Elon Musk’s Neuralink introduced the first patient to receive its brain-computer implant, demonstrating during a livestream that he can now move a computer cursor to play chess using the device. Photo: Neuralink.
#ElonMusk #Neuralink #WSJ
Neuroscientists have taken a step closer to understanding those moments when our thoughts seem to vanish into thin air, a phenomenon known as “mind blanking.” A study published in The Journal of Neuroscience reveals that when people report having no identifiable thoughts — mind blanking — there is a marked reduction in brain activity across several key regions. This intriguing discovery contributes to broader conversations about consciousness and our ability to report experiences.
The authors behind the new study sought to better understand a relatively understudied area of cognitive neuroscience: the phenomenon of mind blanking, where individuals find themselves unable to recount their immediate-past mental content. Unlike mental states with reportable content, such as daydreaming or engaging in a task, mind blanking represents a unique state of consciousness that lacked thorough neural characterization.
“In the past 10 years, I have researched human unconscious states where communication is restricted (post-comatose disorders),” said corresponding author Athena Demertzi, a tenured research associate of the Belgian Fund for Scientific Research and director of the Physiology of Cognition Lab at the University of Liège, Belgium.
The first person with Neuralink’s computer-linked chip implanted in the surface of their brain showed off their “telekinetic” online chess-playing skills while discussing the “life-changing” procedure for the first time in a surprise livestream.
Noland Arbaugh, a 29-year-old with quadriplegia (or paralysis that affects the body from the neck down), volunteered to have the device implanted as part of Neuralink’s ongoing trial of the technology. Until now, his identity had remained a closely guarded secret.
In the last decade, the advances made into the reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) led to great improvements towards their use as models of diseases. In particular, in the field of neurodegenerative diseases, iPSCs technology allowed to culture in vitro all types of patient-specific neural cells, facilitating not only the investigation of diseases’ etiopathology, but also the testing of new drugs and cell therapies, leading to the innovative concept of personalized medicine. Moreover, iPSCs can be differentiated and organized into 3D organoids, providing a tool which mimics the complexity of the brain’s architecture. Furthermore, recent developments in 3D bioprinting allowed the study of physiological cell-to-cell interactions, given by a combination of several biomaterials, scaffolds, and cells.
Here we show that DS2 is an online, synchronous population event accompanied by widespread increases in neural activity and brief arousalions. On the basis of the stationary activation of place cells with fields close to the mouse’s current location, we propose that DS2 may serve as a mechanism to regularly ground the hippocampal representation of position in an environment during immobility. Rapidly switching between current (DS2) and remote (SPW-R) locations would enable cognitive flexibility that varies with sudden changes in the animal’s internal state or changes in the environment (for example, a startling noise). Synchronous neural activity during DS2 may provide opportunity windows for synaptic plasticity, consistent with our findings linking DS2 to associative memory formation.
At the microcircuit level, distinct brain states are shaped by the non-uniform recruitment of local inhibitory cells, which are key for directing information flow27. As arousal-activated AACs heterogeneously innervate principal cells19,20 and are highly active during DS2 but mostly silent during SPW-Rs, this GABAergic cell (and probably others, such as TORO cells) may be important in regulating the distinct ensemble activity between DS2 and SPW-Rs. At a network level, DS2 is thought to be primarily triggered by the medial entorhinal cortex, which contains neurons that encode self-referenced movement variables, locations and environmental borders28,29,30. This self-referenced spatial input may indeed be key for recruiting spatially tuned hippocampal cells corresponding to an animal’s current position during DS2. Both tones and air puffs reliably evoked DS2 and promoted current position encoding, but the identity of the stimulus (tone versus puff) could not be reliably decoded.
In the past 10 years, gene-editing and organoid culture have completely changed the process of biology. Congenital nervous system malformations are difficult to study due to their polygenic pathogenicity, the complexity of cellular and neural regions of the brain, and the dysregulation of specific neurodevelopmental processes in humans. Therefore, the combined application of CRISPR-Cas9 in organoid models may provide a technical platform for studying organ development and congenital diseases. Here, we first summarize the occurrence of congenital neurological malformations and discuss the different modeling methods of congenital nervous system malformations. After that, it focuses on using organoid to model congenital nervous system malformations. Then we summarized the application of CRISPR-Cas9 in the organoid platform to study the pathogenesis and treatment strategies of congenital nervous system malformations and finally looked forward to the future.
Keywords: organoid, CRISPR-Cas9, congenital nervous system malformation, central nervous system, 3D
Brain organoids have become increasingly used systems allowing 3D-modeling of human brain development, evolution, and disease. To be able to make full use of these modeling systems, researchers have developed a growing toolkit of genetic modification techniques. These techniques can be applied to mature brain organoids or to the preceding embryoid bodies (EBs) and founding cells. This review will describe techniques used for transient and stable genetic modification of brain organoids and discuss their current use and respective advantages and disadvantages. Transient approaches include adeno-associated virus (AAV) and electroporation-based techniques, whereas stable genetic modification approaches make use of lentivirus (including viral stamping), transposon and CRISPR/Cas9 systems. Finally, an outlook as to likely future developments and applications regarding genetic modifications of brain organoids will be presented.
The development of brain organoids (Kadoshima et al., 2013; Lancaster et al., 2013) has opened up new ways to study brain development and evolution as well as neurodevelopmental disorders. Brain organoids are multicellular 3D structures that mimic certain aspects of the cytoarchitecture and cell-type composition of certain brain regions over a particular developmental time window (Heide et al., 2018). These structures are generated by differentiation of induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) into embryoid bodies followed by, or combined, with neural induction (Kadoshima et al., 2013; Lancaster et al., 2013). In principle, two different classes of brain organoid protocols can be distinguished, namely: (i) the self-patterning protocols which produce whole-brain organoids; and (ii) the pre-patterning protocols which produce brain region-specific organoids (Heide et al., 2018).
The first patient of Elon Musk’s Neuralink has been presented to the public. Noland Arbaugh had all but given up playing Civilization VI ever since a diving accident dislocated two vertebrae in his cervical spinal cord, leaving him paralyzed from the shoulders down.
When confined to his wheel chair, the 29-year-old American is totally dependent on the care of his parents, who need to shift his weight ever few hours to avoid pressure sores from sitting too long in the same position.
Moving a cursor on a display furthermore required the use of a mouth stick, a specialized assistive device used by quadriplegics.
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Researchers from the Broad Institute of MIT and Harvard, along with colleagues from Harvard Medical School and McLean Hospital, have identified remarkably consistent alterations in gene expression within the brains of individuals with schizophrenia and older adults. This discovery points to a shared biological foundation underlying the cognitive difficulties frequently observed in patients with schizophrenia and in aging populations.
In a study published in Nature, the team describes how they analyzed gene expression in more than a million individual cells from postmortem brain tissue from 191 people. They found that in individuals with schizophrenia and in older adults without schizophrenia, two brain cell types called astrocytes and neurons reduced their expression of genes that support the junctions between neurons called synapses, compared to healthy or younger people. They also discovered tightly synchronized gene expression changes in the two cell types: when neurons decreased the expression of certain genes related to synapses, astrocytes similarly changed expression of a distinct set of genes that support synapses.
The team called this coordinated set of changes the Synaptic Neuron and Astrocyte Program (SNAP). Even in healthy, young people, the expression of the SNAP genes always increased or decreased in a coordinated way in their neurons and astrocytes.
