Study identifies how brain connects memories across time
Study identifies how brain connects memories across time Article taken from: http://www.biosciencetechnology.com/news/2016/05/study-identifies-how-brain-connects-memories-across-time Image Source: (Image: Shutterstock) http://www.biosciencetechnology.com/news/2016/05/study-identifies-how-brain-connects-memories-across-time Using a miniature microscope that opens a window into the brain, UCLA neuroscientists have identified in mice how the brain links different memories over time. While aging weakens these connections, the team devised a way for the middle-aged brain to reconnect separate memories.The findings, which were published today in the advance online edition of Nature, suggest a possible intervention for people suffering from age-related memory problems.“Until now, neuroscientists have focused on how the brain creates and stores single memories,” said principal investigator Alcino Silva, a professor of neurobiology at the David Geffen School of Medicine at UCLA. “We wanted to explore how the brain links two memories and whether the passage of time affects the strength of the connection.” “In the real world, memories don’t happen in isolation,” said first author Denise Cai, a researcher in Silva’s lab. “Our past experiences influence the creation of new memories and help us predict what to expect and make informed decisions in the future.”In an intricate experiment, the UCLA team tested in young and middle-aged mice whether the brain linked memories of experiences separated by five hours versus seven days. Watching neurons in real time The lab used a miniature microscope, called a Miniscope, which was developed by UCLA neuroscientists Dr. Peyman Golshani, Baljit Khakh and Silva with funding from the presidential BRAIN Initiative and the Geffen School. The instrument’s powerful camera allowed the scientists to peer into the brains of young mice and observe their cells in action. The tiny, head-mounted microscope illuminated the animals’ neurons firing as the mice moved freely in their natural environments. For 10 minutes at a time, each mouse was placed in three boxes, all unique in terms of fragrance, shape, lighting and flooring. A week’s time separated placement in the first and second boxes. Only five hours separated time spent in the second and third boxes, where the mouse later received a small shock to the foot.Two days later, the team returned each mouse to all three boxes. As expected, the mice froze with fear when it recognized the inside of the third box. What happened next, however, came as a surprise.“The mouse also froze in the second box, where no shock occurred,” Silva observed. “This suggests that the mouse transferred its memory of the shock in the third box to its experience in the second box five hours earlier.”When Silva and Cai examined the animals’ brains, the neural activity confirmed their hypothesis.“The same brain cells that recorded the mouse’s shock in the third box also encoded its memory of the second box a few hours earlier,” Cai said. “We saw 20 percent more overlap in the neural circuits that recorded the animal’s experiences in the memories that unfolded closer in time.”In other words, says Silva, “The memories became interrelated in how they were encoded and stored by the brain, such that the recall of one memory triggered the recall of another memory related in time.” Exciting the brain Based on an earlier Silva finding, the team knew that a cell is most likely to encode a memory when it’s aroused and ready to fire. Neuroscientists refer to this condition as excitability.“The excitable brain is already warmed up,” Silva said. “It’s like stretching your muscles before exercise or revving your car engine before you drive.”Suspecting that aging weakens neurons’ ability to fully excite, the UCLA researchers conducted a similar experiment in middle-aged mice. They introduced each of the mice to two boxes, five hours apart, and administered a foot shock in the second box.When they returned the animals to the boxes two days later, the results could not have been more clear-cut.“The older mice froze only in the box where they had received a shock,” Cai explained. “They did not react in the first box.”A glimpse into the Miniscopes confirmed that the brains of the mice did not connect the two memories; each memory was encoded on its own neural circuit. Rescuing lost connections Next the team focused on boosting the older animals’ ability to link memories. Cai used a biological tool to excite neurons in a tiny part of the hippocampus — the memory center of the brain — before introducing the mice to the first box.She stimulated the same cells before placing the mice in the first box and the second box, where they received a foot shock two days later.“The proof in the pudding arrived when we reintroduced the middle-aged mice to the first box,” Silva said. “The animals froze — they now linked the shock that happened in the second box to the first. This suggests that increased excitability had reversed their age-related inability to link memories.”Cai and Silva are currently testing an FDA-approved drug’s effect on the ability of middle-aged mice to connect memories.The work was supported by the National Institute on Aging, the National Institute of Neurological Diseases and Stroke and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. The National Institute of Mental Health and the dean’s fund at the David Geffen School of Medicine at UCLA provided funding to Silva, Khakh and Golshani to develop the miniaturized microscopes. Date: May 24th, 2013 Source: https://www.uclahealth.org/news/ucla-study-identifies-how-brain-connects-memories-across-time?
‘Sunscreen gene’ may help protect against skin cancer
‘Sunscreen gene’ may help protect against skin cancer Article taken from: http://news.usc.edu/100824/sunscreen-gene-may-help-protect-against-skin-cancer/ USC-led study reveals that melanoma patients with deficient or mutant copies of the gene are less protected from harmful ultraviolet rays The “UV radiation Resistance Associated Gene” is a tumor suppressor for skin cancer. (Photo/Pixabay) A new USC-led study identified a “sunscreen gene” that may help stave off skin cancer.The researchers found that the “UV radiation Resistance Associated Gene” is a tumor suppressor for skin cancer, the most common form of cancer in the United States —and the deadliest. In fact, melanoma rates have doubled over the last three decades, according to the Centers for Disease Control and Prevention.“If we understand how this UV-resistant gene functions and the processes by which cells repair themselves after ultraviolet damage, then we could find targets for drugs to revert a misguided mechanism back to normal conditions,” said Chengyu Liang, the study’s senior author and an associate professor of molecular microbiology and immunology at the Keck School of Medicine of USC. The study was published in Molecular Cell in time for Melanoma/Skin Cancer Detection and Prevention Month. More than 90 percent of melanoma skin cancers develop because of cell damage from exposure to UV radiation. Melanoma kills about 10,130 people annually, according to the American Cancer Society.“People who have the mutated UV-resistant gene or low levels of the UV-resistant gene may be at higher risk of melanoma or other skin cancers, especially if they go sunbathing or tanning frequently,” Liang said. “Our study suggests that the UV-resistant gene may serve as a biomarker for skin cancer prevention.” A shot in the cell The researchers used data from 340 melanoma patients who participated in The Cancer Genome Atlas. The study also included two experimental groups with either reduced levels of the UV-resistant gene or a mutant copy of that gene in melanoma cells and 50 fly eyes. The control groups were melanoma cells or fly eyes with normal copies of the UV-resistant gene. The scientists gave a UV shot to cells carrying the normal UV-resistant gene and cells carrying defective copies of it. After 24 hours, cells carrying normal versions of the gene had repaired more than 50 percent of the UV-induced damage. In contrast, the defective samples repaired less than 20 percent of the damaged cells. “That means when people sunbathe or go tanning, those who have the normal UV-resistant gene can repair most UV-induced DNA burns in a timely manner, whereas those with the defective UV-resistant gene will have more damage left unrepaired,” Liang said. “After daily accumulation, if they sunbathe or go tanning often, these people will have increased risk for developing skin cancers such as melanoma.” The researchers were able to show a correlation with increased cancer risk. Their study did not definitively say diminished levels or mutant copies of the UV-resistant gene were causes for skin cancer development. Why the UV-resistant gene matters Scientists first discovered the UV-resistant gene nearly two decades ago in relation to a disease called Xeroderma Pigmentosum, which makes people extremely sensitive to sunlight and puts them at high risk for developing skin cancer. Scientists did not examine the function of the UV-resistant gene in people who are healthy or who have skin cancer. The USC-led team has now identified what the UV-resistant gene does and how it operates in a general population, said Yongfei Yang, lead author and a research associate at Keck Medicine of USC. When the UV-resistant gene is lost, the cell cannot efficiently repair UV- and chemical-induced damage. Chengyu Liang “The UV-resistant gene is a tumor suppressor involved in the UV-repair process of a cell’s DNA and is essential for preventing UV-induced genomic instability,” Yang said. “When the UV-resistant gene is lost, the cell cannot efficiently repair UV- and chemical-induced damage.”The UV-resistant gene is involved in the multistep DNA cell-repair process, researchers found. First a known protein scans for damaged DNA. Once it finds lesions, it tags the UV-resistant gene into action. The UV-resistant gene is like a humanitarian convoy dropping off reinforcements or aid to help damaged areas repair at precisely the right time. The researchers did not have data from people without skin cancer, so they were unable to compare their observations of melanoma patients with those of skin cancer-free people.“We found the expression level of the UV-resistant gene is related to melanoma patients’ survival and metastasis stages,” Yang said. “Lower levels of the UV-resistant gene means a lower survival rate and advanced metastases stages.” The UV-resistant gene brings hope UV exposure, frequent trips to the tanning salon and genetics all play a role in developing skin cancer. Studies have shown, for example, that redheads are more prone to skin cancer because of their genetic background. Liang, Yang and their colleagues have identified a new player in the skin cancer field.“To our knowledge, the UV-resistant gene does not have any enzymic activity; It’s a supporter or coordinator,” Liang said. “Although it may not be the direct doer, without it, the whole structure collapses.”Future studies will use mouse models to better understand how the UV-resistant gene functions.“The UV-resistant gene may serve as a good target for drug development,” Yang said. “Perhaps one day a drug could stimulate the repairing functionality of the UV-resistant gene to ensure swift and effective repair of UV-damaged skin cells. That would be a good treatment for people who are at high risk of developing skin cancer.”Scientists at Children’s Hospital Los Angeles, the Korea Advanced Institute of Science and Technology and the Chinese Academy of Sciences in Beijing also contributed to the study. The Margaret Early Trustee Foundation, American Cancer Society, National Institutes of Health grants and GRL Program from the National Research Foundation of Korea funded the research. Date: May 23th. 2016 Source: news.usc.edu/100824/sunscreen-gene-may-help-protect-against-skin-cancer/
More Ancient Viruses Lurk in Human DNA Than Previously Thought
More Ancient Viruses Lurk in Human DNA Than Previously Thought Article taken from: http://www.biosciencetechnology.com/news/2016/03/more-ancient-viruses-lurk-human-dna-previously-thought#at_pco=smlwn-1.0&at_si=573f67fd6e7661e9&at_ab=per-2&at_pos=0&at_tot=1 (Image: Shutterstock)Image Source: http://www.biosciencetechnology.com/news/2016/03/more-ancient-viruses-lurk-human-dna-previously-thought#at_pco=smlwn-1.0&at_si=573f67fd6e7661e9&at_ab=per-2&at_pos=0&at_tot=1 Think your DNA is all human? Think again. And a new discovery suggests it’s even less human than scientists previously thought. Nineteen new pieces of non-human DNA — left by viruses that first infected our ancestors hundreds of thousands of years ago — have just been found, lurking between our own genes.And one stretch of newfound DNA, found in about 50 of the 2,500 people studied, contains an intact, full genetic recipe for an entire virus, say the scientists who published their findings in the Proceedings of the National Academy of Sciences. Whether or not it can replicate, or reproduce, it isn’t yet known. But other studies of ancient virus DNA have shown it can affect the humans who carry it.In addition to finding these new stretches, the scientists also confirmed 17 other pieces of virus DNA found in human genomes by other scientists in recent years. The study looked at the entire span of DNA, or genome, from people from around the world, including a large number from Africa — where the ancestors of modern humans originated before migrating around the world. The team used sophisticated techniques to compare key areas of each person’s genome to the “reference” human genome.Working at Tufts University and the University of Michigan Medical School, the researchers made the findings with funding from the National Institutes of Health. HERV-enly find The findings add to what science already knows about human endogenous retroviruses, or HERVs. That’s the name for the ancient infectious viruses that inserted a DNA-based copy of their own RNA genetic material into our ancestors’ genomes. They’re part of the same type of virus that includes the modern human immunodeficiency virus, which causes AIDS. Over generations, the virus-generated DNA kept getting copied and handed down when humans reproduced. That’s how it ended up in our DNA today. In fact, about 8 percent of what we think of as our “human” DNA actually came from viruses. In some cases, HERV sequences have been adopted by the human body to serve a useful purpose, such as one that helps pregnant women’s bodies build a cell layer around a developing fetus to protect it from toxins in the mother’s blood. The new HERVs are part of the family called HERV-K. The intact whole viral genome, or provirus, just found was on the X chromosome; it’s been dubbed Xq21. It’s only the second intact provirus found to be hiding in human DNA. In the researchers’ own words: “This one looks like it is capable of making infectious virus, which would be very exciting if true, as it would allow us to study a viral epidemic that took place long ago,” said senior author and virologist John Coffin, Ph.D. of the Tufts University School of Medicine. “This research provides important information necessary for understanding how retroviruses and humans have evolved together in relatively recent times.” “Many studies have tried to link these endogenous viral elements to cancer and other diseases, but a major difficulty has been that we haven’t actually found all of them yet,” said co-first author Zachary H. Williams, a Ph.D. student at the Sackler School of Graduate Biomedical Sciences at Tufts University in Boston. “A lot of the most interesting elements are only found in a small percentage of people, which means you have to screen a large number of people to find them.” “This is a thrilling discovery,” said co-first author Julia Wildschutte, Ph.D., who began the work as a Ph.D. student in Coffin’s lab at Tufts. “It will open up many doors to research. What’s more, we have confirmed in this paper that we can use genomic data from multiple individuals compared to the reference human genome to detect new HERVs. But this has also shown us that some people carry insertions that we can’t map back to the reference.” U-M genetics researcher Jeffrey Kidd, Ph.D., worked with Wildschutte when she was a member of his laboratory team. “These are remnants of ancient events that have not been fixed in the population as a whole, but rather happened in the ancestors of some people alive today,” Kidd said. “There have been a number of examples of other HERVs that insert themselves next to human genes or near them, and have impact on their expression. We’re interested in applying these methods to find other types of viral or mobile element insertions.” Genetic teamwork The Michigan team used methods for characterizing repetitive DNA sequences that Kidd and his team had developed, while Coffin and Williams used complementary techniques. Wildschutte is now at Bowling Green State University.Many of the genomes they examined were from the 1000 Genomes Project, an international collaboration. Another set of genomes came from work Kidd and colleagues at Stanford University had done as part of the Human Genome Diversity Project, with a focus on DNA samples from African volunteers. These latter samples showed more signs of HERVs, in line with the high level of genetic diversity in African populations. That diversity stems from the longtime stability and intermixing of the continent’s population – as opposed to other populations in Europe, Asia and the Americas that stem from specific out-migrations in ancient times.Cataloging all the HERV insertions in humans will require even more scanning of whole human genomes, which are becoming easier to come by as technology improves and becomes less expensive. And although intact proviruses lurking in our DNA may be rare, the impact of other HERV sequences on our health or disease is probably not. Date: May 10th, 2016 Source: University of Michigan Health System– http://www.biosciencetechnology.com/news/2016/03/more-ancient-viruses-lurk-human-dna-previously-thought#at_pco=smlwn-1.0&at_si=573f67fd6e7661e9&at_ab=per-2&at_pos=0&at_tot=1
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