Last Week In Science

New Approach to Treating Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the most common form of dementia. In search for new drugs for AD, the research team, led by Professor Mi Hee Lim of Natural Science at UNIST has developed a metal-based substance that works like a pair of genetic scissors to cut out amyloid-β (Aβ), the hallmark protein of AD.

The study has been featured on the cover of the January 2017 issue of the Journal of the American Chemical Society (JACS) and has been also selected as a JACS Spotlight article.

Alzheimer’s disease is the sixth leading cause of death among in older adults. The exact causes of Alzheimer’s disease are still unknown, but several factors are presumed to be causative agents. Among these, the aggregation of amyloid-β peptide (Aβ) has been implicated as a contributor to the formation of neuritic plaques, which are pathological hallmarks of Alzheimer’s disease (AD).

As therapeutics for AD, Professor Lim suggested a strategy that uses metal-based complexes for reducing the toxicity of the amyloid beta (Aβ). Althought various metal complexes have been suggested as therapeutics for AD, none of them work effectively in vivo.

The research team has found that they can hydrolyze amyloid-beta proteins using a crystal structure, called tetra-N methylated cyclam (TMC). Hydrolysis is the process that uses water molecules to split other molecules apart. The metal-mediated TMC structure uses the external water and cut off the binding of amyloid-beta protein effectively.

In this study, the following four metals (cobalt, nickel, copper and zinc) were placed at the center of the TMC structure. When the double-layered cobalt was added to the center, the hydrolysis activity was at the highest.

The research team reported that the cobalt-based metal complex (Co(II)(TMC)) had the potential to penetrate the blood brain barrier and the hydrolysis activity for nonamyloid protein was low. Moreover, the effects of this substance on the toxicity of amyloid-beta protein were also observed in living cell experiments.

“This material has a high therapeutic potential in the treatment of Alzheimer’s disease as it can penetrate the brain-vascular barrier and directly interact with the amyloid-beta protein in the brain,” says Professor Lim.

This study has also attracted attention by the editor of the Journal of the American Chemical Society. “Not only do they develop new materials, but they have been able to propose details of the working principles and experiments that support them,” according to the editor.

“As a scientist, this is such a great honor to know that our recent publication in JACS was highlighted in JACS Spotlights,” says Professor Lim. “This means that our research has not only been recognized as an important research, but also has caused a stir in academia.”

Life Continues Within the Body After Death, Evidence Shows

The body keeps working to repair itself after death, according to a provocative new study that could offer insight into how we might put the big sleep on hold.

Even after someone is declared dead, life continues in the body, suggests a surprising new study with important implications.

Gene expression — when information stored in DNA is converted into instructions for making proteinsor other molecules — actually increases in some cases after death, according to the new paper, which tracked postmortem activity and is published in the journal Open Biology.

“Not all cells are ‘dead’ when an organism dies,” senior author Peter Noble of the University of Washington and Alabama State University told Seeker. “Different cell types have different life spans, generation times and resilience to extreme stress.”  

In fact, some cells seem to fight to live after the organism has died.

“It is likely that some cells remain alive and are attempting to repair themselves, specifically stem cells,” Noble said.

A special organic dye, Nile Red in different solvents.

From left to right I dissolved equal amounts of Nile Red (a dye) in different solvents. The solvents were: methanol, diisopropyl ether, hexane, n-propanol, tetrahydrofuran, toluene, ethanol, acetone.

Depending on the solvents polarity, the dye dissolved to give different colored solutions (upper image), this is called solvatochromism. It is the ability of a chemical substance to change color due to a change in solvent polarity.

Under UV light, these solutions emitted different colors (bottom pics), this is called solvatofluorescence. The emission and excitation wavelength both shift depending on solvent polarity, so it fluoresces with different color depending on the solvent what it’s dissolved in.

Nile Red is a quite expensive dye, which costs a bit over 1000 USD/gram, therefore I had to make it. The purification of the raw material was posted HERE. 

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WATCH: Incredible Fungi Timelapse from Planet Earth II [video]

Scientists are pretty sure that deep inside the moon, there’s water

While Earth’s surface cracks and spouts fire, the moon’s surface, for as long as we’ve known it, has been quiet. 

The youngest sign of volcanic activity scientists have found on the moon’s surface is 18 million years old.

But the traces of that long-ago volcanic activity could help scientists crack an enduring mystery: How much water is on the moon?

A study published Monday in Nature Geoscience suggests it may be more than we thought. Read more (7/24/17)

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Scientists show how drug binds with ‘hidden pocket’ on flu virus

A new study led by scientists at The Scripps Research Institute (TSRI) is the first to show exactly how the drug Arbidol stops influenza infections. The research reveals that Arbidol stops the virus from entering host cells by binding within a recessed pocket on the virus.

The researchers believe this new structural insight could guide the development of future broad-spectrum therapeutics that would be even more potent against influenza virus.

“This is a very interesting molecule, and now we know where it binds and precisely how it works,” said study senior author Ian Wilson, Hanson Professor of Structural Biology, chair of the Department of Integrative Structural and Computational Biology and member of the Skaggs Institute for Chemical Biology at TSRI.

The study was published in the journal Proceedings of the National Academy of Sciences.

Rameshwar U. Kadam, Ian A. Wilson. Structural basis of influenza virus fusion inhibition by the antiviral drug Arbidol. Proceedings of the National Academy of Sciences, 2016; 201617020 DOI: 10.1073/pnas.1617020114

This is a 3-dimensional illustration showing the different features of an influenza virus, including the surface proteins hemagglutinin (HA) and neuraminidase (NA)/CDC

Largest Batch of Earth-size, Habitable Zone Planets

Our Spitzer Space Telescope has revealed the first known system of seven Earth-size planets around a single star. Three of these planets are firmly located in an area called the habitable zone, where liquid water is most likely to exist on a rocky planet.

This exoplanet system is called TRAPPIST-1, named for The Transiting Planets and Planetesimals Small Telescope (TRAPPIST) in Chile. In May 2016, researchers using TRAPPIST announced they had discovered three planets in the system.

Assisted by several ground-based telescopes, Spitzer confirmed the existence of two of these planets and discovered five additional ones, increasing the number of known planets in the system to seven.

This is the FIRST time three terrestrial planets have been found in the habitable zone of a star, and this is the FIRST time we have been able to measure both the masses and the radius for habitable zone Earth-sized planets.

All of these seven planets could have liquid water, key to life as we know it, under the right atmospheric conditions, but the chances are highest with the three in the habitable zone.

At about 40 light-years (235 trillion miles) from Earth, the system of planets is relatively close to us, in the constellation Aquarius. Because they are located outside of our solar system, these planets are scientifically known as exoplanets. To clarify, exoplanets are planets outside our solar system that orbit a sun-like star.

In this animation, you can see the planets orbiting the star, with the green area representing the famous habitable zone, defined as the range of distance to the star for which an Earth-like planet is the most likely to harbor abundant liquid water on its surface. Planets e, f and g fall in the habitable zone of the star.

Using Spitzer data, the team precisely measured the sizes of the seven planets and developed first estimates of the masses of six of them. The mass of the seventh and farthest exoplanet has not yet been estimated.

For comparison…if our sun was the size of a basketball, the TRAPPIST-1 star would be the size of a golf ball.

Based on their densities, all of the TRAPPIST-1 planets are likely to be rocky. Further observations will not only help determine whether they are rich in water, but also possibly reveal whether any could have liquid water on their surfaces.

The sun at the center of this system is classified as an ultra-cool dwarf and is so cool that liquid water could survive on planets orbiting very close to it, closer than is possible on planets in our solar system. All seven of the TRAPPIST-1 planetary orbits are closer to their host star than Mercury is to our sun.

 The planets also are very close to each other. How close? Well, if a person was standing on one of the planet’s surface, they could gaze up and potentially see geological features or clouds of neighboring worlds, which would sometimes appear larger than the moon in Earth’s sky.

The planets may also be tidally-locked to their star, which means the same side of the planet is always facing the star, therefore each side is either perpetual day or night. This could mean they have weather patterns totally unlike those on Earth, such as strong wind blowing from the day side to the night side, and extreme temperature changes.

Because most TRAPPIST-1 planets are likely to be rocky, and they are very close to one another, scientists view the Galilean moons of Jupiter – lo, Europa, Callisto, Ganymede – as good comparisons in our solar system. All of these moons are also tidally locked to Jupiter. The TRAPPIST-1 star is only slightly wider than Jupiter, yet much warmer. 

How Did the Spitzer Space Telescope Detect this System?

Spitzer, an infrared telescope that trails Earth as it orbits the sun, was well-suited for studying TRAPPIST-1 because the star glows brightest in infrared light, whose wavelengths are longer than the eye can see. Spitzer is uniquely positioned in its orbit to observe enough crossing (aka transits) of the planets in front of the host star to reveal the complex architecture of the system. 

Every time a planet passes by, or transits, a star, it blocks out some light. Spitzer measured the dips in light and based on how big the dip, you can determine the size of the planet. The timing of the transits tells you how long it takes for the planet to orbit the star.

The TRAPPIST-1 system provides one of the best opportunities in the next decade to study the atmospheres around Earth-size planets. Spitzer, Hubble and Kepler will help astronomers plan for follow-up studies using our upcoming James Webb Space Telescope, launching in 2018. With much greater sensitivity, Webb will be able to detect the chemical fingerprints of water, methane, oxygen, ozone and other components of a planet’s atmosphere.

At 40 light-years away, humans won’t be visiting this system in person anytime soon…that said…this poster can help us imagine what it would be like: 

Make sure to follow us on Tumblr for your regular dose of space: http://nasa.tumblr.com

Archbishop Ussher’s chronology was taken as gospel in the Western world. Until we turned to another book to find the age of the earth, the one that was written in the rocks themselves.

Today is the Autumn Equinox in the northern hemisphere! What’s behind the changing colours of autumn leaves? http://wp.me/p4aPLT-sn

Shocking New Role Found for the Immune System: Controlling Social Interactions

In a startling discovery that raises fundamental questions about human behavior, researchers at the University of Virginia School of Medicine have determined that the immune system directly affects – and even controls – creatures’ social behavior, such as their desire to interact with others.

So could immune system problems contribute to an inability to have normal social interactions? The answer appears to be yes, and that finding could have significant implications for neurological diseases such as autism-spectrum disorders and schizophrenia.

“The brain and the adaptive immune system were thought to be isolated from each other, and any immune activity in the brain was perceived as sign of a pathology. And now, not only are we showing that they are closely interacting, but some of our behavior traits might have evolved because of our immune response to pathogens,” explained Jonathan Kipnis, chair of UVA’s Department of Neuroscience. “It’s crazy, but maybe we are just multicellular battlefields for two ancient forces: pathogens and the immune system. Part of our personality may actually be dictated by the immune system.”

Evolutionary Forces at Work

It was only last year that Kipnis, the director of UVA’s Center for Brain Immunology and Glia, and his team discovered that meningeal vessels directly link the brain with the lymphatic system. That overturned decades of textbook teaching that the brain was “immune privileged,” lacking a direct connection to the immune system. The discovery opened the door for entirely new ways of thinking about how the brain and the immune system interact.

(Image caption: Normal brain activity, left, and a hyper-connected brain. Credit: Anita Impagliazzo, UVA Health System)

The follow-up finding is equally illuminating, shedding light on both the workings of the brain and on evolution itself. The relationship between people and pathogens, the researchers suggest, could have directly affected the development of our social behavior, allowing us to engage in the social interactions necessary for the survival of the species while developing ways for our immune systems to protect us from the diseases that accompany those interactions. Social behavior is, of course, in the interest of pathogens, as it allows them to spread.

The UVA researchers have shown that a specific immune molecule, interferon gamma, seems to be critical for social behavior and that a variety of creatures, such as flies, zebrafish, mice and rats, activate interferon gamma responses when they are social. Normally, this molecule is produced by the immune system in response to bacteria, viruses or parasites. Blocking the molecule in mice using genetic modification made regions of the brain hyperactive, causing the mice to become less social. Restoring the molecule restored the brain connectivity and behavior to normal. In a paper outlining their findings, the researchers note the immune molecule plays a “profound role in maintaining proper social function.”

“It’s extremely critical for an organism to be social for the survival of the species. It’s important for foraging, sexual reproduction, gathering, hunting,” said Anthony J. Filiano, Hartwell postdoctoral fellow in the Kipnis lab and lead author of the study. “So the hypothesis is that when organisms come together, you have a higher propensity to spread infection. So you need to be social, but [in doing so] you have a higher chance of spreading pathogens. The idea is that interferon gamma, in evolution, has been used as a more efficient way to both boost social behavior while boosting an anti-pathogen response.”

Understanding the Implications

The researchers note that a malfunctioning immune system may be responsible for “social deficits in numerous neurological and psychiatric disorders.” But exactly what this might mean for autism and other specific conditions requires further investigation. It is unlikely that any one molecule will be responsible for disease or the key to a cure. The researchers believe that the causes are likely to be much more complex. But the discovery that the immune system – and possibly germs, by extension – can control our interactions raises many exciting avenues for scientists to explore, both in terms of battling neurological disorders and understanding human behavior.

“Immune molecules are actually defining how the brain is functioning. So, what is the overall impact of the immune system on our brain development and function?” Kipnis said. “I think the philosophical aspects of this work are very interesting, but it also has potentially very important clinical implications.”

Findings Published

Kipnis and his team worked closely with UVA’s Department of Pharmacology and with Vladimir Litvak’s research group at the University of Massachusetts Medical School. Litvak’s team developed a computational approach to investigate the complex dialogue between immune signaling and brain function in health and disease.

“Using this approach we predicted a role for interferon gamma, an important cytokine secreted by T lymphocytes, in promoting social brain functions,” Litvak said. “Our findings contribute to a deeper understanding of social dysfunction in neurological disorders, such as autism and schizophrenia, and may open new avenues for therapeutic approaches.”

The findings have been published online by the prestigious journal Nature.