Cooperation among viral variants helps hepatitis C survive immune system attacks.

Graph shows a cross-immunoreactivity network (CRN) composed of 100 viral variants. Altruistic variants are shown in green, persistent variants in red, and others in yellow. Credit: Georgia Tech/CDC

Source: Phys.org

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Warring armies use a variety of tactics as they struggle to gain the upper hand. Among their tricks is to attack with a decoy force that occupies the defenders while an unseen force launches a separate attack that the defenders fail to notice.
A study published earlier this month in the journal Proceedings of the National Academy of Sciences suggests that the Hepatitis C virus (HCV) may employ similar tactics to distract the body's natural defenses. After infecting patients, Hepatitis C evolves many variants, among them an "altruistic" group of viral particles that appears to sacrifice itself to protect other mutants from the body's immune system.
The findings, reported by researchers from the Georgia Institute of Technology and the Centers for Disease Control and Prevention (CDC), could help guide development of future vaccines and treatments for the virus, which affects an estimated 170 million people in the world. Developing slowly over many years and often without symptoms, Hepatitis C can cause severe liver damage and cancer. There are currently no vaccines for the disease.
"The members of viral populations in Hepatitis C don't act like separate entities; the different variants work together almost like a team," said Leonid Bunimovich, a Regent's Professor in the Georgia Tech School of Mathematics. "There is a clear separation of responsibilities, including variants we call 'altruistic' because they sacrifice themselves for the good of the whole viral population. These variants seem to draw the immune system attack on themselves."
The findings resulted from mathematical modeling done by the scientists, who first developed a model for how the virus variants and immune system antibodies interact. They then used the model to analyze and explain data gathered from a group of patients infected with Hepatitis C, some of whom had been followed for as long as 20 years.
The virus evolves differently in each person, producing a mix of genetically-related variants over time, Bunimovich noted. Ultimately, the virus variants and the antibodies form a complex network in which an antibody to one variant can react to another variant - a phenomenon known as cross-immunoreactivity.
But how do viruses, which lack brains or even neural cells, produce a level of teamwork that's often difficult for humans to achieve?
"The virus variants do not communicate directly with one another, but in this system of viruses and antibodies, they interact through the antibodies," explained Bunimovich. "When one antibody-producing cell responds to one variant, and then to another, that is a form of interaction that affects both variants. An indirect interaction occurs when the virus variants interact with the same antibody in the network."
Unlike HIV - to which it is often compared - Hepatitis C virus doesn't suppress the body's immune system. Many scientists believe that the viral infection evolves like an "arms race," with the virus mutating to stay one step ahead of the body's immune system. Using next-generation gene sequencing data, the research team - which included regular fellow Pavel Skums and microbiologist Yury Khudyakov from the CDC's Division of Viral Hepatitis - analyzed viral populations in detail. The scientists studied the genetic compositions of the populations, and even saw evolution in blood samples taken from the same persons over time.
The populations of variants rose and fell, some remaining in small numbers and others reappearing after they had been seemingly wiped out by the immune system. At late stages of the persistent infection development, the evolution of new variations almost stopped, though the immune system remained strong. The "arms race" theory fails to explain these observations, Bunimovich said.
Using their model to track both variants and antibodies, the researchers found that certain variants were drawing the immune system response on themselves to protect others. They called this newly-observed phenomenon "antigenic cooperation." The antibodies suppressed only the altruistic variants, leaving other viral members of the network unharmed.
"The altruistic variants allow the antibodies to attack them, thereby sacrificing themselves, so other variants can survive," said Skums, the paper's first author. "The altruistic variants fool the immune system, rendering the immune system response to other variants ineffective. In essence, the surviving variants use the altruistic (sacrificing) variants as an umbrella to protect themselves."
The researchers were surprised by the sophisticated behavior, which occurs because the viral variants are part of the complex interconnected network - a social network not unlike the ones created in such environments as Facebook.
"Even such simple organisms as viruses can organize into a network," Skums explained. "Because they are part of a network, they can develop this kind of complex behavior, fighting the immune system through team efforts."
The findings, if supported by additional research, could alter the strategy for developing vaccines for Hepatitis C. Both vaccines and treatment would have to take into account how the virus evolves differently in individuals. The researchers also hope to examine the activity of other viruses to see if this complex interaction may also be found in other viral networks, Bunimovich said.
For the researchers, mathematics allowed them to see patterns that might otherwise have remained hidden in the complex patient data.
"Now that we see this from the mathematical model, everything makes sense," said Skums. "When you look at this mathematically, you can see the whole picture."

Explore further: Sequencing technique unveiling the realm of viral mutations

More information: "Antigenic cooperation among intrahost HCV variants organized into a complex network of cross-immunoreactivity," Proceedings of the National Academy of Sciences, published ahead of print May 4, 2015. www.dx.doi.org/10.1073/pnas.1422942112

Geneticists solve 40-year-old dilemma to explain why duplicate genes remain in the genome.

An informational graphic of the process of gene duplication, showing how sister genes can confer mutational robustness by allowing organisms to adapt to novel environments. Credit: Mario Fares, 2014.

Source: Phys.org

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Geneticists at Trinity College Dublin have made a major breakthrough with important implications for understanding the evolution of genomes in a variety of organisms.
They found a mechanism sought for more than four decades that explains how gene duplication leads to novel functions in individuals.
Gene duplication is a biological phenomenon that leads to the sudden emergence of new genetic material. 'Sister' genes – the products of gene duplication – can survive across long evolutionary timescales, and allow organisms to tolerate otherwise lethal mutations.
The Trinity geneticists have now identified and described the mechanism underlying this increased tolerance, which is known as 'mutational robustness'.
By experimentally demonstrating that this robustness is important for yeast cells to adapt to novel conditions, including those that are stressful to the cells, they have underlined the likely reason for the existence of gene duplication.
"Natural selection - a process that keeps essential things in the cell - also removes genes that are redundant from the genome," said Dr Mario A Fares, Assistant Professor in Genetics at Trinity, and leading author of the study.
"The mechanism resolving the conflict between sister genes and their apparent evolutionary instability had remained a mystery for decades, but we have now cracked this latest part of the genetic code."
Gene duplication is a frequent phenomenon in eukaryotic organisms (which safeguard their genetic material within cell membranes), including yeast, plants, and animals. But understanding how duplication leads to biological innovation is difficult because evolution cannot be easily traced seeing as it occurs on timescales in the order of millions of years.
Despite their apparently redundant nature, duplicate genes that originated 100 million years ago can still be found in today's organisms. This phenomenon has always suggested the existence of a mechanism maintaining them in the genomes. The researchers in this study chose to work with yeast – an organism whose entire genome has been duplicated over time – to join up the dots.
They 'evolved' yeast cells in the laboratory under conditions that allowed the spread of mutations rejected by natural selection, by simply reducing the effect that natural selection had on these 'maladapted' cells. They found that duplicate genes tolerated the maladaptive mutations to a greater degree than non-duplicate genes.
The geneticists' simple experimental approach revealed that these genes, duplicated 100 million years ago, were still able to respond to different environments as they changed, as well as highlighting their potential to generate new adaptations that might give them an advantage in new environments.
"Discovering the mechanism of innovation through gene duplication marks an exciting beginning for a new era of research in which evolution can be conducted in the laboratory and theories hitherto speculative tested," added Dr Fares.
"Our discovery also has implications for explaining the importance of redundancy in the human society as well. The role of increased redundancies in a fashioned job market in lenient economical conditions could lead, in crisis times, to the emergence of new companies, specialized workforces, and the optimization of individual capabilities, for example, although this requires a profound investigation."
The research, recently published online in the high-profile international journal, Genome Research, was supported by Science Foundation Ireland (SFI).

Explore further: New study explains evolution of duplicate genes
Journal reference: Genome Research
Provided by Trinity College Dublin 

Biologists Wake Dormant Viruses and Uncover Mechanism for Survival.

This shows the functioning of Kap1 protein in mouse embrocation cells. (Credit: Pascal Coderay, pascal@salut.ch)

Source: ScienceDaily

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ScienceDaily (Jan. 14, 2010) — It is known that viral "squatters" comprise nearly half of our genetic code. These genomic invaders inserted their DNA into our own millions of years ago when they infected our ancestors. But just how we keep them quiet and prevent them from attack was more of a mystery until EPFL researchers revived them.

The reason we survive the presence of these endogenous retroviruses -- viruses that attack and are passed on through germ cells, the cells that give rise to eggs and sperm -- is because something keeps the killers silent. Now, publishing in the journal Nature, Didier Trono and his team from EPFL, in Switzerland, describe the mechanism. Their results provide insights into evolution and suggest potential new therapies in fighting another retrovirus -- HIV.
By analysing embryonic stem cells in mice within the first few days of life, Trono and team discovered that mouse DNA codes for an army of auxiliary proteins that recognize the numerous viral sequences littering the genome. The researchers also demonstrated that a master regulatory protein called KAP1 appears to orchestrate these inhibitory proteins in silencing would-be viruses. When KAP1 is removed, for example, the viral DNA "wakes up," multiplies, induces innumerable mutations, and the embryo soon dies.
Because retroviruses tend to mutate their host's DNA, they have an immense power and potential to alter genes. And during ancient pandemics, some individuals managed to silence the retrovirus involved and therefore survived to pass on the ability. Trono explains that the great waves of endogenous retrovirus appearance coincide with times when evolution seemed to leap ahead.
"In our genome we find traces of the last two major waves. The first took place 100 million years ago, at the time when mammals started to develop, and the second about fifty million years ago, just before the first anthropoid primates," he says.
The discovery of the KAP1 mechanism could be of interest in the search for new therapeutic approaches to combat AIDS. The virus that causes AIDS can lie dormant in the red blood cells it infects, keeping it hidden from potential treatments. Waking the virus up could expose it to attack.
Co-authors include Helen M. Rowe, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Switzerland; Johan Jakobsson, EPFL and Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Sweden; Daniel Mesnard, EPFL; Jacques Rougemont, EPFL; Séverine Reynard, EPFL; Tugce Aktas, EMBL Heidelberg, Germany; Pierre V. Maillard, EPFL; Hillary Layard-Liesching, EPFL; Sonia Verp, EPFL; Julien Marquis, EPFL; François Spitz, EMBL Heidelberg, Germany; Daniel B. Constam, EPFL; and Didier Trono, EPFL.

Story Source:
Adapted from materials provided by Ecole Polytechnique Fédérale de Lausanne, via EurekAlert!, a service of AAAS.

Chimp and human Y chromosomes evolving faster than expected.

Source: Physorg.com

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Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation.

By conducting the first comprehensive interspecies comparison of Y chromosomes, Whitehead Institute researchers have found considerable differences in the genetic sequences of the human and chimpanzee Ys—an indication that these chromosomes have evolved more quickly than the rest of their respective genomes over the 6 million years since they emerged from a common ancestor. The findings are published online this week in the journal Nature.
"The region of the Y that is evolving the fastest is the part that plays a role in sperm production," say Jennifer Hughes, first author on the Nature paper and a postdoctoral researcher in Whitehead Institute Director David Page's lab. "The rest of the Y is evolving more like the rest of the genome, only a little bit faster."
The chimp Y chromosome is only the second Y chromosome to be comprehensively sequenced. The original chimp genome sequencing completed in 2005 largely excluded the Y chromosome because its hundreds of repetitive sections typically confound standard sequencing techniques. Working closely with the Genome Center at Washington University, the Page lab managed to painstakingly sequence the chimp Y chromosome, allowing for comparison with the human Y, which the Page lab and the Genome Center at Washington University had sequenced successfully back in 2003.
The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content. The chimp Y, for example, has lost one third to one half of the human Y chromosome genes--a significant change in a relatively short period of time. Page points out that this is not all about gene decay or loss. He likens the Y chromosome changes to a home undergoing continual renovation.
"People are living in the house, but there's always some room that's being demolished and reconstructed," says Page, who is also a Howard Hughes Medical Institute investigator. "And this is not the norm for the genome as a whole."

Wes Warren, Assistant Director of the Washington University Genome Center, agrees. "This work clearly shows that the Y is pretty ingenious at using different tools than the rest of the genome to maintain diversity of genes," he says. "These findings demonstrate that our knowledge of the Y chromosome is still advancing."
Hughes and Page theorize that the divergent evolution of the chimp and human Y chromosomes may be due to several factors, including traits specific to Y chromosomes and differences in mating behaviors.
Because multiple male chimpanzees may mate with a single female in rapid succession, the males' sperm wind up in heated reproductive competition. If a given male produces more sperm, that male would theoretically be more likely to impregnate the female, thereby passing on his superior sperm production genes, some of which may be residing on the Y chromosome, to the next generation.
Because selective pressure to pass on advantageous sperm production genes is so high, those genes may also drag along detrimental genetic traits to the next generation. Such transmission is allowed to occur because, unlike other chromosomes, the Y has no partner with which to swap genes during cell division. Swapping genes between chromosomal partners can eventually associate positive gene versions with each other and eliminate detrimental gene versions. Without this ability, the Y chromosome is treated by evolution as one large entity. Either the entire chromosome is advantageous, or it is not.
In chimps, this potent combination of intense selective pressure on sperm production genes and the inability to swap genes may have fueled the Y chromosome's rapid evolution. Disadvantages from a less-than-ideal gene version or even the deletion of a section of the chromosome may have been outweighed by the advantage of improved sperm production, resulting in a Y chromosome with far fewer genes than its human counterpart.
To determine whether this rapid rate of evolution affects Y chromosomes beyond those of chimps and humans, the Page lab and the Washington University Genome Center are now sequencing and examining the Y chromosomes of several other mammals.
Provided by Massachusetts Institute of Technology.

Scientists sequence soybean genome, reveal pathways for improving biodiesel.

Soybean, one of the most important global sources of protein and oil, is now the first legume species with a published complete draft genome sequence. Credit: Roy Kaltschmidt, Lawrence Berkeley National Laboratory.

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Source: Physorg.com

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Soybean, one of the most important global sources of protein and oil, is now the first legume species with a published complete draft genome sequence. The sequence and its analysis appear in the January 14 edition of the journal Nature.

The research team comprised 18 institutions, including the U.S. Department of Energy Joint Genome Institute (DOE JGI), the U.S. Department of Agriculture-Agricultural Research Service (USDA-ARS), Purdue University and the University of North Carolina at Charlotte. The DOE, National Science Foundation, USDA and United Soybean Board supported the research.
"The soybean genome's billion-plus nucleotides afford us a better understanding of the plant's capacity to turn sunlight, carbon dioxide, nitrogen and water, into concentrated energy, protein, and nutrients for human and animal use," said Anna Palmisano, DOE Associate Director of Science for Biological and Environmental Research. "This opens the door to crop improvements that are sorely needed for energy production, sustainable human and animal food production, and a healthy environmental balance in agriculture worldwide."
With the soybean genetic code now determined, the research community has access to a key reference for more than 20,000 legume species and can explore the extraordinary evolutionary innovation of nitrogen-fixing symbiosis that is so critically important to successful agricultural crop rotation strategies.
Jeremy Schmutz, the study's first author and a DOE JGI scientist at the HudsonAlpha Institute for Biotechnology in Alabama, said that the soybean sequencing was the largest plant project done to date at the DOE Joint Genome Institute. "It also happens to be the largest plant that's ever been sequenced by the whole genome shotgun strategy—where we break it apart and reassemble it like a huge puzzle," he said. Of the more than 20 other plant genomes taken on by the DOE JGI, those already sequenced include the black cottonwood (poplar) tree and the grain sorghum, both targeted because of their promise as biomass feedstocks for biofuels production.
"This is a milestone for soybean research and promises to usher in a new era in soybean agronomic improvement," said co-author Gary Stacey, Director, Center for Sustainable Energy and Associate Director and National Center for Soybean Biotechnology, University of Missouri. "The genome provides a parts list of what it takes to make a soybean plant and, more importantly, helps to identify those genes that are essential for such important agronomic traits as protein and oil content."

From the sequence analysis, Stacey said that he and his colleagues have identified more than 46,000 genes of which 1,110 are involved in lipid metabolism. "These genes and their associated pathways are the building blocks for soybean oil content and represent targets that can be modified to bolster output and lead to the increase of the use of soybean oil for biodiesel production."
While biodiesel from soybean oil represents a cleaner, renewable alternative to fossil fuels with desirable properties as a liquid transportation fuel, there simply is not enough oil produced by the plant to be a competitive gasoline on a gallons-of-fuel yield per acre. The availability of the soybean genome may provide some key solutions. "We can now zero in on the control points governing carbon flow towards protein and oil," said Tom Clemente, Professor, Center for Biotechnology, Center for Plant Science Innovation at the University of Nebraska, Lincoln. "With the combination of informatics, biochemistry and genetics we can target the development of a soybean with greater than 40 percent oil content."
The availability of the soybean genome sequence has accelerated other soybean trait discovery efforts as well. For example, researchers have used the sequence to zero in on a mutation that can be used to select for a line that has lower levels of the sugar stachyose, which will improve the ability of animals and humans to digest soybeans.

In another effort, by comparing the genomes of soybean and corn, a single-base pair mutation was found that causes a reduction in phytate production in soybean. Phytate is the form in which phosphorous is stored in plant tissue. Because phytate is not absorbed by the animals that eat the feed, the unabsorbed phytate passes through the gastrointestinal tract, elevating the amount of phosphorus in the manure. Limiting phytate production in the soybean could reduce a major environmental runoff contaminant from swine and poultry waste.
Of additional importance for soybean farmers is that the genome sequence has provided access to the first resistance gene for the devastating disease Asian Soybean Rust (ASR). In countries where ASR is well established, soybean yield losses due to the disease can be as high as 80 percent.

Provided by DOE/Joint Genome Institute

Chimp and Human Y Chromosomes Evolving Faster Than Expected.

Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation. (Credit: iStockphoto/Wesley Jenkins)

Source: ScienceDaily

-------------------------

ScienceDaily (Jan. 13, 2010) — Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation.

By conducting the first comprehensive interspecies comparison of Y chromosomes, Whitehead Institute researchers have found considerable differences in the genetic sequences of the human and chimpanzee Ys -- an indication that these chromosomes have evolved more quickly than the rest of their respective genomes over the 6 million years since they emerged from a common ancestor. The findings are published online this week in the journal Nature.
"The region of the Y that is evolving the fastest is the part that plays a role in sperm production," say Jennifer Hughes, first author on the Nature paper and a postdoctoral researcher in Whitehead Institute Director David Page's lab. "The rest of the Y is evolving more like the rest of the genome, only a little bit faster."
The chimp Y chromosome is only the second Y chromosome to be comprehensively sequenced. The original chimp genome sequencing completed in 2005 largely excluded the Y chromosome because its hundreds of repetitive sections typically confound standard sequencing techniques. Working closely with the Genome Center at Washington University, the Page lab managed to painstakingly sequence the chimp Y chromosome, allowing for comparison with the human Y, which the Page lab and the Genome Center at Washington University had sequenced successfully back in 2003.
The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content. The chimp Y, for example, has lost one third to one half of the human Y chromosome genes--a significant change in a relatively short period of time. Page points out that this is not all about gene decay or loss. He likens the Y chromosome changes to a home undergoing continual renovation.
"People are living in the house, but there's always some room that's being demolished and reconstructed," says Page, who is also a Howard Hughes Medical Institute investigator. "And this is not the norm for the genome as a whole."
Wes Warren, Assistant Director of the Washington University Genome Center, agrees. "This work clearly shows that the Y is pretty ingenious at using different tools than the rest of the genome to maintain diversity of genes," he says. "These findings demonstrate that our knowledge of the Y chromosome is still advancing."
Hughes and Page theorize that the divergent evolution of the chimp and human Y chromosomes may be due to several factors, including traits specific to Y chromosomes and differences in mating behaviors.
Because multiple male chimpanzees may mate with a single female in rapid succession, the males' sperm wind up in heated reproductive competition. If a given male produces more sperm, that male would theoretically be more likely to impregnate the female, thereby passing on his superior sperm production genes, some of which may be residing on the Y chromosome, to the next generation.
Because selective pressure to pass on advantageous sperm production genes is so high, those genes may also drag along detrimental genetic traits to the next generation. Such transmission is allowed to occur because, unlike other chromosomes, the Y has no partner with which to swap genes during cell division. Swapping genes between chromosomal partners can eventually associate positive gene versions with each other and eliminate detrimental gene versions. Without this ability, the Y chromosome is treated by evolution as one large entity. Either the entire chromosome is advantageous, or it is not.
In chimps, this potent combination of intense selective pressure on sperm production genes and the inability to swap genes may have fueled the Y chromosome's rapid evolution. Disadvantages from a less-than-ideal gene version or even the deletion of a section of the chromosome may have been outweighed by the advantage of improved sperm production, resulting in a Y chromosome with far fewer genes than its human counterpart.
To determine whether this rapid rate of evolution affects Y chromosomes beyond those of chimps and humans, the Page lab and the Washington University Genome Center are now sequencing and examining the Y chromosomes of several other mammals.
This research was funded by the National Institutes of Health (NIH) and the Howard Hughes Medical Institute (HHMI).

Story Source:
Adapted from materials provided by Whitehead Institute for Biomedical Research. Original article written by Nicole Giese.
Journal Reference:
1. Jennifer F. Hughes, Helen Skaletsky, Tatyana Pyntikova, Tina A. Graves, Saskia K. M. Van Daalen, Patrick J. Minx, Robert S. Fulton, Sean D. Mcgrath, Devin P. Locke, Cynthia Friedman, Barbara J. Trask, Elaine R. Mardis, Wesley C. Warren, Sjoerd Repping, Steve Rozen, Richard K. Wilson, David C. Page. Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content. Nature, Online January 13, 2010

'Longevity Gene' Helps Prevent Memory Decline and Dementia.

Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a "longevity gene" helps to slow age-related decline in brain function in older adults. Drugs that mimic the gene's effect are now under development, the researchers note, and could help protect against Alzheimer's disease. (Credit: iStockphoto/Anne De Haas)

Source: ScienceDaily

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ScienceDaily (Jan. 13, 2010) — Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a "longevity gene" helps to slow age-related decline in brain function in older adults. Drugs that mimic the gene's effect are now under development, the researchers note, and could help protect against Alzheimer's disease.

The paper describing the Einstein study is published in the January 13 edition of the Journal of the American Medical Association.
"Most work on the genetics of Alzheimer's disease has focused on factors that increase the danger," said Richard B. Lipton, M.D., the Lotti and Bernard Benson Faculty Scholar in Alzheimer's Disease and professor and vice chair in the Saul R. Korey Department of Neurology at Einstein and senior author of the paper. As an example, he cites APOE ε4, a gene variant involved in cholesterol metabolism that is known to increase the risk of Alzheimer's among those who carry it.
"We reversed this approach," says Dr. Lipton, "and instead focused on a genetic factor that protects against age-related illnesses, including both memory decline and Alzheimer's disease."
In a 2003 study, Dr. Lipton and his colleagues identified the cholesteryl ester transfer protein (CETP) gene variant as a "longevity gene" in a population of Ashkenazi Jews. The favorable CETP gene variant increases blood levels of high-density lipoprotein (HDL) -- the so-called good cholesterol -- and also results in larger-than-average HDL and low-density lipoprotein (LDL) particles.
The researchers of the current study hypothesized that the CETP longevity gene might also be associated with less cognitive decline as people grow older. To find out, they examined data from 523 participants from the Einstein Aging Study, an ongoing federally funded project that has followed a racially and ethnically diverse population of elderly Bronx residents for 25 years.
At the beginning of the study, the 523 participants -- all of them 70 or over -- were cognitively healthy, and their blood samples were analyzed to determine which CETP gene variant they carried. They were then followed for an average of four years and tested annually to assess their rates of cognitive decline, the incidence of Alzheimer's disease and other changes.
"We found that people with two copies of the longevity variant of CETP had slower memory decline and a lower risk for developing dementia and Alzheimer's disease," says Amy E. Sanders, M.D., assistant professor in the Saul R. Korey Department of Neurology at Einstein and lead author of the paper. "More specifically, those participants who carried two copies of the favorable CETP variant had a 70 percent reduction in their risk for developing Alzheimer's disease compared with participants who carried no copies of this gene variant."
The favorable gene variant alters CETP so that the protein functions less well than usual. Dr. Lipton notes that drugs are now being developed that duplicate this effect on the CETP protein. "These agents should be tested for their ability to promote successful aging and prevent Alzheimer's disease," he recommends.
The research was funded by the National Institute on Aging, one of the 27 institutes and centers of the National Institutes of Health.

Story Source:
Adapted from materials provided by Albert Einstein College of Medicine.

Journal Reference:
1. Sanders et al. Association of a Functional Polymorphism in the Cholesteryl Ester Transfer Protein (CETP) Gene With Memory Decline and Incidence of Dementia. JAMA The Journal of the American Medical Association, 2010; 303 (2): 150 DOI: 10.1001/jama.2009.1988