Category Archives: Biology
In a recent article published along with cover art engineers showed how simple shape and charge modifications of a nanoparticle can cause tremendous changes in the chemical interactions between the nanoparticle and a cell membrane. (Credit: Image courtesy of Syracuse University)
Jan. 23, 2013 — Researchers at Syracuse University’s Department of Biomedical and Chemical Engineering at L.C. Smith College of Engineering and Computer Science are studying the toxicity of commonly used nanoparticles, particles up to one million times smaller than a millimeter that could potentially penetrate and damage cell membranes.
In a recent article published along with cover art in the journal Langmuir, researchers Shikha Nangia, assistant professor of biomedical and chemical engineering (BMCE), and Radhakrishna Sureshkumar, Department Chair of BMCE and professor of physics, showed how simple shape and charge modifications of a nanoparticle can cause tremendous changes in the chemical interactions between the nanoparticle and a cell membrane.
Nanomaterials, which are currently being used as drug carriers, also pose a legitimate concern, since no universal standards exist to educate and fully protect those who handle these materials. Nanoparticles are comparable to chemicals in their potential threat because they could easily penetrate the skin or be inhaled.
“Nanotechnology has immense potential that is starting to be being realized; a comprehensive understanding of toxicity of nanoparticles will help develop better safe handling procedures in nanomanufacturing and nano-biotechnology” says Sureshkumar and Nangia, In addition, the toxicity levels of various nanoparticles can be used to our advantage in targeting cancer cells and absorbing radiation during cancer therapy. Nanotoxicity is becoming a major concern as the use of nanoparticles in imaging, therapeutics, diagnostics, catalysis, sensing and energy harvesting continues to grow dramatically.
This research project has taken place over the past year utilizing a state of the art 448 core parallel computer nicknamed “Prophet” housed in Syracuse University’s Green Data Center. The research was funded by the National Science Foundation.
Langmuir is a notable, interdisciplinary journal of American Chemical Society publishing articles in: colloids, interfaces, biological interfaces, nano-materials, electrochemistry and devices and applications.
Editing genome with high precision: New method to insert multiple genes in specific locations, delete defective genes
Jan. 3, 2013 — Researchers at MIT, the Broad Institute and Rockefeller University have developed a new technique for precisely altering the genomes of living cells by adding or deleting genes. The researchers say the technology could offer an easy-to-use, less-expensive way to engineer organisms that produce biofuels; to design animal models to study human disease; and to develop new therapies, among other potential applications.
To create their new genome-editing technique, the researchers modified a set of bacterial proteins that normally defend against viral invaders. Using this system, scientists can alter several genome sites simultaneously and can achieve much greater control over where new genes are inserted, says Feng Zhang, an assistant professor of brain and cognitive sciences at MIT and leader of the research team.
“Anything that requires engineering of an organism to put in new genes or to modify what’s in the genome will be able to benefit from this,” says Zhang, who is a core member of the Broad Institute and MIT’s McGovern Institute for Brain Research.
Zhang and his colleagues describe the new technique in the Jan. 3 online edition of Science. Lead authors of the paper are graduate students Le Cong and Ann Ran.
The first genetically altered mice were created in the 1980s by adding small pieces of DNA to mouse embryonic cells. This method is now widely used to create transgenic mice for the study of human disease, but, because it inserts DNA randomly in the genome, researchers can’t target the newly delivered genes to replace existing ones.
In recent years, scientists have sought more precise ways to edit the genome. One such method, known as homologous recombination, involves delivering a piece of DNA that includes the gene of interest flanked by sequences that match the genome region where the gene is to be inserted. However, this technique’s success rate is very low because the natural recombination process is rare in normal cells.
More recently, biologists discovered that they could improve the efficiency of this process by adding enzymes called nucleases, which can cut DNA. Zinc fingers are commonly used to deliver the nuclease to a specific location, but zinc finger arrays can’t target every possible sequence of DNA, limiting their usefulness. Furthermore, assembling the proteins is a labor-intensive and expensive process.
Complexes known as transcription activator-like effector nucleases (TALENs) can also cut the genome in specific locations, but these complexes can also be expensive and difficult to assemble.
The new system is much more user-friendly, Zhang says. Making use of naturally occurring bacterial protein-RNA systems that recognize and snip viral DNA, the researchers can create DNA-editing complexes that include a nuclease called Cas9 bound to short RNA sequences. These sequences are designed to target specific locations in the genome; when they encounter a match, Cas9 cuts the DNA.
This approach can be used either to disrupt the function of a gene or to replace it with a new one. To replace the gene, the researchers must also add a DNA template for the new gene, which would be copied into the genome after the DNA is cut.
Each of the RNA segments can target a different sequence. “That’s the beauty of this — you can easily program a nuclease to target one or more positions in the genome,” Zhang says.
The method is also very precise — if there is a single base-pair difference between the RNA targeting sequence and the genome sequence, Cas9 is not activated. This is not the case for zinc fingers or TALEN. The new system also appears to be more efficient than TALEN, and much less expensive.
The new system “is a significant advancement in the field of genome editing and, in its first iteration, already appears comparable in efficiency to what zinc finger nucleases and TALENs have to offer,” says Aron Geurts, an associate professor of physiology at the Medical College of Wisconsin. “Deciphering the ever-increasing data emerging on genetic variation as it relates to human health and disease will require this type of scalable and precise genome editing in model systems.”
The research team has deposited the necessary genetic components with a nonprofit called Addgene, making the components widely available to other researchers who want to use the system. The researchers have also created a website with tips and tools for using this new technique.
Engineering new therapies
Among other possible applications, this system could be used to design new therapies for diseases such as Huntington’s disease, which appears to be caused by a single abnormal gene. Clinical trials that use zinc finger nucleases to disable genes are now under way, and the new technology could offer a more efficient alternative.
The system might also be useful for treating HIV by removing patients’ lymphocytes and mutating the CCR5 receptor, through which the virus enters cells. After being put back in the patient, such cells would resist infection.
This approach could also make it easier to study human disease by inducing specific mutations in human stem cells. “Using this genome editing system, you can very systematically put in individual mutations and differentiate the stem cells into neurons or cardiomyocytes and see how the mutations alter the biology of the cells,” Zhang says.
In the Science study, the researchers tested the system in cells grown in the lab, but they plan to apply the new technology to study brain function and diseases.
The research was funded by the National Institute of Mental Health; the W.M. Keck Foundation; the McKnight Foundation; the Bill & Melinda Gates Foundation; the Damon Runyon Cancer Research Foundation; the Searle Scholars Program; and philanthropic support from MIT alumni Mike Boylan and Bob Metcalfe, as well as the newscaster Jane Pauley.
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Crayfish Harbor Fungus That’s Wiping Out Amphibians
Freshwater crustaceans could be the key to understanding how the chytrid fungus persists in the ecosystem long after the last amphibian is gone.
Dead frogs killed by the amphibian chytrid fungus.
Photograph by Joel Sartore, National Geographic
Published December 17, 2012
Scientists have found a new culprit in spreading the disease that’s been driving the world’s frogs to the brink of extinction: crayfish.
In the last few decades, the disease caused by the chytrid fungus has been a disaster for frogs and other amphibians. More than 300 species are nearly extinct because of it. Many probably have gone extinct, but it can be difficult to know for sure when a tiny, rare species disappears from the face of the Earth. (Related photos: “Ten Most Wanted ‘Extinct’ Amphibians.”)
“This pathogen is bad news. It’s worse news than any other pathogen in the history of life on Earth as far as we know it,” says Vance Vredenburg, a conservation biologist at San Francisco State University who studies frogs but did not work on the new study.
The chytrid fungus was only discovered in the late 1990s. Since then, scientists have been scrambling to figure out how it spreads and how it works.
One of the biggest mysteries is how chytrid can persist in a frogless pond. Researchers saw it happen many times and were perplexed: If all of a pond’s amphibians were wiped out, and a few frogs or salamanders came back and recolonized the pond, they would also die—even though there were no amphibians in the pond to harbor the disease. (Learn about vanishing amphibians.)
One possible reason is that chytrid infects other animals. For a study published today in Proceedings of the National Academy of Sciences, Taegan McMahon, a graduate student in ecology at the University of South Florida in Tampa, looked at some possible suspects and focused on crayfish, those lobsterlike crustaceans living in freshwater. They seemed like a good possibility because they’re widespread and because their bodies have a lot of keratin, a protein the fungus attacks.
In the lab, McMahon exposed crayfish to the disease and they got sick. More than a third died within seven weeks, and most of the survivors were carrying the fungus. She also put infected crayfish in the water with tadpoles—separated by mesh, so the crustaceans wouldn’t eat the baby frogs—and the tadpoles got infected. When McMahon and her colleagues checked out wetlands in Louisiana and Colorado, they also found infected crayfish.
That means crayfish can probably act as a reservoir for the disease. The fungus seems to be able to dine on crayfish then leap back to amphibians when it gets a chance. No one knows for sure where the fungus originally came from or why it’s been such a problem in recent decades, but this research suggests one way that it could have been spread. Crayfish are sometimes moved from pond to pond as fish bait and are sold around the world as food and aquarium pets. (Related photos: “New Giant ‘Bearded’ Crayfish Species.”)
The study doesn’t answer every last question about the disease. For one thing, crayfish are common, but they aren’t everywhere; there are no crayfish in some of the places where frogs have been hardest hit, Vredenburg says. But, he says, the new research shows that “we need to start looking a little more broadly at other potential hosts.”
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Cancer is a modern disease caused by factors such as pollution and diet, a study of ancient human remains has indicated.
The study of remains and literature from ancient Egypt, ancient Greece and earlier periods shows almost no evidence of the disease, says Professor Rosalie David of the University of Manchester.
Only one case has been discovered during the investigation of hundreds of Egyptian mummies, and there are few references to cancer in historical records. Cancer, and particularly child cancer, has become vastly more prevalent since the Industrial Revolution.
“In industrialised societies, cancer is second only to cardiovascular disease as a cause of death. But in ancient times, it was extremely rare,” says David. “It has to be a man-made disease, down to pollution and changes to our diet and lifestyle.”
The data includes the first ever histological diagnosis of cancer in an Egyptian mummy by Professor Michael Zimmerman of Villanova University, who found rectal cancer in an unnamed mummy from the Ptolemaic period.
“In an ancient society lacking surgical intervention, evidence of cancer should remain in all cases,” says Zimmerman. “The virtual absence of malignancies in mummies must be interpreted as indicating their rarity in antiquity, indicating that cancer causing factors are limited to societies affected by modern industrialization”.
It”s not just that people didn”t live long enough to get cancer, says the team, as individuals in ancient Egypt and Greece did still develop such diseases as atherosclerosis, Paget”s disease of bone, and osteoporosis.
Nor do tumors simply fail to last. Zimmerman”s experiments indicate that mummification preserves the features of malignancy, and that tumours should actually be better preserved than normal tissues.
The first reports in scientific literature of distinctive tumours have only occurred in the past 200 years, such as scrotal cancer in chimney sweeps in 1775, nasal cancer in snuff users in 1761 and Hodgkin’s disease in 1832.
“Extensive ancient Egyptian data, along with other data from across the millennia, has given modern society a clear message – cancer is man-made and something that we can and should address,” says David.
gene”s location on a chromosome plays a significant role in shaping how an organism”s traits vary and evolve, according to findings by genome biologists at New York University”s Center for Genomic and Systems Biology and Princeton University”s Lewis-Sigler Institute for Integrative Genomics. Their research, which appears in the latest issue of the journal Science, suggests that evolution is less a function of what a physical trait is and more a result of where the genes that affect that trait reside in the genome.
Physical traits found in nature, such as height or eye color, vary genetically among individuals. While these traits may differ significantly across a population, only a few processes can explain what causes this variation — namely, mutation, natural selection, and chance.
In the Science study, the NYU and Princeton researchers sought to understand, in greater detail, why traits differ in their amount of variation. But they also wanted to determine the parts of the genome that vary and how this affects expression of these physical traits. To do this, they analyzed the genome of the worm Caenorhabditis elegans (C. elegans). C. elegans is the first animal species whose genome was completely sequenced. It is therefore a model organism for studying genetics. In their analysis, the researchers measured approximately 16,000 traits in C. elegans. The traits were measures of how actively each gene was being expressed in the worms” cells.
The researchers began by asking if some traits were more likely than others to be susceptible to mutation, with some physical features thus more likely than others to vary. Different levels of mutation indeed explained some of their results. Their findings also revealed significant differences in the range of variation due to natural selection — those traits that are vital to the health of the organism, such as the activity of genes required for the embryo to develop, were much less likely to vary than were those of less significance to its survival, such as the activity of genes required to smell specific odors.
However, these results left most of the pattern of variation in physical traits unexplained — some important factor was missing.
To search for the missing explanation, the researchers considered the make-up of C. elegans” chromosomes — specifically, where along its chromosomes its various genes resided.
Chromosomes hold thousands of genes, with some situated in the middle of their linear structure and others at either end. In their analysis, the NYU and Princeton researchers found that genes located in the middle of a chromosome were less likely to contribute to genetic variation of traits than were genes found at the ends. In other words, a gene”s location on a chromosome influenced the range of physical differences among different traits.
The biologists also considered why location was a factor in the variation of physical traits. Using a mathematical model, they were able to show that genes located near lots of other genes are evolutionarily tied to their genomic neighbors. Specifically, natural selection, in which variation among vital genes is eliminated, also removes the differences in neighboring genes, regardless of their significance. In C. elegans, genes in the centers of chromosomes are tied to more neighbors than are genes near the ends of the chromosomes. As a result, the genes in the center are less able to harbor genetic variation.
The research was conducted by Matthew V. Rockman, an assistant professor at New York University”s Department of Biology and Center for Genomics and Systems Biology as well as Sonja S. Skrovanek and Leonid Kruglyak, researchers at Princeton University”s Lewis-Sigler Institute for Integrative Genomics, Department of Ecology and Evolutionary Biology, and Howard Hughes Medical Institute.
The study was supported by grants from the National Institutes of Health.
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by New York University.
- M. V. Rockman, S. S. Skrovanek, L. Kruglyak. Selection at Linked Sites Shapes Heritable Phenotypic Variation in C. elegans. Science, 2010; 330 (6002): 372 DOI: 10.1126/science.1194208
By Ewen Callaway
Don””t be fooled by the playful-looking duck””s bill — platypuses deliver a venom containing more than 80 different toxins.
The finding, from an analysis of the genes encoding the dangerous mixture, also reveals the striking similarities between the poisons of different animals. The genes resemble those of other venomous animals, such as snakes, lizards, starfish and sea anemones.
Like eyes, fins and wings, which have evolved independently in a number of different lineages, platypus venom looks to be an example of convergent evolution, says Wesley Warren, a genomicist at Washington University in St Louis, Missouri, who led the study, published in the journal Genome Biology.1
The platypus — a semi-aquatic egg-laying mammal found in Australia — is one of few mammals to make venom, which males produce in abdominal venom glands and deliver through spurs on their hind legs. They only make the poison during breeding season, and Warren thinks that males probably deploy it to defend their turf against other males.
By some accounts, being poisoned by a platypus could qualify as punishment in one of Dante””s circles of hell. In one case report2, Australian doctors described their treatment of a 57-year-old man a few hours after he grabbed one of the small mammals while fishing. The pain was “so bad I started to become incoherent” the man said, and far worse than the shrapnel wounds he took as a soldier. Ibuprofen and morphine provided no relief, and one finger was swollen and ached more than 4 months after the run-in.
Efforts to find the molecules capable of inflicting such anguish have focused on separating and characterizing proteins in venom extracts. This approach identified three of the most abundant ingredients of platypus venom, but Warren””s team suspected that more molecules were present at lower levels.
What””s your poison?
His team sequenced messenger RNA transcripts from the venom gland of a male platypus, killed by a dog in breeding season. To identify venom ingredients they looked for genes that were not produced in other tissues and which resembled venom genes from other animals. This scan turned up 83 genes in 13 different families of toxins, linked to effects including inflammation, nerve damage, muscle contraction and blood coagulation. For instance, platypuses make 26 different kinds of serine protease enzymes, which are also found in the venom of most snakes, and seven of their venom genes resemble a neurotoxin produced by spiders called α-latrotoxin.
Additional tests will be needed to determine what each venom ingredient does, says Warren. He also thinks that his team””s study undercounted the number of toxin-encoding genes in the platypus ””venome””, because the method used overlooks genes that bear little resemblance to other animal toxins. To find these, his team plans to look for genes switched on during the seasonal development of the platypus venom gland.
Nonetheless, the platypus venome supports work in other animals showing widespread convergence in venom gene evolution. Warren says that this probably happens when genes that perform normal chores, such as blood coagulation, become duplicated independently in different lineages, where they evolve the capacity to carry out other jobs.
Animals end up using the same genes as building blocks for venom because only a subset of the proteins the genes encode have the structural and functional properties to become venoms, he adds.
Despite such convergence, closely related animals tend to produce similar venoms, says Bryan Fry, head of the venomics laboratory at the University of Melbourne, Australia.
An evolutionary outlier such as the platypus is likely to produce a venom with new components, says Fry. “If you want to find something potentially useful in drug design and development from a venom, you””re much likelier to find it in a novel venom such as platypus venom than if you are looking at, say, rattlesnakes.”
An earlier version of this story stated incorrectly that platypuses were marsupials. They are monotremes.
The new silk alone could shake up the textile industry by creating a softer and stronger fabric that still looks like silk. Click to enlarge this image. Hemera
Silkworms have been modified to produce spider silk, creating a fabric that could be used in everything from bulletproof clothing to artificial tendons.
By Eric Bland
- Silkworms have been genetically engineered to spin spider silk.
- The new hybrid silk is finer and tougher than ordinary silk.
- The development could lead to wound-healing, lighter body armor as well as artificial tissue.
If Spider-Man ever ran out of webs, he could now enlist an army of silkworms to spin extra high-tensile spider silk.
Scientists have created a genetically modified silkworm that spins a new kind of silk: a hybrid of silkworm silk and spider silk.
The new material alone could shake up the textile industry, while future silk hybrids could be used in everything from bulletproof clothing to artificial tendons.
“Compared to normal spider silk, it””s not as strong,” said Malcolm Fraser, a scientist from the University of Notre Dame. “But we are confident that, this being our first attempt, that we will be able to tweak the system to bring the system closer to the strength of true spider silk.”
Fraser, along with professor Randy Lewis from the University of Wyoming, developed the spider-silk-spinning silkworms.
Silkworms have helped clothe people for thousands of years by reliably producing large quantities of a soft, supple and luxurious material.
Spider dragline silk is significantly stronger than silkworm silk — so strong that it can best steel wire — but it is hard to make.
“They just don””t produce enough silk,” said Fraser, who notes that a golden cloth on display at the American Museum of Natural History in New York City required more than one million spiders to produce. “One million silkworms can produce considerably more silk than one million spiders.”
The new silk is a hybrid of spider silk and silkworm silk. It is stronger and finer than silkworm silk, but not quite as strong as spider silk. “It would definitely be stronger (than a normal silk shirt),” said Lewis. “But it wouldn””t flow like silkworm silk does.”
“It””s a fabulous accomplishment,” said Cheryl Hayashi, a spider silk expert and a professor at the University of California, Riverside.
Other groups have produced spider silk protein in plants, in bacteria and even in goat””s milk. But spider silk protein is not the same as spun spider silk. The silkworms have the necessary body parts to spin the protein into silk threads — and to produce it in large quantities.
The new silk alone could shake up the textile industry by creating a softer, stronger fabric that still looks like silk.
Fraser and his team, however, have bigger plans in mind.
In this work the Notre Dame and University of Wyoming scientists replaced only one of multiple silk-producing genes in silkworms with spider silk genes. Eventually they want to replace multiple silkworm silk-producing genes with spider silk genes.
In particular, they hope to insert genes from the newly discovered Darwin””s Bark Spider (Caerostris darwini), which produced silk twice as strong as any other. That””s more than 10 times stronger than Kevlar, a fabric commonly found in bulletproof vests.
Mass produced, stronger-than-steel spider silk will also have a range of biomedical applications, said Fraser and Lewis. Hybrid silk could be speed wound-healing, eliminate or reduce the need for cadaver-derived tendons and ligaments.
Published October 13, 2010
An unexpected cast of characters has found a home on Broadway: At least 13 species of ants mingle along the famous thoroughfare and other Manhattan streets, a new study says.
Just like human New Yorkers, the ants are a jumble of personalities, from the tiny thief ant—which, as the name suggests, feeds its colonies with stolen food—to the street-smart pavement ant, a fiercely territorial insect that nests under cement. (See ant pictures in National Geographic magazine.)
Though most of the species are native to North America, the team also found a few foreign species living peacefully among the locals, likely having hitched a ride to the Big Apple in soil from potted plants or wood mulch.
For instance, the poisonous Asian needle ant had never before been found north of Virginia. (Also see “Brain-Controlling Flies to Triumph Over Alien Ants?“)
Not all alien species are detrimental to native species. “Quite the opposite,” study leader Marko Pećarević, a Columbia University ecologist, said in an email. “Given enough time—centuries or millennia—they tend to complement the native richness.
“The problem is that one in a hundred will be an invasive, and cause great damage to the environment, usually by altering habitats and/or directly killing other species,” he added.
Despite this rich diversity, for ants Manhattan is more a mixing bowl than a melting pot, the study authors noted.
“While we humans all belong to the same species and hence can reproduce and ””melt”” our ancestral differences into a beautiful amalgam that is New York, the ants that make up the diversity found on the medians in NYC are truly different species and cannot reproduce, but merely mix and coexist,” Pećarević said.
(Related: “Ants Practice Nepotism, Study Finds.”)
Ants Adapting to City Life
In the summer of 2006, Pećarević and colleagues trapped ants on 44 medians along Broadway, Park Avenue, and the West Side Highway on Manhattan Island. (See pictures of what Manhattan may have looked like in 1609.)
All the medians supported some type of vegetation, from the well-manicured lawns of Park Avenue to the tree-lined patches on Broadway, he said by email.
Since past studies of urban wildlife have focused mostly on areas that more closely mimic nature, such as gardens, observing medians or other built elements could reveal unknown animal habitats, the study said.
Predictably, the larger medians host more species, he said. Some species, such as the pavement ant, prefer medians with more concrete.
Others, such as the Asian Nylanderia flavipes, like areas with more trees, according to the study, which appeared October 5 in the journal PLoS One.
Still other ants live underground, including the cornfield ant, which “herds” aphids like people care for cattle.
Future studies that collect ants from trees may reveal additional species in New York City, for a total of about 30, Pećarević predicted.
Eric Lonsdorf, director of the Urban Wildlife Institute at Chicago””s Lincoln Park Zoo, said he was surprised by how many species were discovered in such small strips of land.
Lonsdorf was also intrigued by the idea of ants adapting to life in the city. For instance, past research has shown that odorous house ants living in cities set up larger colonies with multiple queens, according to the study.
Seeing “urban as a particular kind of habitat for animals, rather than universally unsuitable, is a shift in thinking,” Lonsdorf added.
City Critters Poorly Understood
The new research is a reminder that the pockets of nature urbanites encounter each day remain poorly understood—even as more people move into New York and other cities, the study says.
Indeed, finding such an assortment of ants in a city of eight million humans is “more evidence that we know little about how animals perceive urban areas as habitat,” Lonsdorf said.
According to study leader Pećarević, urban wildlife does a “lot of work that makes life more pleasant for us, such as waste removal, seed dispersal, [and] pollination of flowers, to mention but a few.”
So the next time you””re downtown, “take a few minutes to sit on a bench and look at ants go about their business,” he suggested.
“There is a whole new world to discover out there.”
MIT engineers have developed a way to rapidly perform surgery on single nerve cells in the worm C. elegans. The white lines represent axons — long extensions of nerve cells that carry messages to other cells. (Credit: Craig Millman and Yanik Lab)
Scientists have long sought the ability to regenerate nerve cells, or neurons, which could offer a new way to treat spinal-cord damage as well as neurological diseases such as Alzheimer”s or Parkinson”s. Many chemicals can regenerate neurons grown in Petri dishes in the lab, but it”s difficult and time-consuming to identify those chemicals that work in live animals, which is critical for developing drugs for humans.
Engineers at MIT have now used a new microchip technology to rapidly test potential drugs on tiny worms called C. elegans, which are often used in studies of the nervous system. Using the new technology, associate professor Mehmet Fatih Yanik and his colleagues rapidly performed laser surgery, delivered drugs and imaged the resulting neuron regrowth in thousands of live animals.
“Our technology helps researchers rapidly identify promising chemicals that can then be tested in mammals and perhaps even in humans,” says Yanik. Using this technique, the researchers have already identified one promising class of neuronal regenerators.
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Researchers at the University of Edinburgh report a new experimental compound that can improve memory and cognitive function in aging mice. The compound is being investigated with a view to developing a drug that could slow the natural decline in memory associated with aging.
With support from a Wellcome Trust Seeding Drug Discovery award, the team has identified a preclinical candidate that they hope to take into human trials within a year.
Many people find they become more forgetful as they get older and we generally accept it as a natural part of the aging process. Absent mindedness and a difficulty to concentrate are not uncommon, it takes longer to recall a person”s name, and we can”t remember where we left the car keys. These can all be early signs of the onset of dementia, but for most of us it”s just part of getting old.
Such memory loss has been linked with high levels of ”stress” steroid hormones known as glucocorticoids which have a deleterious effect on the part of the brain that helps us to remember. An enzyme called 11beta-HSD1 is involved in making these hormones and has been shown to be more active in the brain during aging.
In a study published in the Journal of Neuroscience, the team reports the effects of a new synthetic compound that selectively blocks 11beta-HSD1 on the ability of mice to complete a memory task, called the Y maze.
Professor Jonathan Seckl from the University of Edinburgh, who discovered the role of 11beta-HSD1 in the brain, described the findings: “Normal old mice often have marked deficits in learning and memory just like some elderly people. We found that life-long partial deficiency of 11beta-HSD1 prevented memory decline with aging. But we were very surprised to find that the blocking compound works quickly over a few days to improve memory in old mice suggesting it might be a good treatment for the already elderly.”
The effects were seen after only 10 days of treatment.
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