Scientists from Imperial College believe that intelligence may be influenced by two networks of genes, possibly controlled by a master regulatory system 
 
 British scientists believe they have made a huge step forward in the understanding of the mechanisms of human intelligence. That genetic inheritance must play some part has never been disputed. Despite occasional claims later dismissed, no-one has yet produced a single gene that controls intelligence. 
 
 But Michael Johnson of Imperial College London, a consultant neurologist and colleagues report in Nature Neuroscience that they may have discovered a very different answer: two networks of genes, perhaps controlled by some master regulatory system, lie behind the human gift for lateral thinking, mental arithmetic, pub quizzes, strategic planning, cryptic crosswords and the ability to laugh at limericks. 
 
 Diverse parental genes lead to taller, smarter children, finds extensive study Read more 
 
 As usual, such research raises potentially politically-loaded questions about the nature of intelligence. “Intelligence is a composite measure of different cognitive abilities and how they are distributed in a population. It doesn’t measure any one thing. But it is measurable,” Dr Johnson said. 
 
 About 40% of the variation in intelligence is explained by inheritance. The other factors are not yet certain. But the scientists raise the distant possibility that armed with the new information they may be able to devise ways to modify human intelligence. 
 
 “The idea of ultimately using drugs to affect cognitive performance is not in any way new. We all drink coffee to improve our cognitive performance,” Dr Johnson said. “It’s about understanding the pathways that are related to cognitive ability both in health and disease, especially disease so one day we could help people with learning disabilities fulfil their potential. That is very important.” 
 
 The two networks, known just as M1 and M3, one with roughly 1000 genes, the other with more than a 100, also play a role in neurodevelopmental disorders such as epilepsy, schizophrenia and autism. The functions do not seem to overlap, and the role of each network has yet to be settled. 
 
 “We know that genetics plays a major role in intelligence but until now haven’t known which genes are relevant. This research highlights some of the genes involved in human intelligence and how they interact with each other,” Dr Johnson said. “What’s exciting about this is that the genes we have found are likely to share a common regulation, which means that potentially we can manipulate a whole set of genes whose activity is linked to human intelligence.” 
 
 The discovery is testament to the power of patience, patients and the assembly of huge sets of data. The Imperial College scientists started with evidence from 100 mouse brains, 122 samples of human brain, and 102 whole human brains preserved postmortem. Such indicators of a genetic connection between neurodevelopmental problems or memory and understanding were then checked against records of 6,732 people in the “Generation Scotland” family health study, which tracks the life history of thousands of volunteers, and repeated in 1,003 healthy people who had volunteered to take part in a study called the Lothian Birth Cohort 1936. 
 
 Gene linked to long life also protects against mental decline in old age Read more 
 
 It assessed a range of cognitive abilities – among them memory, attention, processing speed and reasoning – and then it combined the results with genetic information donated by healthy people who had taken IQ tests, and from people with autism spectrum disorder and intellectual disability. Included in the research were studies of people who had undergone neurosurgery for epilepsy. 
 
 Then the scientists then harnessed massive computing power to see what the data could tell them. They found that the genes that influenced the intelligence and ability of healthy people were the same ones that impaired cognitive ability and caused epilepsy when mutated. If researchers understand what may go wrong in the interplay of inheritance that delivers human reasoning or memory, they might – the possibility for the moment is only theoretical – be able to devise new ways to deliver help. 
 
 “Traits such as intelligence are governed by large groups of genes working together - like a football team made up of players in different position,” he said. “We found that some of these genes overlap with those that cause severe childhood onset epilepsy or intellectual disability,” 
 
 The researchers may have identified a pool of players in a team: they still have to identify how the players co-operate, which are the key players and precisely what game is being played. 
 
 “Eventually we hope that this sort of analysis will provide new insights into better treatments for neurodevelopmental disease such as epilepsy, and ameliorate or treat the cognitive impairments associated with these devastating diseases.” 
 
 • This article was amended on 29 December 2015 to remove a reference to autism as a neurodevelopmental illness; it is a disorder, not an illness. ||||| Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Estimates vary, but experts suggest that more than 5 million Americans may have Alzheimer’s. 
 
 Alzheimer's disease is currently ranked as the sixth leading cause of death in the United States, but recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people. 
 
 Alzheimer’s is the most common cause of dementia among older adults. Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living. 
 
 The causes of dementia can vary, depending on the types of brain changes that may be taking place. Other dementias include Lewy body dementia, frontotemporal disorders, and vascular dementia. It is common for people to have mixed dementia—a combination of two or more disorders, at least one of which is dementia. For example, some people have both Alzheimer's disease and vascular dementia. 
 
 Alzheimer’s disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau, tangles). 
 
 These plaques and tangles in the brain are still considered some of the main features of Alzheimer’s disease. Another feature is the loss of connections between nerve cells (neurons) in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body. 
 
 Changes in the Brain 
 
 Cross sections of the brain show atrophy, or shrinking, of brain tissue caused by Alzheimer's disease. 
 
 Scientists continue to unravel the complex brain changes involved in the onset and progression of Alzheimer’s disease. It seems likely that damage to the brain starts a decade or more before memory and other cognitive problems appear. During this preclinical stage of Alzheimer’s disease, people seem to be symptom-free, but toxic changes are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons stop functioning, lose connections with other neurons, and die. 
 
 The damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As more neurons die, additional parts of the brain are affected, and they begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly. 
 
 Signs and Symptoms 
 
 Memory problems are typically one of the first signs of cognitive impairment related to Alzheimer’s disease. Some people with memory problems have a condition called mild cognitive impairment (MCI). In MCI, people have more memory problems than normal for their age, but their symptoms do not interfere with their everyday lives. Movement difficulties and problems with the sense of smell have also been linked to MCI. Older people with MCI are at greater risk for developing Alzheimer's, but not all of them do. Some may even go back to normal cognition. 
 
 The first symptoms of Alzheimer's vary from person to person. For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease. Researchers are studying biomarkers (biological signs of disease found in brain images, cerebrospinal fluid, and blood) to see if they can detect early changes in the brains of people with MCI and in cognitively normal people who may be at greater risk for Alzheimer’s. Studies indicate that such early detection may be possible, but more research is needed before these techniques can be relied upon to diagnose Alzheimer's disease in everyday medical practice. 
 
 Mild Alzheimer’s Disease 
 
 As Alzheimer’s disease progresses, people experience greater memory loss and other cognitive difficulties. Problems can include wandering and getting lost, trouble handling money and paying bills (PDF, 159K), repeating questions, taking longer to complete normal daily tasks, and personality and behavior changes. People are often diagnosed in this stage. 
 
 Moderate Alzheimer’s Disease 
 
 In this stage, damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. Memory loss and confusion grow worse, and people begin to have problems recognizing family and friends. They may be unable to learn new things, carry out multistep tasks such as getting dressed, or cope with new situations. In addition, people at this stage may have hallucinations, delusions, and paranoia and may behave impulsively. 
 
 Severe Alzheimer’s Disease 
 
 Ultimately, plaques and tangles spread throughout the brain, and brain tissue shrinks significantly. People with severe Alzheimer’s cannot communicate and are completely dependent on others for their care. Near the end, the person may be in bed most or all of the time as the body shuts down. 
 
 What Causes Alzheimer’s 
 
 Scientists don’t yet fully understand what causes Alzheimer’s disease in most people. In people with early-onset Alzheimer's, a genetic mutation is usually the cause. Late-onset Alzheimer's arises from a complex series of brain changes that occur over decades. The causes probably include a combination of genetic, environmental, and lifestyle factors. The importance of any one of these factors in increasing or decreasing the risk of developing Alzheimer’s may differ from person to person. 
 
 The Basics of Alzheimer’s 
 
 Scientists are conducting studies to learn more about plaques, tangles, and other biological features of Alzheimer’s disease. Advances in brain imaging techniques allow researchers to see the development and spread of abnormal amyloid and tau proteins in the living brain, as well as changes in brain structure and function. Scientists are also exploring the very earliest steps in the disease process by studying changes in the brain and body fluids that can be detected years before Alzheimer’s symptoms appear. Findings from these studies will help in understanding the causes of Alzheimer's and make diagnosis easier. 
 
 One of the great mysteries of Alzheimer’s disease is why it largely strikes older adults. Research on normal brain aging is shedding light on this question. For example, scientists are learning how age-related changes in the brain may harm neurons and contribute to Alzheimer’s damage. These age-related changes include atrophy (shrinking) of certain parts of the brain, inflammation, production of unstable molecules called free radicals, and mitochondrial dysfunction (a breakdown of energy production within a cell). 
 
 Genetics 
 
 Most people with Alzheimer’s have the late-onset form of the disease, in which symptoms become apparent in their mid-60s. The apolipoprotein E (APOE) gene is involved in late-onset Alzheimer’s. This gene has several forms. One of them, APOE ε4, increases a person’s risk of developing the disease and is also associated with an earlier age of disease onset. However, carrying the APOE ε4 form of the gene does not mean that a person will definitely develop Alzheimer’s disease, and some people with no APOE ε4 may also develop the disease. 
 
 Also, scientists have identified a number of regions of interest in the genome (an organism's complete set of DNA) that may increase a person's risk for late-onset Alzheimer's to varying degrees. 
 
 Early-onset Alzheimer’s disease occurs between a person’s 30s to mid-60s and represents less than 10 percent of all people with Alzheimer’s. Some cases are caused by an inherited change in one of three genes, resulting in a type known as early-onset familial Alzheimer’s disease, or FAD. For other cases of early-onset Alzheimer’s, research suggests there may be a genetic component related to factors other than these three genes. 
 
 Most people with Down syndrome develop Alzheimer's. This may be because people with Down syndrome have an extra copy of chromosome 21, which contains the gene that generates harmful amyloid. 
 
 For more about this area of research, see NIA's Alzheimer’s Disease Genetics Fact Sheet. 
 
 Health, Environmental, and Lifestyle Factors 
 
 Research suggests that a host of factors beyond genetics may play a role in the development and course of Alzheimer’s disease. There is a great deal of interest, for example, in the relationship between cognitive decline and vascular conditions such as heart disease, stroke, and high blood pressure, as well as metabolic conditions such as diabetes and obesity. Ongoing research will help us understand whether and how reducing risk factors for these conditions may also reduce the risk of Alzheimer’s. 
 
 A nutritious diet, physical activity, social engagement, and mentally stimulating pursuits have all been associated with helping people stay healthy as they age. These factors might also help reduce the risk of cognitive decline and Alzheimer’s disease. Clinical trials are testing some of these possibilities. 
 
 Diagnosis of Alzheimer’s Disease 
 
 Doctors use several methods and tools to help determine whether a person who is having memory problems has “possible Alzheimer’s dementia” (dementia may be due to another cause) or “probable Alzheimer’s dementia” (no other cause for dementia can be found). 
 
 To diagnose Alzheimer’s, doctors may: 
 
 Ask the person and a family member or friend questions about overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality 
 
 Conduct tests of memory, problem solving, attention, counting, and language 
 
 Carry out standard medical tests, such as blood and urine tests, to identify other possible causes of the problem 
 
 Perform brain scans, such as computed tomography (CT), magnetic resonance imaging (MRI), or positron emission tomography (PET), to rule out other possible causes for symptoms. 
 
 These tests may be repeated to give doctors information about how the person’s memory and other cognitive functions are changing over time. 
 
 Alzheimer's disease can be definitely diagnosed only after death, by linking clinical measures with an examination of brain tissue in an autopsy. 
 
 People with memory and thinking concerns should talk to their doctor to find out whether their symptoms are due to Alzheimer’s or another cause, such as stroke, tumor, Parkinson’s disease, sleep disturbances, side effects of medication, an infection, or a non-Alzheimer's dementia. Some of these conditions may be treatable and possibly reversible. 
 
 If the diagnosis is Alzheimer's, beginning treatment early in the disease process may help preserve daily functioning for some time, even though the underlying disease process cannot be stopped or reversed. An early diagnosis also helps families plan for the future. They can take care of financial and legal matters, address potential safety issues, learn about living arrangements, and develop support networks. 
 
 In addition, an early diagnosis gives people greater opportunities to participate in clinical trials that are testing possible new treatments for Alzheimer's disease or other research studies. 
 
 Treatment of Alzheimer’s Disease 
 
 Alzheimer’s disease is complex, and it is unlikely that any one drug or other intervention can successfully treat it. Current approaches focus on helping people maintain mental function, manage behavioral symptoms, and slow or delay the symptoms of disease. Researchers hope to develop therapies targeting specific genetic, molecular, and cellular mechanisms so that the actual underlying cause of the disease can be stopped or prevented. 
 
 Maintaining Mental Function 
 
 Several medications are approved by the U.S. Food and Drug Administration to treat symptoms of Alzheimer’s. Donepezil (Aricept®), rivastigmine (Exelon®), and galantamine (Razadyne®) are used to treat mild to moderate Alzheimer’s (donepezil can be used for severe Alzheimer’s as well). Memantine (Namenda®) is used to treat moderate to severe Alzheimer’s. These drugs work by regulating neurotransmitters, the chemicals that transmit messages between neurons. They may help maintain thinking, memory, and communication skills, and help with certain behavioral problems. However, these drugs don’t change the underlying disease process. They are effective for some but not all people, and may help only for a limited time. 
 
 Managing Behavior 
 
 Common behavioral symptoms of Alzheimer’s include sleeplessness, wandering, agitation, anxiety, and aggression. Scientists are learning why these symptoms occur and are studying new treatments—drug and non-drug—to manage them. Research has shown that treating behavioral symptoms can make people with Alzheimer’s more comfortable and makes things easier for caregivers. 
 
 Looking for New Treatments 
 
 Alzheimer’s disease research has developed to a point where scientists can look beyond treating symptoms to think about addressing underlying disease processes. In ongoing clinical trials, scientists are developing and testing several possible interventions, including immunization therapy, drug therapies, cognitive training, physical activity, and treatments used for cardiovascular and diabetes. 
 
 Support for Families and Caregivers 
 
 Caring for a person with Alzheimer’s disease can have high physical, emotional, and financial costs. The demands of day-to-day care, changes in family roles, and decisions about placement in a care facility can be difficult. There are several evidence-based approaches and programs that can help, and researchers are continuing to look for new and better ways to support caregivers. 
 
 Becoming well-informed about the disease is one important long-term strategy. Programs that teach families about the various stages of Alzheimer’s and about ways to deal with difficult behaviors and other caregiving challenges can help. 
 
 Good coping skills, a strong support network, and respite care are other ways that help caregivers handle the stress of caring for a loved one with Alzheimer’s disease. For example, staying physically active provides physical and emotional benefits. 
 
 Some caregivers have found that joining a support group is a critical lifeline. These support groups allow caregivers to find respite, express concerns, share experiences, get tips, and receive emotional comfort. Many organizations sponsor in-person and online support groups, including groups for people with early-stage Alzheimer’s and their families. 
 
 For more information, see Caring for a Person with Alzheimer’s Disease: Your Easy-to-Use Guide from the National Institute on Aging. 
 
 For More Information 
 
 To get information about Alzheimer's and learn about support groups and services for people with the disease and their caregivers, contact the following organizations: 
 
 Alzheimer’s Disease Education and Referral (ADEAR) Center 
 
 1-800-438-4380 (toll-free) 
 
 adear@nia.nih.gov 
 
 www.nia.nih.gov/alzheimers 
 
 The National Institute on Aging’s ADEAR Center offers information and publications for families, caregivers, and professionals on diagnosis, treatment, patient care, caregiver needs, long-term care, education and training, and research related to Alzheimer’s disease. Staff members answer telephone, email, and written requests and make referrals to local and national resources. Visit the ADEAR website to learn more about Alzheimer's and other dementias, find clinical trials, and sign up for email updates. 
 
 Alzheimer’s Association 
 
 1-800-272-3900 (toll-free) 
 
 1-866-403-3073 (TTY/toll-free) 
 
 info@alz.org 
 
 www.alz.org 
 
 Alzheimer’s Foundation of America 
 
 1-866-232-8484 (toll-free) 
 
 info@alzfdn.org 
 
 www.alzfdn.org 
 
 Eldercare Locator 
 
 1-800-677-1116 (toll-free) 
 
 www.eldercare.gov 
 
 Family Caregiver Alliance 
 
 1-800-445-8106 (toll-free) 
 
 info@caregiver.org 
 
 www.caregiver.org 
 
 MedlinePlus 
 
 www.nlm.nih.gov/medlineplus/alzheimersdisease.html 
 
 Alzheimer’s Disease Education and Referral (ADEAR) Center 
 
 A service of the National Institute on Aging 
 
 National Institutes of Health 
 
 NIH...Turning Discovery Into Health® 
 
 U.S. Department of Health and Human Services ||||| Women who display the early signs of mental decline that can precede Alzheimer’s disease deteriorate faster than men with the same condition, a new study has found. 
 
 Another study suggests that women’s daily activities and cognitive abilities decline faster than men’s after undergoing surgery with general anesthesia. A third study has found that an abnormal protein that plays a key role in triggering Alzheimer’s accumulates at higher rates in women’s brains than in men’s. 
 
 The new research, presented this week at the Alzheimer’s Association International Conference in Washington, lends additional support to the view that women run a higher risk than men of developing Alzheimer’s disease and may be more vulnerable to its damaging effects once the illness gets going. 
 
 “The bottom line is, more and more we think there are some differences,” said Kristine Yaffe, a professor of psychiatry, neurology and epidemiology at the University of California at San Francisco. “It’s not just that women are living to be older — that’s true, and that drives some of this. But there’s something else going on in terms of biology [and] environment for women compared to men that may make them at greater risk or, if they have some symptoms, may change the progression.” 
 
 [Here’s a look at why women may be more at risk for Alzheimer’s than men] 
 
 Of an estimated 5.4 million people with Alzheimer’s in the United States, about 3.4 million are female. Women have twice the lifetime risk of developing Alzheimer’s disease, which is the leading cause of dementia. The disease is progressive and incurable. 
 
 The distinguishing features of Alzheimer’s include the buildup of abnormal proteins that destroy brain cells in areas critical to memory and learning. These proteins — beta-amyloid, which forms waxy, insoluble plaques; and tau, which creates fibrous tangles — begin accumulating well ahead of symptoms such as memory loss, and advances in technology have allowed scientists to obtain images of them. 
 
 For a year or more, the Alzheimer’s Association has highlighted the disease’s disparate impact on women, both in its incidence and in the burden of caring for those who have it. The findings shared Tuesday bolster the theory that gender differences may have an effect on determining Alzheimer’s risk, perhaps because of hormonal interactions with genes, biochemistry and development in the brain. 
 
 [How fear of Alzheimer’s reshapes some people’s lives] 
 
 Roberta Diaz Brinton, a professor at the University of Southern California’s School of Pharmacy, said her research has shown that women may have higher Alzheimer’s risk because estrogen has such an important effect on regulating the energy supply in the brain. At menopause, women’s bodies undergo radical transformations that can alter the brain’s ability to change glucose, a kind of sugar, into energy. 
 
 “Every cell — every single cell in your body — has a sex. The X chromosome or the XY chromosome is within all of our cells, and that very likely has an effect on cell function,” said Brinton, who helped organize the Alliance of Women Alzheimer’s Researchers, a professional interest group within the Alzheimer’s Association. 
 
 A study led by scientists at UC San Francisco explored the connection between gender and a gene whose ability to raise the risk of developing Alzheimer’s disease is already well known. The study — conducted by Duygu Tosun, an assistant professor of radiology, and others — used data from brain scans to investigate links between gender and a gene variant known as APOE4. 
 
 The gene is one of several variants that code for an apolipoprotein, a protein that shuttles cholesterol and fatty substances in the body and the brain. Having a single copy of the gene raises the risk of Alzheimer’s at least twofold; having a copy from each parent boosts the odds even higher. 
 
 The study found that men who carried the APOE4 gene had higher accumulations of beta-amyloid in their brains than men who did not. But the study’s major finding was that women had higher accumulations of the abnormal protein in their brains, regardless of whether they carried the APOE4 gene. 
 
 “This study shows women have more amyloid in their brain than men in general, and especially once the women are in the late stages where they’re having dementia. They’re going to have higher levels than men, and the APOE4 isn’t going to affect that,” said Michael W. Weiner, a radiology professor at UC San Francisco and principal investigator of the Alzheimer’s Disease Neuroimaging Initiative. 
 
 That heightened vulnerability may also affect the rate of decline among women who already show signs of dementia. 
 
 Katherine Amy Lin, an undergraduate at Duke University, said her team used data from the neuroimaging initiative to track the erosion of cognitive ability in men and women who already suffered mild cognitive impairment. 
 
 Lin, who worked with the university’s medical school, said the study examined 257 men and 141 women, mostly in their mid-70s, and their performance on cognitive tests over an eight-year period. 
 
 The study found that people with the APOE4 gene had a faster rate of decline. But after adjusting for genetic disposition and other factors, the study showed that women who suffered from mild cognitive decline saw their performance deteriorate twice as fast as men’s. 
 
 “Our findings do suggest that there is greater vulnerability to women,” Lin said. She cautioned, however, that the results are preliminary and in need of further gender-specific research. 
 
 In a similar study, Katie J. Schenning, a physician at Oregon Health & Science University in Portland, said her team explored gender differences in people who suffer cognitive decline after undergoing surgery with general anesthesia. Though most people do not experience any lasting effects from surgery involving anesthesia, recent research has found that older people are susceptible to progressive cognitive and functional decline after such procedures. Older adults receive about a third of the anesthesia administered in the United States, Schenning said. 
 
 Using data from the Oregon Brain Aging Study and a project called Intelligent Systems for Assessing Aging Changes, the team looked at 527 people, including 182 who underwent 331 procedures using general anesthesia. The average follow-up was seven years. It found that men who were exposed to general anesthesia during surgery declined faster on measures of cognitive performance and daily activity than men who had not had surgery; women who underwent surgery with anesthesia also declined faster than women who did not. But women also declined more rapidly than men. The rate was even faster for women who had multiple surgeries using anesthesia. 
 
 Women had more rapid erosion in measures of both cognition and ability to perform daily activities. 
 
 “I do want to stress that, at this time, it’s uncertain which specific surgical or anesthetic factors might contribute to postoperative cognitive or functional decline,” Schenning said. “It’s also very important to note that this is just not an effect of anesthesia itself but rather a combination of the effects of anesthesia and surgery together.” 
 
 But Schenning also said the findings suggest that physicians should advise older patients of the risk of decline after surgery with a general anesthetic and perhaps urge them to carefully weigh whether to undergo nonessential procedures.
– Researchers from London's Imperial College think they've found two networks of genes, possibly controlled by a master system, that control cognitive functions—a find that may allow them to modify human intelligence down the line, the Guardian reports. In a study published in Nature Neuroscience, scientists say these M1 and M3 clusters control cognitive functions such as memory, attention, and reasoning, per the Daily Express. "Traits such as intelligence are governed by large groups of [genes] working together—like a football team made up of players in different [positions]," study co-author Dr. Michael Johnson says, per the Guardian. By figuring out how these "players" work together, scientists could perhaps boost cognitive abilities by simply flicking the equivalent of a master switch. And based on other findings in the study linking mutations of those same genes to cognitive impairments, research in this area may be lead to treatment of cognitive issues that accompany neurodevelopmental diseases such as epilepsy, Dr. Johnson notes, per the Guardian. Researchers analyzed "huge sets of data" taken from samples of mouse and human brains, the paper notes, as well as info from a previous health study and genetic data from volunteers (both healthy ones and those with autism and other intellectual disabilities) who took IQ tests. Not only did they find evidence for the disparate gene networks—they also found that the same genes that apparently contribute to the intelligence of healthy subjects damaged cognitive abilities if they were mutated. "Eventually we hope that this sort of analysis will provide new insights into better treatments for neurodevelopmental disease … and ameliorate or treat the cognitive impairments associated with these devastating diseases," Johnson says. Not everyone is thrilled with the idea of flipping a switch to play around with intelligence functioning. "Genetics is the science of inheritance, not pre-determinism, and there is no substitute for hard work and application," a University of Kent genetics professor tells the Express. (Predict your kid's intelligence—with a raisin.)