Chapter 7. Life-Span Development of the Brain and Behavior
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By Dominic Howell BBC News Gum disease has been linked to a greater rate of cognitive decline in people with Alzheimer's disease, early stage research has suggested. The small study, published in PLOS ONE, looked at 59 people who were all deemed to have mild to moderate dementia. It is thought the body's response to gum inflammation may be hastening the brain's decline. The Alzheimer's Society said if the link was proven to be true, then good oral health may help slow dementia. The body's response to inflammatory conditions was cited as a possible reason for the quicker decline. Inflammation causes immune cells to swell and has long been associated with Alzheimer's. Researchers believe their findings add weight to evidence that inflammation in the brain is what drives the disease. 'Six-fold increase' The study, jointly led by the University of Southampton and King's College London, cognitively assessed the participants, and took blood samples to measure inflammatory markers in their blood. Their oral health was also assessed by a dental hygienist who was unaware of the cognitive outcomes. Of the sample group, 22 were found to have considerable gum disease while for the remaining 37 patients the disease was much less apparent. The average age of the group with gum disease was 75, and in the other group it was 79. A majority of participants - 52 - were followed up at six months, and all assessments were repeated. The presence of gum disease - or periodontitis as it is known - was associated with a six-fold increase in the rate of cognitive decline, the study suggested. © 2016 BBC
Link ID: 21976 - Posted: 03.12.2016
Susan Gaidos Most people would be happy to get rid of excess body fat. Even better: Trade the spare tire for something useful — say, better-functioning knees or hips, or a fix for an ailing heart or a broken bone. The idea is not far-fetched, some scientists say. Researchers worldwide are repurposing discarded fat to repair body parts damaged by injury, disease or age. Recent studies in lab animals and humans show that the much-maligned material can be a source of cells useful for treating a wide range of ills. At the University of Pittsburgh, bioengineer Rocky Tuan and colleagues extract buckets full of yellow fat from volunteers’ bellies and thighs and turn the liposuctioned material into tissue that resembles shock-absorbing cartilage. If the cartilage works as well in people as it has in animals, Tuan’s approach might someday offer a kind of self-repair for osteoarthritis, the painful degeneration of cartilage in the joints. He’s also using fat cells to grow replacement parts for the tendons and ligaments that support the joints. Foremost among fat’s virtues is its richness of stem cells, which have the ability to divide and grow into a wide variety of tissue types. Fat stem cells — also known as adipose-derived stem cells — can be coerced to grow into bone, cartilage, muscle tissue or, of course, more fat. Cells from fat are being tested to mend tissues found in damaged joints, hearts and muscle, and to regrow bone and heal wounds. © Society for Science & the Public 2000 - 2016
Rich Stanton In 1976, the driving simulation Death Race was removed from an Illinois amusement park. There had, according to a news story at the time, been complaints that it encouraged players to run over pedestrians to score points. Through a series of subsequent newspaper reports, the US National Safety Council labelled the game “gross” and motoring groups demanded its removal from distribution. The first moral panic over video game violence had begun. This January, a group of four scholars published a paper analysing the links between playing violent video games at a young age and aggressive behaviour in later life. The titles mentioned in the report are around 15-years-old – one of several troubling ambiguities to be found in the research. Nevertheless, the quality and quantity of the data make this an uncommonly valuable study. Given that game violence remains a favoured bogeyman for politicians, press and pressure groups, it should be shocking that such a robust study of the phenomenon is rare. But it is, and it’s important to ask why. A history of violence With the arrival of Pong in 1973, video games became a commercial reality, but now, in 2016, they are still on the rocky path to mass acceptance that all new media must traverse. The truth is that the big targets of moral concern – Doom, Grand Theft Auto, Call of Duty – are undeniably about killing and they are undeniably popular among male teenagers. An industry report estimates that 80% of the audience for the Call of Duty series is male, and 21% is aged 10-14. Going by the 18 rating on the last three entries, that means at least a fifth of the game’s vast audience shouldn’t be playing. © 2016 Guardian News and Media Limited
By GINA KOLATA Marty and Matt Reiswig, two brothers in Denver, knew that Alzheimer’s disease ran in their family, but neither of them understood why. Then a cousin, Gary Reiswig, whom they barely knew, wrote a book about their family, “The Thousand Mile Stare.” When the brothers read it, they realized what they were facing. In the extended Reiswig family, Alzheimer’s disease is not just a random occurrence. It results from a mutated gene that is passed down from parent to child. If you inherit the mutated gene, Alzheimer’s will emerge at around age 50 — with absolute certainty. Your child has a 50-50 chance of suffering the same fate. The revelation came as a shock. And so did the next one: The brothers learned that there is a blood test that can reveal whether one carries the mutated gene. They could decide to know if they had it. Or not. It’s a dilemma more people are facing as scientists discover more genetic mutations linked to diseases. Often the newly discovered gene increases risk, but does not guarantee it. Sometimes knowing can be useful: If you have a gene mutation that makes colon cancer much more likely , for example, then frequent colonoscopies may help doctors stave off trouble. But then there are genes that make a dreaded disease a certainty: There is no way to prevent it, and no way to treat it. Marty Reiswig, 37, saw his father, now in the final stages of Alzheimer’s, slowly lose his ability to think, to remember, to care for himself, or even to recognize his wife and sons. Mr. Reiswig knows that if he has the gene, he has perhaps a bit more than a decade before the first symptoms appear. If he has it, his two young children may have it, too. He wavers about getting tested. © 2016 The New York Times Company
By DONALD G. McNEIL Jr. and CATHERINE SAINT LOUIS The Zika virus damages many fetuses carried by infected and symptomatic mothers, regardless of when in pregnancy the infection occurs, according to a small but frightening study released on Friday by Brazilian and American researchers. In a separate report published on Friday, other scientists suggested a mechanism for the damage, showing in laboratory experiments that the virus targets and destroys fetal cells that eventually form the brain’s cortex. The reports are far from conclusive, but the studies help shed light on a mysterious epidemic that has swept across more than two dozen countries in the Western Hemisphere, alarming citizens and unnerving public health officials. In the first study, published in The New England Journal of Medicine, researchers found that 29 percent of women who had ultrasound examinations after testing positive for infection with the Zika virus had fetuses that suffered “grave outcomes.” They included fetal death, tiny heads, shrunken placentas and nerve damage that suggested blindness. “This is going to have a chilling effect,” said Dr. Anthony S. Fauci, the director of the National Institute of Allergy and Infectious Diseases. “Now there’s almost no doubt that Zika is the cause.” The small size of the study, which looked at 88 women at one clinic in Rio de Janeiro, was a limitation, Dr. Fauci added. From such a small sample, it is impossible to be certain how often fetal damage may occur in a much larger population. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21957 - Posted: 03.05.2016
Ewan Birney The Daily Mail recently ran an article about how alcohol abuse could harm future generations, via the (exciting-sounding) mechanism of trans-generational epigenetics. This is an emotive topic, combining a commonplace habit (drinking beer and wine) with a scary outcome (harming your children, grandchildren and future generations) and adding a twist of science for gravitas. It’s not surprising that this research has been handed a megaphone by the mainstream press – but does the science stack up? To start with, the research was carried out in rats, as multi-generational experiments on humans are both grossly unethical and logistically extremely hard. This crucial bit of information is missing from both the Daily Mail headline and the paper’s title. Secondly, the big effects of alcohol consumption were mainly seen on the rats’ children and grandchildren – the effects on their great grandchildren were smaller. That is really important, because if there’s no effect on great grandchildren, it’s probably not due to epigenetics. Drinking large amounts of alcohol (for a rat) whilst pregnant would be expected to have an effect on the children and even the grandchildren. This is because the eggs of female mammals are made early on in foetal development, whilst a daughter is developing in the womb. So if that cell (the egg) also gives rise to a daughter, she will have directly experienced exposures that occurred during her maternal grandmother’s pregnancy. © 2016 Guardian News and Media Limited or its affiliated companies.
By Meeri Kim Teenagers tend to have a bad reputation in our society, and perhaps rightly so. When compared to children or adults, adolescents are more likely to engage in binge drinking, drug use, unprotected sex, criminal activity, and reckless driving. Risk-taking is like second nature to youth of a certain age, leading health experts to cite preventable and self-inflicted causes as the biggest threats to adolescent well-being in industrialized societies. But before going off on a tirade about groups of reckless young hooligans, consider that a recent study may have revealed a silver lining to all that misbehavior. While adolescents will take more risks in the presence of their peers than when alone, it turns out that peers can also encourage them to learn faster and engage in more exploratory acts. A group of 101 late adolescent males were randomly assigned to play the Iowa Gambling Task, a psychological game used to assess decision making, either alone or observed by their peers. The task involves four decks of cards: two are “lucky” decks that will generate long-term gain if the player continues to draw from them, while the other two are “unlucky” decks that have the opposite effect. The player chooses to play or pass cards drawn from one of these decks, eventually catching on to which of the decks are lucky or unlucky — and subsequently only playing from the lucky ones.
Laura Sanders In a multivirus competition, a newcomer came out on top for its ability to transport genetic cargo to a mouse’s brain cells. The engineered virus AAV-PHP.B was best at delivering a gene that instructed Purkinje cells, the dots in the micrograph above, to take on a whitish glow. Unaffected surrounding cells in the mouse cerebellum look blue. Cargo carried by viruses like AAV-PHP.B could one day replace faulty genes in the brains of people. AAV-PHP.B beat out other viruses including a similar one called AAV9, which is already used to get genes into the brains of mice. Genes delivered by AAV-PHP.B also showed up in the spinal cord, retina and elsewhere in the body, Benjamin Deverman of Caltech and colleagues report in the February Nature Biotechnology. Similar competitions could uncover viruses with the ability to deliver genes to specific types of cells, the researchers write. Selective viruses that can also get into the brain would enable deeper studies of the brain and might improve gene therapy techniques in people. © Society for Science & the Public 2000 - 2016
By DONALD G. McNEIL Jr. A baby with a shrunken, misshapen head is surely a heartbreaking sight. But reproductive health experts are warning that microcephaly may be only the most obvious consequence of the spread of the Zika virus. Even infants who appear normal at birth may be at higher risk for mental illnesses later in life if their mothers were infected during pregnancy, many researchers fear. The Zika virus, they say, closely resembles some infectious agents that have been linked to the development of autism, bipolar disorder and schizophrenia. Schizophrenia and other debilitating mental illnesses have no single cause, experts emphasized in interviews. The conditions are thought to arise from a combination of factors, including genetic predisposition and traumas later in life, such as sexual or physical abuse, abandonment or heavy drug use. But illnesses in utero, including viral infections, are thought to be a trigger. “The consequences of this go way beyond microcephaly,” said Dr. W. Ian Lipkin, who directs The Center for Infection and Immunity at Columbia University. Here is a look at the most prominent rumors and theories about Zika virus, along with responses from scientists. Among children in Latin America and the Caribbean, “I wouldn’t be surprised if we saw a big upswing in A.D.H.D., autism, epilepsy and schizophrenia,” he added. “We’re looking at a large group of individuals who may not be able to function in the world.” © 2016 The New York Times Company
By Nicholas Bakalar The popular heartburn drugs known as proton pump inhibitors have been linked to a range of ills: bone fractures, kidney problems, infections and more. Now a large new study has found that they are associated with an increased risk for dementia as well. Proton pump inhibitors, or P.P.I.s, are widely available both by prescription and over the counter under various brand names, including Prevacid, Prilosec and Nexium. German researchers, using a database of drug prescriptions, studied P.P.I. use in 73,679 men and women older than 75 who were free of dementia at the start of the study. Over an average follow-up period of more than five years, about 29,000 developed Alzheimer’s disease or other dementias. The study is in JAMA Neurology. After controlling for age, sex, depression, diabetes, stroke, heart disease and the use of other medicines, they found that regular use of P.P.I.s increased the risk for dementia in men by 52 percent and in women by 42 percent, compared with nonusers. “Our study does not prove that P.P.I.s cause dementia,” said the senior author, Britta Haenisch of the German Center for Neurodegenerative Diseases. “It can only provide a statistical association. This is just a small part of the puzzle. “Clinicians, pharmacists and patients have to weigh the benefits against the potential side effects,” she continued, “and future studies will help to better inform these decisions.” © 2016 The New York Times Company
Link ID: 21910 - Posted: 02.19.2016
By Gretchen Reynolds Some forms of exercise may be much more effective than others at bulking up the brain, according to a remarkable new study in rats. For the first time, scientists compared head-to-head the neurological impacts of different types of exercise: running, weight training and high-intensity interval training. The surprising results suggest that going hard may not be the best option for long-term brain health. As I have often written, exercise changes the structure and function of the brain. Studies in animals and people have shown that physical activity generally increases brain volume and can reduce the number and size of age-related holes in the brain’s white and gray matter. Exercise also, and perhaps most resonantly, augments adult neurogenesis, which is the creation of new brain cells in an already mature brain. In studies with animals, exercise, in the form of running wheels or treadmills, has been found to double or even triple the number of new neurons that appear afterward in the animals’ hippocampus, a key area of the brain for learning and memory, compared to the brains of animals that remain sedentary. Scientists believe that exercise has similar impacts on the human hippocampus. These past studies of exercise and neurogenesis understandably have focused on distance running. Lab rodents know how to run. But whether other forms of exercise likewise prompt increases in neurogenesis has been unknown and is an issue of increasing interest, given the growing popularity of workouts such as weight training and high-intensity intervals. So for the new study, which was published this month in the Journal of Physiology, researchers at the University of Jyvaskyla in Finland and other institutions gathered a large group of adult male rats. The researchers injected the rats with a substance that marks new brain cells and then set groups of them to an array of different workouts, with one group remaining sedentary to serve as controls. © 2016 The New York Times Company
Link ID: 21902 - Posted: 02.17.2016
Meghan Rosen The people of Flint, Mich., are drinking bottled water now, if they can get it. Volunteers deliver it door-to-door and to local fire stations. The goal is to keep the city’s residents from ingesting so much lead. Success – or lack thereof – could have consequences not just now, but for generations to come. Late last year, scientists raised alarms over a link between the city’s lead-tainted water and the growing number of children with high lead levels in their blood. It’s a serious problem. Lead is toxic to the brain, something scientists have long known. “Lead is probably the most well-known neurotoxin to man,” says Mona Hanna-Attisha, the pediatrician who first connected lead in Flint’s water to lead exposure in kids. And as scientists are beginning to find out, the damage that lead inflicts on children may be long-lasting. In addition to harming kids during youth, lead could contribute to disorders that develop later in life, such as Alzheimer’s disease or schizophrenia. Lead’s reach could extend even further, too — beyond those who drank the contaminated water to their children and grandchildren. Flint’s kids “will have to be followed throughout their whole life, and maybe into the next generation or two,” says Douglas Ruden, a neural toxicologist at Wayne State University in Detroit. A few months of drinking clean water will help bring the kids’ lead levels back down, he says. “But the damage is done.” And it’s permanent. In the United States, lead is everywhere. Decades of burning leaded gasoline spewed lead into the air, and the element settled in the upper layer of soil, clinging to particles of dirt. © Society for Science & the Public 2000 - 2016.
By Lindsey Tanner CHICAGO — Two blood-building drugs injected soon after birth may give premature babies a lasting long-term edge, boosting brain development and IQ by age 4, a first-of-its-kind study found. The study was small but the implications are big if larger, longer studies prove the drugs help level the playing field for these at-risk newborns, the researchers and other experts say. Preemies who received the medicines scored much better by age 4 on measures of intelligence, language and memory than those who did not. The medicine-receiving group’s scores on an important behavior measure were just as high as a control group of 4-year-olds born on time at a normal weight. The results are “super exciting,” said Robin Ohls, the lead author and a pediatrics professor at the University of New Mexico. She said it is the first evidence of long-term benefits of the drugs when compared with no blood-boosting treatment. Although the treated babies didn’t do as well as the normal-weight group on most measures, their scores were impressive and suggest greater brain development than the other preemies, Ohls said. They scored about 12 points higher on average on IQ tests than the untreated infants but about 10 points lower than the normal-weight group. On tests measuring memory and impulsive behavior, the treated babies fared as well as those born at normal weight.
Keyword: Development of the Brain
Link ID: 21896 - Posted: 02.15.2016
Laura Sanders WASHINGTON — Tiny orbs of brain cells swirling in lab dishes may offer scientists a better way to study the complexities of the human brain. Toxicologist Thomas Hartung described these minibrains, grown from stem cells derived from people’s skin cells, at the annual meeting of the American Association for the Advancement of Science. Insights from experiments on animals are often difficult to apply to humans, Hartung, of Johns Hopkins University, said in a news briefing February 12. “We need something else,” he said. “We are not 150-pound rats.” These minibrains aren’t flashy. Other minibrain systems created by scientists in the past have complex neural structures and elaborate development (SN: 9/21/13, p. 5), representing the Ferraris and Maseratis of minibrains, Hartung said. In contrast, he said, his minibrains are Mini Coopers. But these bare-bones models, made of busy nerve cells and support cells in a sphere about the size of a fly eye, offer a standardized system that can reliably test the effects of a wide range of drugs. Hartung and colleagues are developing a company to make minibrains quickly available to researchers who could use them to study such disorders as autism, depression and Alzheimer’s disease, he said. The minibrains would cost about as much as a lab rat. © Society for Science & the Public 2000 - 2016
Keyword: Development of the Brain
Link ID: 21895 - Posted: 02.15.2016
By Uri Bram Early-life exposure to pathogenic bacteria can induce a lifelong imprinted olfactory memory in C. elegans through two distinct neural circuits, according to a study published today (February 11) in Cell. Researchers from Rockefeller University in New York City have shown that early-life pathogen exposure leads the nematode to have a lifelong aversion to the specific associated bacterial odors, whereas later-in-life exposure spurs only transient aversion. “This study is very exciting,” said Yun Zhang of Harvard who studies learning in C. elegans but was not involved in the present work. “Imprinting is a form of learning widely observed in many animals [but] finding this in C. elegans is very meaningful because this nematode is genetically tractable, and its small nervous system is well described.” A classic example of imprinting is how geese form attachments to the first moving object they see after birth; Nobel laureate Konrad Lorenz famously showed that the “moving object” could be himself instead of a mother goose. During the critical period at the start of life, animals often have unusual abilities to create and maintain long-term memories. For the present study, Rockefeller’s Xin Jin and colleagues described a form of aversive imprinting in their C. elegans: newly hatched nematodes exposed to Pseudomonas aeruginosa PA14 or toxin-emitting Escherichia coli BL21 established a long-term olfactory aversion to it. Animals that experienced the pathogen immediately after hatching were able to synthesize and maintain the aversive memory for the whole of their four-day lifespans, while animals trained in adulthood only retained the aversive memory for up to 24 hours. © 1986-2016 The Scientist
Alan Yuhas in Washington DC Scientists working on genetically modified worms have made what they hope are the first steps towards developing a preventative treatment for Alzheimer’s disease. The study, published in the journal Science Advances and presented at the American Association for the Advancement of Science conference, describes how researchers modified nematode worms to develop Alzheimer’s-like symptoms, and then applied the existing anti-cancer drug, bexarotene, at various stages of the disease. “We showed that these worms that were doomed to develop Alzheimer’s disease could be rescued,” said study author Michele Vendruscolo, of the University of Cambridge. “It is a powerful first step,” he said. “It is very exciting, but at the same time we are very aware it the first step and many things can go wrong.” Researchers believe that Alzheimer’s destroys brain function through a catastrophic cascade of events: natural proteins start folding and glomming onto each other in dysfunctional ways, a process that in turn creates the toxic molecules thought to kill brain cells. When the proteins started malfunctioning in the worms, the drug could do nothing to save them. But if administered before symptoms developed, it prevented the first stage of the process. © 2016 Guardian News and Media Limited
By PAM BELLUCK The risk of developing dementia is decreasing for people with at least a high school education, according to an important new study that suggests that changes in lifestyle and improvements in physical health can help prevent or delay cognitive decline. The study, published Wednesday in The New England Journal of Medicine, provides the strongest evidence to date that a more educated population and better cardiovascular health are contributing to a decline in new dementia cases over time, or at least helping more people stave off dementia for longer. The findings have implications for health policy and research funding, and they suggest that the long-term cost of dementia care may not be as devastatingly expensive as policy makers had predicted, because more people will be able to live independently longer. There are wild cards that could dampen some of the optimism. The study participants were largely white and suburban, so results may not apply to all races and ethnicities. Still, a recent study showed a similar trend among African-Americans in Indianapolis, finding that new cases of dementia declined from 1992 to 2001. The 2001 participants had more education, and although they had more cardiovascular problems than the 1992 participants, those problems were receiving more medical treatment. Another question mark is whether obesity and diabetes, which increase dementia risk, will cause a surge in dementia cases when the large number of overweight or diabetic 40- and 50-year-olds become old enough to develop dementia. © 2016 The New York Times Company
By CARL ZIMMER The Zika virus has quickly gained Ebola-level notoriety as it has spread through the Western Hemisphere in recent months. Researchers in Brazil, where it was first detected in May, have linked infections in pregnant women to a condition known as microcephaly: infants born with undersize heads. Where birth defects are concerned, however, the Zika virus is far from unique. A number of other viruses, such as rubella and cytomegalovirus, pose a serious risk during pregnancy. Researchers have uncovered some important clues about how those pathogens injure fetuses — findings that are now helping to guide research into the potential link between Zika and microcephaly. “I think we’ll discover a lot of parallels,” said Dr. Mark R. Schleiss, the director of pediatric infectious diseases and immunology at the University of Minnesota Medical School. The risk that viruses pose during pregnancy came to light in the mid-1900s, when outbreaks of rubella, or German measles, led to waves of birth defects, including microcephaly, cataracts and deformed hearts and livers. The number of infants affected was staggering. In an epidemic in Philadelphia in 1965, 1 percent of all babies were born with congenital rubella syndrome, which can also cause deafness, developmental disability, low birth weight and seizures. Because of vaccinations, such devastation is now rare in the United States and a number of other countries. “I’m 52, and I’ve seen one case of congenital rubella syndrome,” said Dr. David W. Kimberlin, a professor of pediatrics at the University of Alabama at Birmingham. But the virus is still a grave threat in developing countries. Worldwide, more than 100,000 children are born each year with congenital rubella syndrome. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21883 - Posted: 02.10.2016
By Nicholas Bakalar Eating seafood is linked to a reduced risk of dementia-associated brain changes in people who carry the ApoE4 gene variation, which increases the risk for Alzheimer’s disease. Eating seafood was not linked to similar changes in those who carried other forms of the ApoE gene. The study, published in JAMA, looked at 286 autopsied brains and also found that eating seafood was linked to increased mercury in the brain, but that mercury levels were not linked to brain abnormalities. After controlling for age, sex, education and other factors, the researchers found that compared with those who ate less seafood, ApoE4 carriers who had one seafood meal or more a week had lower densities of the amyloid plaques and neurofibrillary tangles typical of Alzheimer’s disease. Over all, they had a 47 percent lower likelihood of having a post-mortem diagnosis of Alzheimer’s. Consumption of fish oil supplements was not correlated with pathological brain changes. The lead author, Martha Clare Morris, a professor of epidemiology at Rush University, said that mercury from fish appears to pose little risk for aging people. But, she said, there are studies that show that mercury consumption in pregnancy can cause cognitive problems in babies. “Most studies in dementia have found that one seafood meal a week is beneficial,” she said, though “they haven’t found that the more you eat, the lower the risk.” © 2016 The New York Times Company
Link ID: 21879 - Posted: 02.10.2016
Laura Sanders A preliminary report from scientists at the biotech company Amgen Inc. questions a cancer drug’s ability to fight Alzheimer’s disease. In experiments described February 4 in F1000Research, bexarotene, a drug approved by the FDA to treat lymphoma, didn’t reduce levels of the Alzheimer’s-related amyloid-beta protein. In the original work, described in Science in 2012 (SN: 3/10/12, p. 5), neuroscientist Gary Landreth of Case Western Reserve University in Cleveland and colleagues showed that bexarotene swiftly clears A-beta from the brains of mice, reducing both the sticky plaques and smaller forms of the protein that circulate in the brain. The mice also showed signs of improved learning and memory. A year after that work appeared, four reports, also in Science, disputed some of those findings. In tests on rats, the Amgen scientists found that bexarotene didn’t drop levels of plaques or smaller forms of A-beta. The new study didn’t describe behavioral tests. Landreth points out that this study, and previous experiments that failed to find a benefit, used a formulation of the drug that wouldn’t persist at high enough levels in the brain to be useful. “The controversy with the preclinical data is going to go away in the face of solid clinical trials,” Landreth says. A small clinical trial published online January 29 in Alzheimer’s Research & Therapy found that bexarotene reduced A-beta in the brains of people, but only people without a particular version of the ApoE gene, a known risk factor for Alzheimer’s. © Society for Science & the Public 2000 - 2016
Link ID: 21871 - Posted: 02.09.2016