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“We took skin biopsies from patients living with Huntington’s disease and reprogrammed the skin biopsies into neurons. We then compared these neurons with reprogrammed neurons from healthy people. The results are very interesting. We have found several defects that explain some of the disease mechanisms in neurons from patients with Huntington’s disease. Among other things, we observed that neurons from patients with Huntington’s disease show problems in breaking down and recycling a particular kind of protein – which can lead to a lack of energy in these cells”, says Johan Jakobsson, professor of neuroscience at Lund University.

The researchers have also measured the biological age of the cells and observed that the reprogrammed neurons retain their biological age, which is significant if they are to be used for research in the new model system.

The posterior parietal cortex (PPC) plays a key role in integrating sensory inputs from different modalities to support adaptive behavior. Neuronal activity in PPC reflects perceptual decision-making across behavioral tasks, but the mechanistic involvement of PPC is unclear. In an audiovisual change detection task, we tested the hypothesis that PPC is required to arbitrate between the noisy inputs from the two different modalities and help decide in which modality a sensory change occurred. In trained male mice, we found extensive single-neuron and population-level encoding of task-relevant visual and auditory stimuli, trial history, as well as upcoming behavioral responses. However, despite these rich neural correlates, which would theoretically be sufficient to solve the task, optogenetic inactivation of PPC did not affect visual or auditory performance. Thus, despite neural correlates faithfully tracking sensory variables and predicting behavioral responses, PPC was not relevant for audiovisual change detection. This functional dissociation questions the role of sensory-and task-related activity in parietal associative circuits during audiovisual change detection. Furthermore, our results highlight the necessity to dissociate functional correlates from mechanistic involvement when exploring the neural basis of perception and behavior.

SIGNIFICANCE STATEMENT The posterior parietal cortex (PPC) is active during many daily tasks, but capturing its function has remained challenging. Specifically, it is proposed to function as an integration hub for multisensory inputs. Here, we tested the hypothesis that, rather than classical cue integration, mouse PPC is involved in the segregation and discrimination of sensory modalities. Surprisingly, although neural activity tracked current and past sensory stimuli and reflected the ongoing decision-making process, optogenetic inactivation did not affect task performance. Thus, we show an apparent redundancy of sensory and task-related activity in mouse PPC. These results narrow down the function of parietal circuits, as well as direct the search for those neural dynamics that causally drive perceptual decision-making.

Yes, it does. Although OrganEx helps revitalize pigs’ organs, it’s far from a deceased animal being brought back to life. Rather, their organs were better protected from low oxygen levels, which occur during heart attacks or strokes.

“One could imagine that the OrganEx system (or components thereof) might be used to treat such people in an emergency,” said Porte.

The technology could also help preserve donor organs, but there’s a long way to go. To Dr. Brendan Parent, director of transplant ethics and policy research at NYU Grossman School of Medicine, OrganEx may force a rethink for the field. For example, is it possible that someone could have working peripheral organs but never regain consciousness? As medical technology develops, death becomes a process, not a moment.

Discussion panel with:
- Swati Chavda, a science fiction writer and former brain surgeon.
- Ron S. Friedman, a science fiction writer and an Information Technologies Specialist.

August 13th 2022, When Words Collide festival.

#booktube #authortube #writingtube #braincomputerinterface #neuralink.

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Neuralink, a company co-founded by Elon Musk, has been working on an implantable brain-machine interface since 2016. While it previously demonstrated its progress by showing a Macaque monkey controlling the cursor.

It’s unclear what kind of deal Musk has offered — whether it’s a collaboration or a financial investment —since none of the players responded or confirmed the report with the news organization.


Elon Musk’s last update on Neuralink — his company that is working on technology that will connect the human brain directly to a computer — featured a pig with one of its chips implanted in its brain. Now Neuralink is demonstrating its progress by showing a Macaque with one of the Link chips playing Pong. At first using “Pager” is shown using a joystick, and then eventually, according to the narration, using only its mind via the wireless connection.

Today we are pleased to reveal the Link’s capability to enable a macaque monkey, named Pager, to move a cursor on a computer screen with neural activity using a 1,024 electrode fully-implanted neural recording and data transmission device, termed the N1 Link. We have implanted the Link in the hand and arm areas of the motor cortex, a part of the brain that is involved in planning and executing movements. We placed Links bilaterally: one in the left motor cortex (which controls movements of the right side of the body) and another in the right motor cortex (which controls the left side of the body).

Hui Li, PhD, a Department of Pathology researcher, along with his team discovered that a gene responsible for the deadliest type of brain tumor is also found to be responsible for two forms of childhood cancer. The new discovery may open the door to the first targeted treatments for two types of rhabdomyosarcoma, a cancer of the soft tissue that primarily strikes young children. Research also suggests the gene may play an important role in other cancers that form in muscle, fat, nerves and other connective tissues in both children and adults. Hui Li, PhD, and team published their findings in the scientific journal PNAS.

Summary: Increasing neurogenesis by deleting the Bax gene in mouse models of Alzheimer’s improved the animals’ performance in tests measuring spatial recognition and contextual memory.

Source: Rockefeller University.

Researchers at the University of Illinois Chicago have discovered that increasing the production of new neurons in mice with Alzheimer’s disease (AD) rescues the animals’ memory defects.