Posts Tagged ‘science’

Biology encodes information in DNA and RNA, which are complex molecules finely tuned to their functions. But are they the only way to store hereditary molecular information? Some scientists believe life as we know it could not have existed before there were nucleic acids, thus understanding how they came to exist on the primitive Earth is a fundamental goal of basic research. The central role of nucleic acids in biological information flow also makes them key targets for pharmaceutical research, and synthetic molecules mimicking nucleic acids form the basis of many treatments for viral diseases, including HIV. Other nucleic acid-like polymers are known, yet much remains unknown regarding possible alternatives for hereditary information storage. Using sophisticated computational methods, scientists from the Earth-Life Science Institute (ELSI) at the Tokyo Institute of Technology, the German Aerospace Center (DLR) and Emory University explored the “chemical neighbourhood” of nucleic acid analogues. Surprisingly, they found well over a million variants, suggesting a vast unexplored universe of chemistry relevant to pharmacology, biochemistry and efforts to understand the origins of life. The molecules revealed by this study could be further modified to gives hundreds of millions of potential pharmaceutical drug leads.

Nucleic acids were first identified in the 19th century, but their composition, biological role and function were not understood by scientists until the 20th century. The discovery of DNA’s double-helical structure by Watson and Crick in 1953 revealed a simple explanation for how biology and evolution function. All living things on Earth store information in DNA, which consists of two polymer strands wrapped around each other like a caduceus, with each strand being the complement of the other. When the strands are pulled apart, copying the complement on either template results in two copies of the original. The DNA polymer itself is composed of a sequence of “letters”, the bases adenine (A), guanine (G), cytosine (C) and thymine (T), and living organisms have evolved ways to make sure during DNA copying that the appropriate sequence of letters is almost always reproduced. The sequence of bases is copied into RNA by proteins, which then is read into a protein sequence. The proteins themselves then enable a wonderland of finely-tuned chemical processes which make life possible.

Small errors occasionally occur during DNA copying, and others are sometimes introduced by environmental mutagens. These small errors are the fodder for natural selection: some of these errors result in sequences which produce fitter organisms, though most have little effect, and many even prove lethal. The ability of new sequences to allow their hosts to better survive is the “ratchet” which allows biology to almost magically adapt to the constantly changing challenges the environment provides. This is the underlying reason for the kaleidoscope of biological forms we see around us, from humble bacteria to tigers, the information stored in nucleic acids allows for “memory” in biology. But are DNA and RNA the only way to store this information? Or are they perhaps just the best way, discovered only after millions of years of evolutionary tinkering?

“There are two kinds of nucleic acids in biology, and maybe 20 or 30 effective nucleic acid-binding nucleic acid analogues. We wanted to know if there is one more to be found or even a million more. The answer is, there seem to be many, many more than was expected,” says professor Jim Cleaves of ELSI.

Though biologists don’t consider them organisms, viruses also use nucleic acids to store their heritable information, though some viruses use a slight variant on DNA, RNA, as their molecular storage system. RNA differs from DNA in the presence of a single atom substitution, but overall RNA plays by very similar molecular rules as DNA. The remarkable thing is, among the incredible variety of organisms on Earth, these two molecules are essentially the only ones biology uses.

Biologists and chemists have long wondered why this should be. Are these the only molecules that could perform this function? If not, are they perhaps the best, that is to say, other molecules could play this role, and perhaps biology tried them out during evolution?

The central importance of nucleic acids in biology has also long made them drug targets for chemists. If a drug can inhibit the ability of an organism or virus to pass its knowledge of how to be infectious on to offspring, it effectively kills the organisms or virus. Mucking up the heredity of an organism or virus is a great way to knock it dead. Fortunately for chemists, and all of us, the cellular machinery which manages nucleic acid copying in each organism is slightly different, and in viruses often very different.

Organisms with large genomes, like humans, need to be very careful about copying their hereditary information and thus are very selective about not using the wrong precursors when copying their nucleic acids. Conversely, viruses, which generally have much smaller genomes, are much more tolerant of using similar, but slightly different molecules to copy themselves. This means chemicals that are similar to the building blocks of nucleic acids, known as nucleotides, can sometimes impair the biochemistry of one organism worse than another. Most of the important anti-viral drugs used today are nucleotide (or nucleoside, which are molecule differing by the removal of a phosphate group) analogues, including those used to treat HIV, herpes and viral hepatitis. Many important cancer drugs are also nucleotide or nucleoside analogues, as cancer cells sometimes have mutations that make them copy nucleic acids in unusual ways.

“Trying to understand the nature of heredity, and how else it might be embodied, is just about the most basic research one can do, but it also has some really important practical applications,” says co-author Chris Butch, formerly of ELSI and now a professor at Nanjing University.

Since most scientists believe the basis of biology is heritable information, without which natural selection would be impossible, evolutionary scientists studying the origins of life have also focused on ways of making DNA or RNA from simple chemicals that might have occurred spontaneously on primitive Earth. Once nucleic acids existed, many problems in the origins of life and early evolution would make sense. Most scientists think RNA evolved before DNA, and for subtle chemical reasons which make DNA much more stable than RNA, DNA became life’s hard disk. However, research in the 1960s soon split the theoretical origins field in two: those who saw RNA as the simple “Occam’s Razor” answer to the origins-of-biology problem and those who saw the many kinks in the armour of RNA’s abiological synthesis. RNA is still a complicated molecule, and it is possible structurally simpler molecules could have served in its place before it arose.

Co-author Dr. Jay Goodwin, a chemist with Emory University says “It is truly exciting to consider the potential for alternate genetic systems, based on these analogous nucleosides – that these might possibly have emerged and evolved in different environments, perhaps even on other planets or moons within our solar system. These alternate genetic systems might expand our conception of biology’s ‘central dogma’ into new evolutionary directions, in response and robust to increasingly challenging environments here on Earth.”

Examining all of these basic questions, which molecule came first, what is unique about RNA and DNA, all at once by physically making molecules in the laboratory, is difficult. On the other hand, computing molecules before making them could potentially save chemists a lot of time. “We were surprised by the outcome of this computation,” says co-author Dr. Markus Meringer, “it would be very difficult to estimate a priori that there are more than a million nucleic-acid like scaffolds. Now we know, and we can start looking into testing some of these in the lab.”

“It is absolutely fascinating to think that by using modern computational techniques we might stumble upon new drugs when searching for alternative molecules to DNA and RNA that can store hereditary information. It is cross-disciplinary studies such as this that make science challenging and fun yet impactful,” says co-author Dr. Pieter Burger, also of Emory University.

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Reference:

Henderson James Cleaves, II*1,2,3, Christopher Butch1,3,4, Pieter Buys Burger4, Jay Goodwin4, and Markus Meringer5, One Among Millions: The Chemical Space of Nucleic Acid-Like Molecules, Journal of Chemical Information and Modeling, DOI: 10.1021/acs.jcim.9b00632

1. Earth-Life Science Institute, Tokyo Institute of Technology, 2-12-IE-1 Ookayama, Meguro-ku, Tokyo 152-8551, Japan
2. Institute for Advanced Study, Princeton, New Jersey 08540, United States

3. Blue Marble Space Institute for Science, 1515 Gallatin St. NW, Washington, DC 20011, United States

4. Department of Chemistry, Emory University, 1515 Dickey Dr., Atlanta, Georgia 30322, United States

5. German Aerospace Center (DLR), Earth Observation Center (EOC), Münchner Straße 20, 82234 Oberpfaffenhofen-Wessling, Germany

https://www.eurekalert.org/pub_releases/2019-11/tiot-dio103119.php


Francisco Lopera, a neurologist at the University of Antioquia in Medellin, Colombia, has been painstakingly collecting brains, birth and death records from one sprawling Colombian family to study Alzheimer’s.Credit…Federico Rios Escobar for The New York Times


A woman with lots of beta-amyloid buildup (red) in her brain remained cognitively healthy for decades.

by Kelly Servick

In 2016, a 73-year-old woman from Medellín, Colombia, flew to Boston so researchers could scan her brain, analyze her blood, and pore over her genome. She carried a genetic mutation that had caused many in her family to develop dementia in middle age. But for decades, she had avoided the disease. The researchers now report that another rare mutation—this one in the well-known Alzheimer’s disease risk gene APOE—may have protected her. They can’t prove this mutation alone staved off disease. But the study draws new attention to the possibility of preventing or treating Alzheimer’s by targeting APOE—an idea some researchers say has spent too long on the sidelines.

“This case is very special,” says Yadong Huang, a neuroscientist at the Gladstone Institutes in San Francisco, California, who was not involved with the research. “This may open up a very promising new avenue in both research and therapy.”

APOE, the strongest genetic risk factor for Alzheimer’s, has three common forms. A variant called APOE2 lowers risk of the disease. The most common variant, APOE3, doesn’t influence risk. APOE4 raises risk; roughly half of the people with the disease have at least one copy of this variant.

Researchers have long contemplated targeting APOE with therapies. A team at Cornell University will soon start a clinical trial that infuses the protective APOE2 gene into the cerebrospinal fluid of people with two copies of APOE4.

But mysteries about APOE have kept it from becoming a front-runner among drug targets. “It does so many things that it’s confusing,” says Eric Reiman, a neuroscientist at the Banner Alzheimer’s Institute in Phoenix and a co-author on the new paper. The APOE protein binds and transports fats and is abundant in the brain. And the APOE4 variant seems to encourage the formation of sticky plaques of the protein beta-amyloid, which clog the brain in Alzheimer’s. But powerful amyloid-busting drugs have repeatedly failed to benefit patients in clinical trials. Some researchers saw no reason to try an APOE-targeting therapy that seemed to be “just a poor man’s antiamyloid treatment,” Reiman says.

The Colombian woman’s case suggests other ways APOE could affect Alzheimer’s risk. The woman participated in a study led by researchers at the University of Antioquia in Medellín that has tracked roughly 6000 members of her extended family. About one-fifth of them carried an Alzheimer’s-causing mutation in a gene called presenilin 1; these carriers generally developed dementia in their late 40s. Yet the woman didn’t show the first signs of the disease until her 70s, even though she, too, carried the mutation. “She’s definitely an outlier,” says cell biologist Joseph Arboleda-Velasquez of Harvard Medical school in Boston. (The research team is keeping the woman’s name confidential to protect her privacy.)

In Boston, a positron emission tomography scan of the woman’s brain revealed more amyloid buildup than in any other family member who has been scanned. “It was very striking,” says Yakeel Quiroz, a clinical neuropsychologist at Massachusetts General Hospital and Harvard Medical School. But the team found no signs of major damage to neurons, and minimal buildup of another Alzheimer’s hallmark: the misfolded protein tau. Whatever protection this woman had didn’t depend on keeping the brain amyloid-free. Instead, her case supports the idea that tau has a “critical role … in the clinical manifestations of Alzheimer’s disease,” says Jennifer Yokoyama, a neurogeneticist at the University of California, San Francisco.

Genome sequencing revealed two copies of a rare mutation in the APOE gene, the researchers report this week in Nature Medicine. First discovered in 1987, the mutation, known as Christchurch, occurs in a region separate from those that determine a person’s APOE2, 3, or 4 status. (The woman has the neutral APOE3 variant.) Previous research found that the Christchurch mutation—like the more common protective APOE2 mutation—impairs APOE’s ability to bind to and clear away fats and sometimes leads to cardiovascular disease.

The researchers also found that the mutation prevents APOE from binding strongly to other molecules called heparan sulfate proteoglycans (HSPGs), which coat neurons and other cells “like a carpet,” says Guojun Bu, a neuroscientist at the Mayo Clinic in Jacksonville, Florida, who has studied the interaction between these molecules and APOE.

APOE2 may also impair the protein’s ability to bind HSPGs. But how that could protect against disease isn’t clear. One possible clue: Research by neuroscientist Marc Diamond of the University of Texas Southwestern Medical Center in Dallas and his colleagues suggest the toxic tau protein relies on HSPGs to help it spread between cells. Maybe the less APOE binds to HSPGs, the harder it is for tau to spread.

But, Diamond cautions, “It will require much more study to understand if this relationship exists.” The Christchurch mutation might have protective effects unrelated to HSPGs; it’s also possible that mutations other than Christchurch protected the woman.

If hampering APOE’s normal binding really staved off her Alzheimer’s, future treatments might aim to mimic that effect. An antibody or small molecule could latch onto the APOE protein to interfere with binding, gene editing could change the structure of APOE to imitate the Christchurch variant, or a “gene silencing” approach could reduce production of APOE altogether.

Reiman hopes the new study will rally researchers to pursue treatments related to APOE. He, Quiroz, Arboleda-Velasquez, and other collaborators also posted a preprint on the medRxiv server on 2 November showing that people with two copies of APOE2 have lower Alzheimer’s risk than previously thought—about 99% lower than people with two copies of APOE4. “When it comes to finding a treatment that could have a profound impact on the disease,” Reiman says, “APOE may be among the lowest hanging fruit.”

https://science.sciencemag.org/content/366/6466/674


With pressure to “publish or perish,” some scientists fake their research results. Elisabeth Bik spends her days correcting them.

by Gemma Milne

Elisabeth Bik spends her days trawling scientific papers, life sciences papers in particular, looking for signs of image manipulation. Put another way, she plays a backward game of “spot the difference” (backward because it’s more like “spot the similarity”) to seek out fraudulent work posing as science. She does this for free, week after week, along with other online science misconduct sleuths, in the pursuit of correcting the record upon which the world’s knowledge is based.

She is a self-appointed, image-manipulation detective — the Sherlock Holmes of science fraud.

It started with plagiarism before plagiarism became easy to catch. After reading about its prevalence in scientific papers, Bik, who had a 15-year career as a microbiology researcher, searched Google Scholar and found her own work had been copied. Then she set about finding other instances of this particular fraud. On one such investigation, she found a PhD thesis that not only had plagiarized text, but also an image that was reused throughout. The author had been trying to pass off the same image as a series of distinct results. “[The image] was mirrored, or turned around, but it had a very distinct little smear, which I recognized,” she says.

After reporting the fraudulent thesis to the university, resulting in its retraction, Bik realized she’d stumbled upon a new, strange hobby. “That was something I was good at, recognizing these patterns,” she says, “and so I started doing that more and more.” She soon found herself going through swaths of research papers during her evenings and weekends, and looking forward to getting home from her day job to continue.

It wasn’t long before Bik had amassed a huge collection of fraudulent papers. In 2016, she co-authored a paper revealing the fruits of her labor. Within her manual search of more than 20,000 pieces of biomedical research, 4% contained manipulated images. She reported those 800 papers, and she’s continued searching, sharing, and reporting ever since.

One of the initial 800 papers she reported was by Min-Jean Yin, who led the Pfizer California cancer lab at the time of the paper’s publication. It contained duplicated images of western blots, a common test used to detect specific protein molecules. The images produced from the test are the data, so editing them essentially amounts to chopping and changing results to fit whatever hypothesis the scientist is trying to prove.

After Bik reported the abnormalities both on popular research discussion forum PubPeer as well as on the science misconduct blog For Better Science, Pfizer not only fired Yin but also opened up a larger investigation into her years of work at their lab. This led them to retract many of her published papers focused on cancer therapeutics.


Image from the PubPeer listing questioning of one of Yin’s 2011 papers, with the red box annotating a copied crop. Credit: PubPeer

Bik is prolific on PubPeer and on Twitter, where she posts multicolored annotated graphics that point out how images have been manipulated to nearly 40,000 followers. “I’ve been a very quiet microbiologist until a few years ago when I joined Twitter,” she says with a laugh.

After earning a PhD in the Netherlands, 15 years at Stanford, and a few years in the science startup scene, this year, both Bik and her husband decided to take the leap into working on personal projects instead of for companies. Looking for fraud in research is more than just a fun hobby for Bik. “I’ve found this niche that I feel I can make a difference in,” she says. “I felt it was calling me.”

Bik often picks open-access journals, as they’re easier to flick through, or papers that are requested by other scientists who are tipping her off. “What I’m doing now is going into all the image manipulation cases I’ve already found and finding other papers by the same author, which could be in other journals.”

Living off savings, Bik reckons she has about a year’s leeway to work on her image manipulation sleuthing and hopes to find a way of monetizing her expertise as a science misconduct consultant to journals.

Published work in prestigious academic journals is the main currency of the science world, and career progression, respect, and compensation are often linked to publishing reputation. The most significant journals only publish research with big implications and strong evidence that represents a leap in knowledge, not just an incremental addition. Unfortunately, this can’t always be achieved through grit, hard work, and the right area of research, so some scientists succumb to “publish or perish” pressure by editing their images to show clearer results, re-using images to convey “desirable” scientific claims, or photoshopping their graphs to back up false, but exciting findings.

Other scientists may spend years of time and huge amounts of research funding trying to build upon false science. “My goal is not to have people disciplined; my goal is to correct the science,” Bik explains.

Despite Bik’s work finding these manipulations, she estimates that only 30% of those papers have been corrected or retracted. “By tweeting about it, I hope to accomplish two things,” she explains. “First, put pressure on journals to react, like those viral videos where people are mistreated on airplanes. And second, make them aware that fraud happens, so when they see a paper, they know what to look for.”

Journals are notoriously bad at handling scientific misconduct. Sometimes this failing is understandable: Correcting or retracting a published paper could mean getting in touch with a myriad of authors, who may have since changed universities, never reply, or be unable to produce the original data. It requires time and patience to hunt down either the rationale for an honest mistake or the admission of misconduct, and it reduces the bottom line of these profit-making enterprises.

But sometimes the lack of investigation is unjustified. Journals have been known to reject complaints that aren’t submitted correctly through their complex and out-of-date online systems, or — more worryingly — come from anonymous submissions. Ivan Oransky, co-founder of Retraction Watch, which keeps track of scientific retractions, says: “I would love for scientists, journals, and universities who refuse to take seriously anonymous complaints and allegations about papers to tell me how they feel about the anonymous whistle-blower [who brought forth concerns about President Donald Trump’s dealings with Ukraine].”

Because reputation is paramount in science, anonymity is often required.

Much of the sleuthing is done by active scientists who use pseudonyms for fear of being ousted by their university or ostracized by the affected researchers. One such sleuth is Smut Clyde who, like Bik, spends huge amounts of time finding irregularities, knowing that their anonymous posts may not be accepted by the journals. “There are an awful lot of scientists [committing fraud]. Just picking out one or two doesn’t really make much of a difference — it’s just a drop in the ocean,” they told OneZero. “The best we can hope for is to raise awareness that the ocean is rather full already and ultimately shift the incentives. It’s more long-term than identifying one particular person who is up to no good.”

Bik is well-known and well-respected within the science misconduct community, not only for the prolific nature of her work but also because she writes and reports under her own name. In some ways, then, Bik is a surrogate for so many. She posts and reports publicly, often after being tipped off to papers from those who aren’t able to do it themselves: “Every day I get a new request.”

“I hope more people join me in the image manipulation search, as I feel we need more people doing this. There’s so many papers and I feel we need to clean ship.”
It’s the volunteers, the puzzle aficionados, the ones who do it because they feel they must, that are holding science to account. Conan Doyle’s fictional Sherlock Holmes famously inspired changes in police reporting; maybe one day the tenacity and sharp eyes of Bik and the rest of the image manipulation sleuths might inspire the institutions of science to do the same.

https://onezero.medium.com/this-science-vigilante-calls-out-bogus-results-in-prestigious-journals-eb5a414c7f76

By Julie Zaugg and Jared Peng

Authorities in China have approved a drug for the treatment of Alzheimer’s disease, the first new medicine with the potential to treat the cognitive disorder in 17 years.

The seaweed-based drug, called Oligomannate, can be used for the treatment of mild to moderate Alzheimer’s, according to a statement from China’s drug safety agency. The approval is conditional however, meaning that while it can go on sale during additional clinical trials, it will be strictly monitored and could be withdrawn should any safety issues arise.

In September, the team behind the new drug, led by Geng Meiyu at the Shanghai Institute of Materia Medica under the Chinese Academy of Sciences, said they were inspired to look into seaweed due to the relatively low incidence of Alzheimer’s among people who consume it regularly.

In a paper in the journal Cell Research, Geng’s team described how a sugar contained within seaweed suppresses certain bacteria contained in the gut which can cause neural degeneration and inflammation of the brain, leading to Alzheimer’s.

This mechanism was confirmed during a clinical trial carried out by Green Valley, a Shanghai-based pharmaceutical company that will be bringing the new drug to market.

Conducted on 818 patients, the trial found that Oligomannate — which is derived from brown algae — can statistically improve cognitive function among people with Alzheimer’s in as little as four weeks, according to a statement from Green Valley.

“These results advance our understanding of the mechanisms that play a role in Alzheimer’s disease and imply that the gut microbiome is a valid target for the development of therapies,” neurologist Philip Scheltens, who advises Green Valley and heads the Alzheimer Center Amsterdam, said in the statement.

Vincent Mok, who heads the neurology division at the Chinese University of Hong Kong, said the new drug showed “encouraging results” when compared to acetylcholinesterase inhibitors — the existing treatment for mild to severe Alzheimer’s.

“It is just as effective but it has fewer side effects,” he told CNN. “It will also open up new avenues for Alzheimer’s research, focusing on the gut microbiome.”

Since very little is known about the mechanisms of the new drug, Mok said it should also be probed to see if it could have a protective effect and possibly slow down the progression of the disease in patients who have yet to develop strong symptoms of dementia.

The company said Oligomannate will be available in China “very soon,” and it is currently seeking approval to market it abroad, with plans to launch third-phase clinical trials in the US and Europe in early 2020.

Alzheimer’s disease, which starts with memory loss and escalates to severe brain damage, is believed to cause 60% to 70% of the cases of dementia reported worldwide, according to the World Health Organization. Dementia affects an estimated 50 million people worldwide, including 9.5 million people in mainland China, Hong Kong and Taiwan.

Named after Alois Alzheimer, the neuropathologist who discovered the disease in 1906, it has so far confounded researchers and pharmaceutical companies.

In October, US pharmaceutical giant Biogen said it would pursue Food and Drug Administration (FDA) approval for an experimental treatment called aducanumab, after announcing in March it was canceling a large clinical trial for the drug.

Johnson & Johnson, Merck, Pfizer and Eli Lilly have all previously abandoned projects to develop a drug for Alzheimer’s after unsatisfactory clinical data.

https://www.cnn.com/2019/11/03/health/china-alzheimers-drug-intl-hnk-scli/index.html

Our thinking skills in childhood could offer a glimpse into how our minds might work at the age of 70, according to a study spanning decades.

The research started in 1946, when 502 8-year-olds, who were born in the U.K. in the same week, took tests to measure their thinking and memory skills. The participants took cognitive tests again between the ages of 69 and 71.

The participants also had scans, including a positron emission tomography (PET) scan that detects amyloid-beta plaques in the brain. These sticky collections of protein are linked to Alzheimer’s disease.

The study, published in the journal Neurology, shows those with the highest test scores in childhood were more likely to have high scores later in life. Kids in the top 25 percent had a greater chance of being in that same quartile at 70.

Educational attainment and socioeconomic status also appeared to make a difference. Those who were college-educated scored around 16 percent better in tests than those who left school before they hit 16. Participants who had a white-collar job were able to remember, on average, 12 details from a short story, versus 11 if they had a manual job. Overall, women did better than men when their memory and thinking speed were tested.

Participants who were found to have amyloid-beta plaques in their brains, meanwhile, scored lower on cognitive tests. In one assessment where participants had to find the missing pieces in five geometric shapes, those with the plaque got 23 out of 32 problems correct, versus 25 for those without the plaques.

Dr. Jonathan M. Schott of University College London commented: “Finding these predictors is important because if we can understand what influences an individual’s cognitive performance in later life, we can determine which aspects might be modifiable by education or lifestyle changes like exercise, diet or sleep, which may, in turn, slow the development of cognitive decline.

“Our study found that small differences in thinking and memory associated with amyloid plaques in the brain are detectable in older adults even at an age when those who are destined to develop dementia are still likely to be many years away from having symptoms.”

Earlier this year, Schott and his team published a separate study in the journal The Lancet Neurology that showed having high blood pressure in a person’s mid-30s was linked to higher levels of blood vessel damage in the brain, as well as shrinkage of the organ.

Professor Tara Spires-Jones from the UK Dementia Research Institute at the University of Edinburgh, who did not work on the new study, told Newsweek the findings add to other studies that suggest our genetics, as well as environmental factors, play a role in how we maintain our thinking skills as we age.

“However, this does not mean that all of your brain power during aging is determined during childhood,” she said. “There is good scientific evidence from this study and many others that keeping your brain and body active are likely to reduce your risk of developing Alzheimer’s disease, even as adults.”

Learning, socializing and exercise can all help, she said.

“One way this works is by building new connections between brain cells, called synapses. Synapses are the building blocks of memory, so building up a robust network of synapses, sometimes called ‘brain reserve’ is thought to be the biology behind the finding that more education is associated with a lower risk of dementia and age-related cognitive decline,” explained Spires-Jones.

Spires-Jones suggested amyloid-beta plaques might be linked with lower tests scores in the study because they build up and damage the connections between brain cells, called synapses, impairing brain function.

“Amyloid plaques are also widely thought to initiate a toxic cascade that leads to dementia in Alzheimer’s disease, including the build-up and spread of another pathology called ‘tangles,'” she said.

She said the study was “very strong” but limited because observational studies can’t explain the links that emerge, and the participants were all white so the results might not relate to other populations.

“It will be important in future work to try and understand the biological underpinnings for the associations between childhood intelligence and better cognitive ability during aging,” she said.

https://www.newsweek.com/dementia-aging-study-brains-tests-1468657

By Priyanka Runwal

From spooky abandoned houses to dark forest corners, spider webs have an aura of eternal existence. In reality, the silk threads can last hours to weeks without rotting. That’s because bacteria that would aid decomposition are unable to access the silk’s nitrogen, a nutrient the microbes need for growth and reproduction, a new study suggests.

Previous research had hinted that spider webs might have antimicrobial properties that outright kill bacteria. But subjecting the webs of three spider species to four types of bacteria revealed that the spiders use a resist strategy instead, researchers report October 23 in the Journal of Experimental Biology.

The scientists “challenge something that has gone significantly overlooked,” says Jeffery Yarger, a biochemist at Arizona State University in Tempe, who wasn’t involved in the research. “We just assumed [the silk] has some kind of standard antimicrobial property.”

Spiders spin strings of silk to trap food, wrap their eggs and rappel. Their silk webs can sport leaf debris for camouflage amidst tree canopies or leftover dead insects for a meal later. These bits and bobs lure bacteria and fungi involved in decomposition to the web, exposing the protein-rich web silks to the microbes.

“But [the microbes] don’t seem to affect spider silk,” says Dakota Piorkowski, a biologist at Tunghai University in Taichung, Taiwan.

To check if the silk was lethal to bacteria, Piorkowski’s team placed threads from three tropical spider species — giant golden orb weaver (Nephila pilipes), lawn wolf spider(Hippasa holmerae) anddome tent spider (Cyrtophora moluccensis) — in petri dishes and grew four types of bacteria, including E. coli, in perpendicular lines across the silk. “The idea is that if the silk has antibacterial properties, you should see no growth between the piece of silk and … bacteria,” Piorkowski says.

There was no evidence of this “clear zone” of dead bacteria in spots where the bacteria came in direct contact with the silk, the researchers found. So the team then tested if the silk kept hungry bacteria at bay by blocking them from its nitrogen reserves. Wetting the silk threads with an assortment of nutrient solutions showed that the bacteria readily grew on all three types of spider silk when extra nitrogen was available. That indicated that the bacteria are capable of growing on and possibly decomposing the silk, as long as the threads themselves aren’t the only source of nitrogen.

The researchers hypothesize that an outer coating of fat or complex protein on the silk may block bacteria’s access to nitrogen.

Randy Lewis, a spider silk biologist at Utah State University in Logan, cautions against ruling out antibacterial features in all spider silks, though. Underground webs of tarantulas (SN: 5/23/11), for example, can face environments rife in microorganisms compared with that experienced by aerial web-spinning spiders, he says, and may need the extra protection.

Spider webs don’t rot easily and scientists may have figured out why

Researchers at the University of Bordeaux say the combination of ingredients in a traditional chocolate cookie trigger the same addictive response in your brain as cocaine or marijuana.

“Overall, this research has revealed that sugar and sweet reward can not only substitute to addictive drugs, like cocaine, but can even be more rewarding and attractive,” the study’s abstract posits.

Like your cookies with a dash of salt? Your brain does too. Salt consumption activates the brain’s reward centers, compounding the already addictive effects of these chocolaty treats.

So the next time your cookie cravings compel you to act against your better judgement, don’t beat yourself up about it. It’s basically a natural human response, the study shows.

Chocolate chip cookies account for about a fifth of the global cookie market, which is expected to become a $38 billion industry by 2022.

Study: Chocolate chip cookies as addictive as cocaine