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Researchers at Texas A&M University have developed the first molecular therapeutic for Angelman syndrome to advance into clinical development.

In a new article, published today in Science Translational Medicine, Dr. Scott Dindot, an associate professor and EDGES Fellow in the Texas A&M School of Veterinary Medicine and Biomedical Sciences’ (VMBS) Department of Veterinary Pathobiology, and his team share the process through which they developed this novel therapeutic candidate, also known as 4.4.PS.L, or GTX-102. Dindot is also the executive director of molecular genetics at Ultragenyx, which is leading the development of GTX-102.

Angelman syndrome (AS) is a devastating, rare neurogenetic disorder that affects approximately 1 in 15,000 per year; the disorder is triggered by a loss of function of the maternal UBE3A gene in the brain, causing , absent speech, movement or balance disorder, and seizures.

Changes in the brain caused by Alzheimer’s disease are associated with shortening of the telomeres—the protective caps on the ends of chromosomes that shorten as cells age—according to a new study led by Anya Topiwala of Oxford Population Health, part of the University of Oxford, UK, published March 22 in the open-access journal PLOS ONE.

Telomeres on chromosomes protect DNA from degrading, but every time a cell divides, the telomeres lose some of their length. Short telomeres are a sign of stress and cellular aging, and are also associated with a higher risk of neurological and psychiatric disorders. Currently, little is known about the links between and changes that occur in the brains of people with neurological conditions. Understanding those relationships could offer insights into the biological mechanisms that cause neurodegenerative disorders.

In the new study, researchers compared telomere length in to results from brain MRIs and from more than 31,000 participants in the UK Biobank, a large-scale biomedical database and research resource containing anonymized genetic, lifestyle and from half a million UK participants.

“This interface could revolutionize the way we interact with technology.”

Researchers from the University of Cambridge have created a new type of neural implant that could restore limb function in paralyzed limbs.

There have been former attempts at using neural implants to restore limb function, but these mostly failed. This is because scar tissue can envelop the electrodes over time, disrupting the connection between the device and the nerve.


University of Cambridge.

The developed device works in sync between the brain and paralyzed limbs — it combines flexible electronics and human stem cells to “better integrate” with the nerve and drive limb function, according to a press release.

Near Death Experience Research Foundation the largest collection of Near Death Experiences (NDE) in over 23 Languages. With thousands of full-text near death experiences posted. Share your near death experience, research, spiritually transforming events, consciousness studies, extensive information and research.

In this video, we will explore the positional system of the brain — hippocampal place cells. We will see how it relates to contextual memory and mapping of more abstract features.

OUTLINE:
00:00 Introduction.
00:53 Hippocampus.
1:27 Discovery of place cells.
2:56 3D navigation.
3:51 Role of place cells.
4:11 Virtual reality experiment.
7:47 Remapping.
11:17 Mapping of non-spatial dimension.
13:36 Conclusion.

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REFERENCES:

1) Anderson, M.I., Jeffery, K.J., 2003. Heterogeneous Modulation of Place Cell Firing by Changes in Context. J. Neurosci. 23, 8827–8835. https://doi.org/10.1523/JNEUROSCI.23-26-08827.

2) Aronov, D., Nevers, R., Tank, D.W., 2017. Mapping of a non-spatial dimension by the hippocampal–entorhinal circuit. Nature 543719–722. https://doi.org/10.1038/nature21692

3) Bostock, E., Muller, R.U., Kubie, J.L., 1991. Experience-dependent modifications of hippocampal place cell firing. Hippocampus 1193-205. https://doi.org/10.1002/hipo.

For individuals suffering from drug addiction, certain cues—whether it’s specific people, places or things—can trigger powerful cravings for repeated use.

A new University of Michigan study has identified signals, traditionally associated with inflammation, contributing to people’s vulnerability to . With repeated drug use with the same exposure to cues, some individuals develop an inability to control their drug use, even in the face of negative consequences.

The study is published in the journal eNeuro.