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Weird magic neurons in the spine can make people with paralysis walk again

All they need is electrical stimulation, and once activated, they re-establish the lost connection between different regions of the spinal cord.

Imagine you are stuck inside a room, you want to get out, but your body is not moving. No matter how hard you try, you are unable to move your body parts. You are not even able to move your finger, how would you feel? Well, that’s what chronic paralysis feels like.

Unfortunately, there is no known permanent cure for this neurological disorder, and this is what makes the situation worse. The physical and mental struggle that a patient with chronic paralysis goes through is unimaginable.


Ozgu Arslan/iStock.

However, a team of international researchers has recently made nine patients with severe spinal cord injuries (SCIs) walk again. They claim to have identified neurons that can restore mobility in patients with SCI. This new and interesting development raises great hopes for people suffering from chronic paralysis.

A new large-scale virtual model of the visual cortex is highly successful in solving visual tasks

Human Brain Project researchers have trained a large-scale model of the primary visual cortex of the mouse to solve visual tasks in a highly robust way. The model provides the basis for a new generation of neural network models. Due to their versatility and energy-efficient processing, these models can contribute to advances in neuromorphic computing.

Modeling the brain can have a massive impact on (AI): Since the brain processes images in a much more energy-efficient way than artificial networks, scientists take inspiration from neuroscience to create neural networks that function similarly to the biological ones to significantly save energy.

In that sense, brain-inspired neural networks are likely to have an impact on future technology, by serving as blueprints for in more energy-efficient neuromorphic hardware. Now, a study by Human Brain Project (HBP) researchers from the Graz University of Technology (Austria) showed how a large data-based model can reproduce a number of the brain’s visual processing capabilities in a versatile and accurate way. The results were published in the journal Science Advances.

Brainwave-reading implant lets paralyzed man spell out 1,100 words

A paralyzed man who cannot speak or type was able to spell out over 1,000 words using a neuroprosthetic device that translates his brain waves into full sentences, US researchers said Tuesday.

“Anything is possible,” was one of the man’s favorite phrases to spell out, said the first author of a new study on the research, Sean Metzger of the University of California San Francisco (UCSF).

Last year the team of UCSF researchers showed that a called a brain-computer interface could translate 50 very common when the man attempted to say them in full.

Monoclonal antibodies preserve stem cells in mouse brains, bring promise for future studies

A new approach to stem cell therapy that uses antibodies instead of traditional immunosuppressant drugs robustly preserves cells in mouse brains and has potential to fast-track trials in humans, a Michigan Medicine study suggests.

For this study, researchers used to suppress the in mice and compared the results to traditional immunosuppression with the medications tacrolimus and mycophenolate mofetil. They tracked implanted human neural stem using luciferase, the protein that makes fireflies glow.

Results published in Clinical and Translational Medicine reveal that suppression with monoclonal enabled long-term survival of human stem cell transplants in mouse brains for at least six to eight months, while the cell grafts did not survive more than two weeks in most animals when using standard immunosuppressant drugs.

Disruption of mTORC1 rescues neuronal overgrowth and synapse function dysregulated by Pten loss

). At P7, Ptenflx/flx and Ptenflx/flxRaptorflx/flx animals were co-injected into the dentate gyrus with a retrovirus encoding a fluorophore (GFP) with a downstream Cre, and a control retrovirus with just a fluorophore (mCherry) and no Cre (Figure 3A). Here, the GFP-expressing newborn granule neurons are KOs for their respective flox genes, while mCherry-expressing neurons serve as their in-tissue WT controls. To investigate the role of mTORC1 in development of Pten KO-mediated somal hypertrophy, we quantified soma size of retrovirally infected immunolabeled granule neurons at P28. We observed that Pten KO neurons had significantly greater soma size when compared with their WT control. This increase in soma size was completely rescued in Pten and Raptor double knockout (DKO) neurons (Table S1A and Figures 3B and 3D). We further examined the role of mTORC1 in aberrant migration of Pten KO granule neurons. The Pten KO neurons migrate significantly farther from the hilus along the GCL, when compared with their WT control. This farther migration was completely rescued in Pten and Raptor DKO neurons (Table S1B and Figures 3B and 3E). The dendritic spine density was also found to be significantly increased in Pten KO neurons. This increase in number of spines in middle molecular layer was reduced to WT density in Pten and Raptor DKO neurons (Table S1C and Figures 3C and 3F). Additionally, the decrease in spine head diameter seen in Pten KO neurons was rescued in Pten and Raptor DKO neurons (Table S1D). However, the increased spine length of Pten KO neurons persisted in the Pten and Raptor DKO neurons (Table S1E). These data suggest that Pten loss-mediated neuronal hypertrophy can be rescued by targeting Raptor to disrupt mTORC1.

To examine the role of mTORC1 in the Pten loss-mediated dendritic overgrowth of granule neurons, we reconstructed and quantified retrovirally infected immunolabeled Pten KO granule neurons, as well as Pten and Raptor DKO granule neurons at P28 (Figures 4A and 4B). We observed that Pten KO granule neurons had more elaborate dendritic arbor. Sholl analysis revealed that Pten KO neurons had an increased number of intersections, when compared with WT control neurons. This increase was completely rescued in Pten and Raptor DKO neurons (Table S1F and Figure 4C). The total dendritic length was also increased in Pten KO neurons, which was rescued in Pten and Raptor DKO neurons (Table S1G and Figure 4D). Further analysis revealed that Pten KO neurons have more primary dendrites protruding directly out of the soma, when compared with their WT control. This increase in number of primary dendrites was completely rescued in Pten and Raptor DKO neurons (Table S4A and Figure S2A).

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