Lifeboat Foundation

). At P7, Pten^flx/flx and Pten^flx/flxRaptor^flx/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).

In a study recently published in the journal Nature Biomedical Engineering, researchers from Kanazawa University use a method called “lasso-grafting” to design therapeutics with enhanced longevity and brain penetration.

Cell growth and repair are stimulated by biomolecules known as cytokines and growth factors. Unfortunately, delivering adequate concentrations of these molecules to the brain for treating neurological conditions like Alzheimer’s disease is challenging as they are either cleared out of the blood very quickly or do not penetrate neural tissue effectively.

A research team led by Kunio Matsumoto and Katsuya Sakai at Kanazawa University in collaboration with Junichi Takagi, Osaka University and Hiroaki Suga, the University of Tokyo has now used a technique called “lasso-grafting” to design molecules that replicate growth factors with longer retention in the body and brain penetration.

A woman once baffled doctors when she came back to life after being dead for more than 17 hours. Velma Thomas had a heart attack at her home in Virginia in 2008 and was rushed to hospital. While there she had two more heart attacks and was placed on life support — in all, her heart stopped beating three times and she was clinically dead, with no brain activity, for 17 hours.

This time I come to talk about a new concept in this Age of Artificial Intelligence and the already insipid world of Social Networks. Initially, quite a few years ago, I named it “Counterpart” (long before the TV series “Counterpart” and “Black Mirror”, or even the movie “Transcendence”).

It was the essence of the ETER9 Project that was taking shape in my head.

Over the years and also with the evolution of technologies — and of the human being himself —, the concept “Counterpart” has been getting better and, with each passing day, it makes more sense!

Imagine a purely digital receptacle with the basics inside, like that Intermediate Software (BIOS⁽¹⁾) that computers have between the Hardware and the Operating System. That receptacle waits for you. One way or another, it waits patiently for you, as if waiting for a Soul to come alive in the ether of digital existence.

Continue reading “Digital Doubles and Second Selves” »

Summary: Female mice who have not been pregnant or given birth show activation in the anterior cingulate cortex when they acquire maternal behaviors after exposure to pups. The findings reveal through repeated exposure to pups, virgin female mice are capable of learning maternal behaviors that resemble those of mothers following birth.

Source: Medical University of Vienna.

Various conditions such as postpartum depression or postpartum psychosis can lead to an alteration in maternal behavior and disrupt the mother-child bonding process.

It gives new meaning to the phrase “speak your mind.

Do you remember how legendary cosmologist Stephen Hawking communicated using his special screen-equipped chair? Well, that was a brain-computer interface (BCI), a device that allows a person to communicate using their brain signals.

Continue reading “People with speech paralysis can now talk using this intelligent spelling device” »

“This is the first system that combines all the pieces; efficient energy harvesting, energy storage, and the controlled brain stimulator.”

Researchers have devised an ingenious way to power deep brain simulators — Using the person’s breathing movements.

About 150,000 deep brain stimulators are implanted every year. Normally placed under the skin in the chest area with electrodes implanted in the brain, these stimulators are known to help with neurological and psychiatric diseases when traditional treatments fail.

Summary: Mutations of the PTEN gene cause neurons to grow to twice the size and form four times the number of synaptic connections to other neurons as a normal neuron. Removing the RAPTOR gene, an essential gene in the mTORC1 signaling pathway, prevents the neuronal and synaptic overgrowth associated with PTEN mutations. Using Rapamycin to inhibit mTORC1 rescues all the changes in neuronal overgrowth.

Source: the geisel school of medicine at dartmouth.

Findings from a new study published in Cell Reports, involving a collaborative effort between researchers at the Luikart Laboratory at Dartmouth’s Geisel School of Medicine and the Weston Laboratory at the University of Vermont, are providing further insight into the neurobiological basis of autism spectrum disorders (ASD) and pointing to possible treatments.

Past neuroscience studies have consistently demonstrated that the aging of the mammalian nervous system is liked with a decline in the volume and functioning of white matter, nerve fibers found in deep brain tissues. Although this is now a well-established finding, the mechanisms underpinning the decline of white matter and associated pathologies are poorly understood.

Researchers at Ludwig Maximilian University (LMU) of Munich, Technical University of Munich, the German Center for Neurodegenerative Diseases, Munich Cluster of Systems Neurology and University Hospital Würzburg have recently carried out a study aimed at better understanding the neural mechanisms that might result in the deterioration of white matter. Their findings, published in Nature Neuroscience, suggest that adaptive immune responses could promote the loss of cells in aging white matter.

“Among the hallmarks of brain aging is a decline in white matter volume and function which leads to an increase in neurological disorders,” Mikael Simons and Özgün Gökce, two of the researchers who carried out the study, told Medical Xpress. “White matter contains nerve fibers (axons), which are extensions of nerve cells (neurons). Many of these nerve fibers are surrounded by a type of sheath or covering called myelin, which allows our neurons to communicate fast, and gives white matter its color.”