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A remarkable new study has successfully used the CRISPR-Cas9 gene editing technique to edit a specific gene in mice engineered to have fragile X syndrome (FXS), a single-gene disorder often related to autism. The single gene edit in the live mice resulted in significant improvements in repetitive and obsessive behaviors, making this the first time gene editing has been used to effectively target behavioral symptoms related to autism spectrum disorder (ASD).

FXS is a genetic disorder associated with intellectual disability, seizures and exaggerated repetitive behavior. Previous studies have shown that the repetitive behaviors associated with FXS are related to a specific excitatory receptor in the brain that, when dysregulated, causes exaggerated signaling between cells.

The CRISPR technique homes in on the gene that controls that excitatory receptor, the metabotropic glutamate receptor 5 (mGluR5), and essentially disables it, dampening the excessive signaling the corresponds with repetitive behaviors. In mice treated with the new system, obsessive digging behavior was reduced by 30 percent and repetitive leaping actions dropped by 70 percent.

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For the first time ever researchers have had a breakthrough in creating a cocktail of drugs that caused new neurons to grow in the brains of mice.

In my last article I gave a detailed account on the debate of neurogenesis. While some neuroscientists claim that neurogenesis takes place within the adult mammalian human brain other researchers contest that idea claiming that new neurons stop developing at a very young age. Whichever side of the debate you are on one thing remains certain, that there are neurological diseases that leave negative impacts on cognitive function. This has left researchers looking for various ways to treat Alzheimer’s, Parkinson’s, and other brain damage.

While the brain is incredibly complex and past research has failed to offer much hope for Alzheimer’s disease, Hongkui Deng at Paking University Health Science Center in China may finally be able to change that.

For the first time ever researchers have had a breakthrough in creating a cocktail of drugs that caused new neurons to grow in the brains of mice.

What this cocktail does when injected into the brain is it hijacks the astrocytes into behaving like new neurons. This is significant for a number of reasons. One important detail about astrocyte cells is that they can survive after a stroke while regular neurons die. Another important detail is that there are 10 times more astrocytes in the brain than neurons. That means that there are 1 trillion glia cells within the brain. So not only are they more resilient than neurons they outnumber them too.

Deng and his team of researchers have found that when the cocktail is injected into the brains of mice that it effectively gives the cell a new identity by erasing its old one and giving it a new one. Not only did the cells change shape but they showed change in gene activity too.

The results were substantial. While it remains speculative as to how closely the cells resemble normal neurons, around 80 to 90 per cent of the astrocytes started to resemble neurons and even mimicked their behavior by electrical signals the same way regular neurons do.

“They are unlikely to be a 100 percent match” Deng stated. “But the treatment was safe and none of the mice developed any health problems”.

Matthew Grubb at King’s College London states that “if it holds up it’s absolutely amazing, and has a lot of potential applications and exciting consequences. If you’ve got a degenerating brain, for example in Alzheimer’s disease, and you could get the brain to regrow neurons itself, it would be a huge step forward.”

The next step for the researchers will be to test the cocktail in mice that have had a stroke. The hope is that the cocktail will cause the astrocytes to behave as neurons and help the mice recover.

While Grubb admits it is difficult to predict the effects of the treatment in humans, if it works in mice then it offers new hope for those who suffer from neurodegenerative diseases such as Alzheimer’s or Parkinson’s. While it is unlikely to bring back lost memories Grubb thinks it might restore the ability to create new ones.

Even though the research is promising there still remain challenges as Roger Barker at the University of Cambridge points out. The sheer numbers of cells lost in a neurodegenerative disease is something to consider. “In Parkinson’s, a quarter of a million cells are lost from either side of the brain. Currently Barker is conducting clinical trials of implants of brain tissue taken from aborted fetuses as a treatment for Parkinson’s.

Another challenge is to distinguish the types of neurons the drugs will make. As Grubb points out, if you make too many of the type of neurons that excites their neighbors you end up triggering epilepsy. Grubb also points out that different brain disorders effects different types of neurons which is another reason why we need to be capable of distinguishing them. The neurons that die from Parkinson’s are the neurons that create the chemical dopamine for example.

Another example is balancing the risks for rewards. As Grubb points out “you’d have to have extremely good control over what cells you’re programming, where they’re going to go, and which cells they’ll connect to. If the treatment were to be used to boost grey matter, for example, this could provide a way to improve skills like memory. However, too much grey matter has been linked to causing people to be being easily distracted.

While the research is definitely groundbreaking it is still in its early stages. Hopefully in the near future it will offer treatments to those who need them.

New Scientist

Buzz Aldrin wants people to know that he has some cool new ideas about how to get to the moon — not just because they’re cool, but also because they show his mind is working.

“That’s not an inactive, incapacitated, dependent mind,” the 88-year-old Aldrin, who became one of the first humans to walk on the moon during 1969’s Apollo 11 mission, told me today during a wide-ranging telephone interview.

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Chemical innovation plays a key role in developing cutting-edge technologies for the military. Research chemists design and synthesize new molecules that could enable a slew of next-generation military products, such as novel propellants for spacecraft engines; new pharmaceuticals and medicines for troops in the field; lighter and longer-lasting batteries and fuel cells; advanced adhesives, coatings and paints; and less expensive explosives that are safer to handle. The problem, however, is that existing molecule design and production methods rely primarily on experts’ intuition in a laborious, trial-and-error research process.

DARPA’s Make-It program, currently in year three of a four-year effort, is developing software tools based on machine learning and expert-encoded rules to recommend synthetic routes (i.e., the “recipe” to make a particular molecule) optimized for factors such as cost, time, safety, or waste reduction. The program seeks to free chemists so that they may focus their energy on chemical innovation, rather than testing various molecular synthesis pathways. The program also is developing automated devices that uniformly and reproducibly create the desired chemical based on the software-generated recipe – this one-device, many-molecules concept is a departure from the traditional dedicated reactors in chemical production. Make-It research teams have recently demonstrated significant progress toward fully automated rapid molecule production, which could speed the pace of chemical discovery for a range of defense products and applications.

“A seasoned research chemist may spend dozens of hours designing synthetic routes to a new molecule and months implementing and optimizing the synthesis in a lab,” said Anne Fischer, program manager in DARPA’s Defense Sciences Office. “Make-It is not only freeing chemists to expend brain power in other areas such as molecular discovery and innovation, it is opening chemical synthesis and discovery to a much broader community of scientific researchers who will benefit from faster development of new molecules.”

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Today, we have part one of a two-part interview with Dr. Michael Fossel, the driving force behind Telocyte, a new company focused on telomerase therapy for various diseases, and a strong advocate of telomerase therapy to treat human disease over the past three decades.

I interviewed Dr. Fossel as an individual thought leader in this field and not in his role representing Telocyte, so the opinions stated here are purely his own.

Born in 1950, Michael Fossel grew up in New York and lived in London, Palo Alto, San Francisco, Portland, and Denver. He graduated cum laude from Phillips Exeter Academy, received a joint B.A. and M.A. in psychology in four years from Wesleyan University in Connecticut, and, after completing a Ph.D. in neurobiology at Stanford University in 1978, went on to finish his M.D. at Stanford Medical School in two and a half years. He was awarded a National Science Foundation Fellowship and taught at Stanford University, where he began studying aging with an emphasis on premature aging syndromes. Dr. Fossel was a Clinical Professor of Medicine at Michigan State University for almost three decades and taught the Biology of Aging at Grand Valley State University.

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We have a ‘thirst for knowledge’ but sometime ‘ignorance is bliss’, so how do we choose between these two mind states at any given time?

UCL psychologists have discovered our brains use the same algorithm and neural architecture to evaluate the opportunity to gain information, as it does to evaluate rewards like food or money.

Funded by the Wellcome Trust, the research, published in the Proceedings of the National Academy of Sciences, also finds that people will spend money to both obtain advance knowledge of a good upcoming event and to remain ignorant of an upcoming bad event.

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In the past experimentation round Wendelstein 7-X achieved higher temperatures and densities of the plasma, longer pulses and the stellarator world record for the fusion product. Moreover, first confirmation for the optimisation concept on which Wendelstein 7-X is based, was obtained. Wendelstein 7-X at Max Planck Institute for Plasma Physics (IPP) in Greifswald, the world’s largest fusion device of the stellarator type, is investigating the suitability of this concept for application in power plants.

Unlike in the first experimentation phase 2015/16 the plasma vessel of Wendelstein 7-X has been fitted with interior cladding since September last year. The vessel walls are now covered with graphite tiles, thus allowing higher temperatures and longer plasma discharges. With the so-called divertor it is also possible to control the purity and density of the plasma: The divertor tiles follow the twisted contour of the plasma edge in the form of ten broad strips along the wall of the plasma vessel. In this way, they protect particularly the wall areas onto which the particles escaping from the edge of the plasma ring are made to impinge. Along with impurities, the impinging particles are here neutralised and pumped off.

“First experience with the new wall elements are highly positive”, states Professor Dr. Thomas Sunn Pedersen. While by the end of the first campaign pulse lengths of six seconds were being attained, plasmas lasting up to 26 seconds are now being produced. A heating energy of up to 75 megajoules could be fed into the plasma, this being 18 times as much as in the first operation phase without divertor. The heating power could also be increased, this being a prerequisite to high plasma density.

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