Neurons programmed to fire at specific faces—such as the famously reported “Jennifer Aniston neuron”—may be more in line with the conscious recognition of faces than the actual images seen. Subjects presented with a blended face, such as an amalgamation of Bill Clinton and George W. Bush, had significantly more firing of such face-specific neurons when they recognized the blended or morphed face as one person or the other. Results of the study led by Christof Koch at the Allen Institute for Brain Science, and carried out by neuroscientists Rodrigo Quian Quiroga at the University of Leicester, Alexander Kraskov at University College London and Florian Mormann at the University of Bonn, under the clinical supervision of the neurosurgeon Itzhak Fried at the University of California at Los Angeles Medical School, are published online today in the journal Neuron.
Some neurons in the region of the brain known as the medial temporal lobe are observed to be extremely selective in the stimuli to which they respond. A cell may only fire in response to different pictures of a particular person who is very familiar to the subject (such as loved one or a celebrity), the person’s written or spoken name, or simply recalling the person from memory.
“These highly specific cells are an entry point to investigate how the brain makes meaning out of visual information,” explains Christof Koch, Chief Scientific Officer at the Allen Institute for Brain Science and senior author on the paper. “We wanted to know how these cells responded not just to a simple image of a person’s face, but to a more ambiguous image of that face averaged or morphed with another person’s face.”
For the trials, subjects were shown either the face of individuals such as Bill Clinton or George W. Bush (the “adaptor” image), and then an ambiguous face which was a blend of both faces. Primed with the Clinton image, subjects tended to recognize Bush’s face in the blended image, while subjects who saw Bush’s face first recognized the blended face as Clinton. That is, even though the blended images were identical, subjects tended to consciously perceive the identity of face to which they were not adapted.
Researchers wanted to know whether these selective neurons responded to the actual image on the screen, or whether they responded more to the perception that the image caused in the brain of the subject. When subjects recognized the ambiguous face as belonging to Clinton, their Clinton-specific neurons fired. However, when subjects recognized that same face as Bush, the neurons fired significantly less. These results indicated that conscious recognition of the face played a crucial role in whether the neurons fired, rather than the raw visual stimulus.
“This study provides further evidence that stimulus-specific neurons in the medial temporal lobe follow the subjective perception of the person, as opposed to faithfully reporting the visual stimulus the person sees,” explains Koch. “This distinction may help us glean insight into how the brain takes raw visual information and transforms it into something meaningful, which can be further modulated by other aspects of experience in the brain.”
(Image caption: In the two brain regions IPF (lateral prefrontal cortex) and V4, a region of the visual system, the brain activity oscillates in a specific frequency range. Credit: © Stefanie Liebe, MPI for biological Cybernetics)
School children and university students are often big fans of the short-term memory – not least when they have to cram large volumes of information on the eve of an exam. Although its duration is brief, short term memory is a complex network of neurons in the brain that includes different brain regions. To store the information, these regions must work together. Researchers from the Max Planck Institute for Biological Cybernetics in Tübingen have now discovered that the participating regions must be active at the same time to enable us to form short-term memories of things that happen.
When we see something, signals from the eyes are processed in areas of the cerebral cortex located at the back of the head. For short-term memory, in contrast, regions in the front part of the cerebral cortex must be active. In order for us to remember something we have seen briefly, these far-apart regions of the brain must collate their information.
How this works can only be examined in apes. Scientists from Nikos Logothetis’s Department at the Max Planck Institute for Biological Cybernetics in Tübingen measured the electrical activity in an optic region and in the front area of the brain while the animals had to remember different images.
In the process, the scientists observed electrical vibrations, known as theta-band oscillations, in the two regions of brain. Surprisingly, these oscillations did not arise independently, but were synchronous. The more synchronously active the regions, the better the animals were able to remember an image.
Accordingly, the functioning of short-term memory can be envisaged as two revolving doors: While the memory is at work, the two doors move in time with each other and, in this way, facilitate the more effective exchange of information.
The study shows how important synchronised brain oscillations are for the communication between the different regions of the brain. Almost all higher intellectual capacities result from the complex interplay of specialised neuronal networks in different parts of the brain.
Neural networks are formed by the interconnection of specific neurons in the brain. The molecular mechanisms involved in creating these connections, however, have so far eluded scientists. Research led by Jun Aruga from the RIKEN Brain Science Institute has now identified an interaction between two proteins that is crucial for making connections between specific types of neurons, with implications for some neurological disorders.
Connections between neurons are made via synapses—small gaps across which chemicals called neurotransmitters pass, relaying signals from a presynaptic neuron to a postsynaptic neuron. Aruga and his colleagues focused on a protein called mGluR7, which is found only at synapses with a specific type of postsynaptic neuron in an area of the brain involved in forming memories.
“mGluR7 is located on the presynaptic side of connections made with hippocampal local inhibitory neurons,” explains Aruga. “Previous studies have proposed that this protein prevents neurotransmitter release from the presynaptic neuron when the neurotransmitter glutamate binds to it.”
The researchers discovered that the localization of mGluR7 to specific synapses is determined by the presence of another protein called Elfn1. This protein is found on the other side of the same synapses, directly opposite mGluR7. When the researchers artificially introduced Elfn1 into cultured cells, mGluR7 became associated with the same cells, and they showed that this was due to a physical interaction between the two proteins. Conversely, deleting Elfn1 in the brains of mice reduced the amount of mGluR7 at the synapses.
These changes interfered with the process of strengthening connections at synapses, which takes place during memory formation, and caused patterns of brain waves that indicated abnormally high levels of electrical activity. Genetically altered mice also exhibited other symptoms that resembled human conditions.
“Deleting Elfn1 increased the susceptibility of mice to seizures,” explains Aruga. “It also enhanced behaviors similar to attention deficit hyperactivity disorder (ADHD).”
Indeed, the researchers found that humans with epilepsy and ADHD also had a faulty version of the gene encoding Elfn1, suggesting that a deficit in the ability of Elfn1 to localize mGluR7 and form specific connections in neural networks is important in some neurological conditions.
“In combination, the human and mouse results implicate the Elfn1–mGluR7 complex in the pathophysiology of epilepsy and ADHD, at least in part,” explains Aruga, although he remains cautious at this early stage of research. “Because of sample size limitations, the human genetics result is not conclusive, but we are now awaiting the results of follow-up studies with additional subjects.”
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Researchers at University of California, San Diego School of Medicine have identified a control mechanism for an area of the brain that processes sensory and emotive information that humans experience as “disappointment.”
The discovery of what may effectively be a neurochemical antidote for feeling let-down is reported Sept. 18 in the online edition of Science.
“The idea that some people see the world as a glass half empty has a chemical basis in the brain,” said senior author Roberto Malinow, MD, PhD, professor in the Department of Neurosciences and neurobiology section of the Division of Biological Sciences. “What we have found is a process that may dampen the brain’s sensitivity to negative life events.”
Because people struggling with depression are believed to register negative experiences more strongly than others, the study’s findings have implications for understanding not just why some people have a brain chemistry that predisposes them to depression but also how to treat it.
Specifically, in experiments with rodents, UC San Diego researchers discovered that neurons feeding into a small region above the thalamus known as the lateral habenula (LHb) secrete both a common excitatory neurotransmitter, glutamate, and its opposite, the inhibitory neurotransmitter GABA.
Excitatory neurotransmitters promote neuronal firing while inhibitory ones suppress it, and although glutamate and GABA are among two of the most common neurotransmitters in the mammalian brain, neurons are usually specialists, producing one but not both kinds of chemical messengers.
Indeed, prior to the study, there were only two other systems in the brain where neurons had been observed to co-release excitatory and inhibitory neurotransmitters – in a particular connection in the hippocampus and in the brainstem during development of the brain’s auditory map.
“Our study is one of the first to rigorously document that inhibition can co-exist with excitation in a brain pathway,” said lead author Steven Shabel, a postdoctoral researcher with Department of Neurosciences and neurobiology section of the Division of Biological Sciences. “In our case, that pathway is believed to signal disappointment.”
The LHb is a small node-like structure in the epithalamus region of the brain that is critical for processing a variety of inputs from the basal ganglia, hypothalamus and cerebral cortex and transmitting encoded responses (output) to the brainstem, an ancient part of the brain that mammals share with reptiles.
Experiments with primates have shown that activity in the LHb increases markedly when monkeys are expecting but don’t get a sip of fruit juice or other reward, hence the idea that this region is part of a so-called disappointment pathway.
Proper functioning of the LHb, however, is believed to be important in much more than just disappointment and has been implicated in regulating pain responses and a variety of motivational behaviors. It has also been linked to psychosis.
Depression, in particular, has been linked to hyperactivity of the LHb, but until this study, researchers had little empirical evidence as to how this overstimulation is prevented in healthy individuals given the apparent lack of inhibitory neurons in this region of the brain.
"The take-home of this study is that inhibition in this pathway is coming from an unusual co-release of neurotransmitters into the habenula," Shabel said. Researchers do not know why this region of the brain is controlled in this manner, but one hypothesis is that it allows for a more subtle control of signaling than having two neurons directly counter-acting each other.
Researchers were also able to show that neurons of rodents with aspects of human depression produced less GABA, relative to glutamate. When these animals were given an antidepressant to raise their brain’s serotonin levels, their relative GABA levels increased.
"Our study suggests that one of the ways in which serotonin alleviates depression is by rebalancing the brain’s processing of negative life events vis-à-vis the balance of glutamate and GABA in the habenula," Shabel said. "We may now have a precise neurochemical explanation for why antidepressants make some people more resilient to negative experiences."
Pictured: Basal ganglia neurons (green) feed into the brain and release glutamate (red) and GABA (blue) and sometimes a mix of both neurotransmitters (white).
The World Alzheimer Report 2014 ‘Dementia and Risk Reduction: An analysis of protective and modifiable factors’, released today, calls for dementia to be integrated into both global and national public health programmes alongside other major non communicable diseases (NCDs).
Alzheimer’s Disease International (ADI) commissioned a team of researchers, led by Professor Martin Prince from King’s College London, to produce the report. ADI is publishing this report, in conjunction with World Alzheimer’s Day (21 September) and as a part of World Alzheimer’s Month, an international campaign to raise awareness and challenge stigma.
The report reveals that control of diabetes and high blood pressure as well as measures to encourage smoking cessation and to reduce cardiovascular risk, have the potential to reduce the risk of dementia even in late-life. The report found that diabetes can increase the risk of dementia by 50%. Obesity and lack of physical activity are important risk factors for diabetes and hypertension, and should, therefore, also be targeted.
While cardiovascular health is improving in many high income countries, many low and middle income countries show a recent pattern of increasing exposure to cardiovascular risk factors, with rising rates of diabetes, heart disease and stroke.
Smoking cessation is strongly linked in the report with a reduction in dementia risk. For example, studies of dementia incidence among people aged 65 years and over show that ex-smokers have a similar risk to those who have never smoked, while those who continue to smoke are at much higher risk.
Furthermore, the study revealed that those who have had better educational opportunities have a lower risk of dementia in late-life. Evidence suggests that education has no impact on the brain changes that lead to dementia, but reduces their impact on intellectual functioning.
The evidence in the report suggest that if we enter old age with better developed, healthier brains we are likely to live longer, happier and more independent lives, with a much reduced chance of developing dementia. Brain health promotion is important across the life span, but particularly in mid-life, as changes in the brain can begin decades before symptoms appear.
The report also urges NCD programs to be more inclusive of older people, with the message that it’s never too late to make a change, as the future course of the global dementia epidemic is likely to depend crucially upon the success or failure of efforts to improve global public health, across the population. Combining efforts to tackle the increasing global burden of NCDs will be strategically important, efficient and cost effective. Leading a healthier lifestyle is a positive step towards preventing a range of long-term diseases, including cancer, heart disease, stroke and diabetes.
However, survey data released by Bupa* has shown that many people are unclear about the causes and actions they can take to potentially reduce their risk of dementia. Just over a sixth (17%) of people realised that social interaction with friends and family could impact on the risk. Only a quarter (25%) identified being overweight as a possible factor, and only one in five (23%) said physical activity could affect the risk of developing dementia and losing their memories. The survey also revealed that over two thirds (68%) of people surveyed around the world are concerned about getting dementia in later life.
Professor Martin Prince, from King’s College London’s Institute of Psychiatry, Psychology & Neuroscience (IoPPN) and author of the report, commented: “There is already evidence from several studies that the incidence of dementia may be falling in high income countries, linked to improvements in education and cardiovascular health. We need to do all we can to accentuate these trends. With a global cost of over US$ 600 billion, the stakes could hardly be higher.”
Marc Wortmann, Executive Director, Alzheimer’s Disease International said: “From a public health perspective, it is important to note that most of the risk factors for dementia overlap with those for the other major non communicable diseases (NCDs). In high income countries, there is an increased focus on healthier lifestyles, but this is not always the case with lower and middle income countries. By 2050, we estimate that 71% of people living with dementia will live in these regions, so implementing effective public health campaigns may help to reduce the global risk.”
Professor Graham Stokes, Global Director of Dementia Care, Bupa, said: “While age and genetics are part of the disease’s risk factors, not smoking, eating more healthily, getting some exercise, and having a good education, coupled with challenging your brain to ensure it is kept active, can all play a part in minimising your chances of developing dementia. People who already have dementia, or signs of it, can also do these things, which may help to slow the progression of the disease.”
* These figures, unless otherwise stated, are from YouGov Plc. Total sample size was 8,513, from the UK (2,401), Australia (1,000), Chile (1,000), China (1,031), Poland (1,002), and Spain (1,077). Fieldwork was undertaken online, between 17–25 July 2014. The figures have been weighted and are representative of all adults (aged 18+) in each country. An even weighting was applied to each country to find a ‘Global Average’.
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