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Sensory hypersensitivity in mice with the Grin2b gene mutation found in patients is related to hyperactivity of the anterior cingulate cortex (ACC) and hyperconnectivity between the ACC and other brain regions. Credit: Institute for Basic Science.

Director Kim Eunjoon states, “This new research demonstrates the involvement of the anterior cingulate cortex (ACC), which has been known for its deep association with cognitive and social functions, in sensory hypersensitivity in autism.”

The hyperactivity of the ACC was also associated with the enhanced functional connectivity between the ACC and other brain areas. It is believed both hyperactivity and the hyperconnectivity of the ACC with various other brain regions are involved with sensory hypersensitivity in Grin2b-mutant mice.

Enhanced neuron growth in the hippocampus, achieved through exercise or genetic methods, aids mice in forgetting strong, maladaptive memories, offering potential for new treatments for PTSD or drug addiction.

Researchers at the University of Toronto, Canada, and Kyushu University, Japan, discovered that enhancing neuron production and subsequently altering neural connections in the hippocampus—through exercise or genetic intervention—enables mice to forget memories associated with trauma or drugs. The findings, reported in the journal Molecular Psychiatry, could offer a new approach to treating mental health conditions like post-traumatic stress disorder (PTSD) or drug addiction.

PTSD is a mental health condition that can be triggered by experiencing or seeing a traumatic event, such as a natural disaster, serious accident, or attack. Worldwide, around 3.9% of the general population has PTSD, with symptoms including vivid flashbacks and avoidance behaviors, such as staying away from places or pushing away people that remind them of the traumatic event.

The human genome is massive, and it contains many highly repetitive sequences that confounded researchers for years. Many of these repeats were simply written off as junk DNA that had no function. However, new research is revealing that many of these regions are much more important than we thought. Some of the repetitive portions of the genome are known to be human endogenous retroviruses (HERVs). These sequences originated from viruses that infected human germ cells millions of years ago and affected our evolution. About eight percent of our genome is thought to be made up of HERVs. These HERVs have also been associated with a variety of psychiatric disorders, although the connection is unclear.

A new study reported in Nature Communications has suggested that HERVs are making a significant but unappreciated contribution to the development of psychiatric disorders, and that they may help explain a genetic component of these disorders that is thought to exist but has not yet been identified.

One tool, called Find My Understudied Genes (FMUG), emerged from a study published in March¹, which first explores why interesting, but relatively under-researched, genes are not highlighted in genetic surveys, and then offers FMUG as a remedy.

The second tool is the Unknome database, created by a team led by Matthew Freeman at the University of Oxford, UK, and Sean Munro at the MRC Laboratory of Molecular Biology, Cambridge, UK, that was described² in 2023.

“We are in the lucky position to know what we don’t know,” says Thomas Stoeger, a biologist at Northwestern University in Chicago, Illinois, and co-author of the FMUG study.

New study could improve the ability to make genetic diagnoses and treat neurodevelopmental disorders.

Imagine a technology that could genetically rewire organisms in real-time, silencing critical genes across entire ecosystems with unknown effects.

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Scientists have pinpointed genetic changes that can leave children born with little to no immune defense against infection.

Retinitis pigmentosa and macular degeneration lead to photoreceptor death and loss of visual perception. Despite recent progress, restorative technologies for photoreceptor degeneration remain largely unavailable. Here, we describe a novel optogenetic visual prosthesis (FlexLED) based on a combination of a thin-film retinal display and optogenetic activation of retinal ganglion cells (RGCs). The FlexLED implant is a 30 µm thin, flexible, wireless µLED display with 8,192 pixels, each with an emission area of 66 µm2. The display is affixed to the retinal surface, and the electronics package is mounted under the conjunctiva in the form factor of a conventional glaucoma drainage implant. In a rabbit model of photoreceptor degeneration, optical stimulation of the retina using the FlexLED elicits activity in visual cortex. This technology is readily scalable to hundreds of thousands of pixels, providing a route towards an implantable optogenetic visual prosthesis capable of generating vision by stimulating RGCs at near-cellular resolution.

### Competing Interest Statement.

All authors have a financial interest in Science Corporation.