When Less Is More: Evolutionary Origins of the Affect Heuristic

The human mind is built for approximations. When considering the value of a large aggregate of different items, for example, we typically do not summate the many individual values. Instead, we appear to form an immediate impression of the likeability of the option based on the average quality of the full collection, which is easier to evaluate and remember. While useful in many situations, this affect heuristic can lead to apparently irrational decision-making. For example, studies have shown that people are willing to pay more for a small set of high-quality goods than for the same set of high-quality goods with lower-quality items added [e.g. 1]. We explored whether this kind of choice behavior could be seen in other primates. In two experiments, one in the laboratory and one in the field, using two different sets of food items, we found that rhesus monkeys preferred a highly-valued food item alone to the identical item paired with a food of positive but lower value. This finding provides experimental evidence that, under certain conditions, macaque monkeys follow an affect heuristic that can cause them to prefer less food. Conservation of this affect heuristic could account for similar ‘irrational’ biases in humans, and may reflect a more general complexity reduction strategy in which averages, prototypes, or stereotypes represent a set or group.

Drug Reverses Abnormal Brain Function in Rett Syndrome Mice

A promising study out today in the prestigious Journal of Neuroscience showed that in a mouse model of Rett syndrome, researchers were able to reverse abnormalities in brain activity and improve neurological function by treating the animals with an FDA-approved anesthesia drug, ketamine. Rett syndrome is among the most severe autism-related disorders, affecting about one in 10,000 female births per year, with no effective treatments available.

“These studies provide new evidence that drug treatment can reverse abnormalities in brain function in Rett syndrome mice,” says David Katz, PhD, professor of neurosciences, Case Western Reserve University School of Medicine and senior author of the study. “They also provide new leads as to what kinds of drugs might be effective in individuals with Rett syndrome.”

Neuroscientists at Case Western Reserve University School of Medicine were able to successfully map differences in the brain activity of normal mice and those with a genetic mutation that mirrors the cause of Rett syndrome in humans. They found that – compared to normal mice – Rett syndrome mice showed regions of abnormally low activity in the front of the brain (forebrain) and regions of abnormally high activity in the back of the brain (brainstem). Importantly, they found that the regions of low activity overlap with regions of the brain that are also under-active in humans with classic autism. This indicates there may be common mechanisms underlying abnormal behaviors in the two diseases.

The identification of these brain regions provided clues into specific areas to target for treatment. Based on previously published findings that ketamine activated neurons in the forebrain, the researchers gave the drug to the Rett syndrome mice and found it increased levels of brain activity in those regions and improved neurological function. Importantly, the drug was effective at a low dose that did not produce anesthesia.

New de novo Genetic Mutations in Schizophrenia Identified

Columbia University Medical Center (CUMC) researchers have identified dozens of new spontaneous genetic mutations that play a significant role in the development of schizophrenia, adding to the growing list of genetic variants that can contribute to the disease. The study, the largest and most comprehensive of its kind, was published today in the online edition of the journal Nature Genetics.

Although schizophrenia typically onsets during adolescence and early adulthood, many of the mutations were found to affect genes with higher expression during early-to-mid fetal development. Together, the findings show that both the function of the mutated gene and when the gene is expressed are critically important in determining the risk for schizophrenia.

The findings inform epidemiologic studies showing that environmental factors, such as malnutrition or infections during pregnancy, can contribute to the development of schizophrenia. “Our findings provide a mechanism that could explain how prenatal environmental insults during the first and second trimester of pregnancy increase one’s risk for schizophrenia,” said study leader Maria Karayiorgou, MD, professor of psychiatry at CUMC, and acting chief, division of Psychiatric and Medical Genetics, New York State Psychiatric Institute. “Patients with these mutations were much more likely to have had behavioral abnormalities, such as phobias and anxiety in childhood, as well as worse disease outcome.”

Not getting sleepy? Research explains why hypnosis doesn’t work for all

Not everyone is able to be hypnotized, and new research from the Stanford University School of Medicine shows how the brains of such people differ from those who can easily be.

The study, published in the October issue of Archives of General Psychiatry, uses data from functional and structural magnetic resonance imaging to identify how the areas of the brain associated with executive control and attention tend to have less activity in people who cannot be put into a hypnotic trance.

“There’s never been a brain signature of being hypnotized, and we’re on the verge of identifying one,” said David Spiegel, MD, the paper’s senior author and a professor of psychiatry and behavioral sciences. Such an advance would enable scientists to understand better the mechanisms underlying hypnosis and how it can be used more widely and effectively in clinical settings, added Spiegel, who also directs the Stanford Center for Integrative Medicine.

Spiegel estimates that one-quarter of the patients he sees cannot be hypnotized, though a person’s hypnotizability is not linked with any specific personality trait. “There’s got to be something going on in the brain,” he said.

New research proves the validity of one of the most promising approaches for combating Alzheimer’s disease (AD) with medicines that treat not just some of the symptoms, but actually stop or prevent the disease itself, scientists are reporting. The study, in the journal ACS Medicinal Chemistry Letters, also identifies a potential new oral drug that the scientists say could lead the way.

Wenhui Hu and colleagues point out that existing drugs for AD provide only “minimal” relief of memory loss and other symptoms, creating an urgent need for new medicines that actually combat the underlying destruction of brain cells. Research suggests that inflammation of nerve cells in the brain is a key part of that process. One medicine, Minozac, is in clinical trials. But Hu says Minozac still has more space to improve its efficacy. So the scientists sifted through compounds with a molecular architecture similar to Minozac in an effort to find more active substances.

The report describes success in doing so. They discovered one compound that appeared especially effective in relieving nerve inflammation and in improving learning and memory in lab mice widely used in AD research. “In general, this study not only proves that countering neuroinflammation is indeed a potential therapeutic strategy for Alzheimer’s disease, but also provides a good lead compound with efficacy comparable to donepezil [an existing AD medicine] for further oral anti-AD drug discovery and development,” the report states.

Home-Based Assessment Tool for Dementia Screening

Georgia Tech researchers have created a tool that allows adults to screen themselves for early signs of dementia. The home-based computer software is patterned after the paper-and-pencil Clock Drawing Test, one of health care’s most commonly used screening exams for cognitive impairment.

“Technology allows us to check our weight, blood-sugar levels and blood pressure, but not our own cognitive abilities,” said project leader Ellen Yi-Luen Do. “Our ClockMe System helps older adults identify early signs of impairment, while allowing clinicians to quickly analyze the test results and gain valuable insight into the patient’s thought processes.”

Georgia Tech’s ClockMe system eliminates the paper trail and computerizes the test into two main components: the ClockReader Application and the ClockAnalyzer Application. Click here to see a video demo.

Genetic diseases diagnosed within 50 hours

The new technology screens the whole genome of the baby from a drop of their blood before homing in on abnormalities in single genes that could explain their ill health.

Genetic diseases are thought to affect up to one in a hundred children and are one of the leading causes of admission to intensive care units immediately after birth.

In about 500 of the conditions - including Krabbe disease, a nervous system disorder - early treatment can prevent the development of severe disability and life-threatening symptoms.

Most of the diseases are extremely rare and many are unfamiliar to doctors, but analysing a baby’s genes to find the cause of their condition currently takes up to six weeks.