wash out waste products, including toxins associated with Alzheimer’s disease.

Neurogenetic disorders, such as neurofibromatosis type 1 (NF1), are diseases caused by a defect in one or more genes, which can sometimes result in cognitive and motor impairments. Better understanding the neural underpinning of these disorders and how they affect motor and cognitive abilities could contribute to the development of new treatment strategies.

Researchers at Stanford University and Washington University School of Medicine recently performed a study on mice aimed at investigating the impact of Nf1 gene mutations, which cause the NF1 neurogenetic disorder, on oligodendroglial plasticity, an adaptive brain process known to contribute to cognitive and motor functions.

Their findings, published in Nature Neuroscience, provide strong evidence that Nf1 mutations delay the development of oligodendroglia, a type of glial cells that support the functioning of the central nervous system, causing disruptions in motor learning.

From the dynamical point of view, most cognitive phenomena are hierarchical, transient and sequential. Such cognitive spatio-temporal processes can be represented by a set of sequential metastable dynamical states together with their associatedions: The state is quasi-stationary close to one metastable state before a rapidion to another state. Hence, we postulate that metastable states are the central players in cognitive information processing. Based on the analogy of quasiparticles as elementary units in physics, we introduce here the quantum of cognitive information dynamics, which we term “cognon”. A cognon, or dynamical unit of thought, is represented by a robust finite chain of metastable neural states. Cognons can be organized at multiple hierarchical levels and coordinate complex cognitive information representations.

MIT just produced three groundbreaking innovations that allowed them to map whole hemispheres of the human brain.

A parasitic fungus compels its insect host to behave in strange ways by hijacking secretory neurons and circadian pathways.

Current computing systems rely on Boolean logic and von Neumann architecture, where computing cells are based on high-speed electron-conducting complementary metal-oxide-semiconductor (CMOS) transistors. In contrast, ions play an essential role in biological neural computing. Compared with CMOS units, the synapse/neuron computing speed is much lower, but the human brain performs much better in many tasks such as pattern recognition and decision-making. Recently, ionic dynamics in oxide electrolyte-gated transistors have attracted increasing attention in the field of neuromorphic computing, which is more similar to the computing modality in the biological brain. In this review article, we start with the introduction of some ionic processes in biological brain computing. Then, electrolyte-gated ionic transistors, especially oxide ionic transistors, are briefly introduced. Later, we review the state-of-the-art progress in oxide electrolyte-gated transistors for ionic neuromorphic computing including dynamic synaptic plasticity emulation, spatiotemporal information processing, and artificial sensory neuron function implementation. Finally, we will address the current challenges and offer recommendations along with potential research directions.

Keywords: bio-inspired computing; ionic transistors; oxide semiconductors.

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Memristive devices with both electrically and optically induced synaptic dynamic behaviors will be crucial to the accomplishment of brain-inspired neuromorphic computing systems, in which the resistive materials and device architectures are two of the most important cornerstones, but still under challenge. Herein, kuramite Cu3SnS4 is newly introduced into poly-methacrylate as the switching medium to construct memristive devices, and the expected high-performance bio-mimicry of diverse optoelectronic synaptic plasticity is demonstrated. In addition to the excellent basic performances, such as stable bipolar resistive switching with On/Off ratio of ∼486, Set/Reset voltage of ∼-0.88/+0.96 V, and good retention feature of up to 104 s, the new designs of memristors possess not only the multi-level controllable resistive-switching memory property but also the capability of mimicking optoelectronic synaptic plasticity, including electrically and visible/near-infrared light-induced excitatory postsynaptic currents, short-/long-term memory, spike-timing-dependent plasticity, long-term plasticity/depression, short-term plasticity, paired-pulse facilitation, and “learning-forgetting-learning” behavior as well. Predictably, as a new class of switching medium material, such proposed kuramite-based artificial optoelectronic synaptic device has great potential to be applied to construct neuromorphic architectures in simulating human brain functions.

© 2023 Author(s). Published under an exclusive license by AIP Publishing.

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BOSTON — There currently is no cure for Parkinson’s disease, but scientists may have discovered a potential path to slow or stop the disease. Parkinson’s disease is a brain disorder that can cause movement problems such as tremors, poor balance, and walking difficulties, and it can also impair cognitive function. There is no cure and treatments aim to simply reduce symptoms. But a new study in mice by researchers at Johns Hopkins offers new hope. They found that the interaction of two proteins is key to the buildup of protein clumps in the brain that damage healthy brain cells in Parkinson’s. They also suggest that disrupting these proteins with a drug already approved by the FDA to treat cancer could potentially slow or stop the brain damage associated with Parkinson’s. The next step would be to conduct clinical trials in humans, but that will take time.