Posts tagged science
Articles and news from the latest research reports.
Scientists show how bigger brains could help us see better
It has become increasingly common to hear reports that big brains are not necessary, or even an evolutionary fluke. However, the new article found that increases in the size of brain areas, such as the visual cortex, are an essential element of evolution.
As part of the study, the researchers found that an increase in the size of the visual part of the brain in different primate species, including humans, apes, and monkeys, is associated with enhanced visual processing.
It is controversial whether overall brain size can predict intelligence. However the size of specialised areas within the brain is associated with specific changes in behaviour such as reducing the susceptibility to visual illusions and increasing the visual acuity or fine details that can be seen.
First author, Dr Alexandra de Sousa explained: “Primates with a bigger visual cortex have better visual resolution, the precision of vision, and reduced visual illusion strength. In essence, the bigger the brain area, the better the visual processing ability.
“The size of brain areas predicts not only the number of neurons (brain cells) in that area, but also the likelihood of connections between neurons. These connections allow for increasingly complex computations to be made that allow for more accurate, and more difficult, visual perception.”
Co-author, Dr Michael Proulx, Senior Lecturer (Associate Professor) in Psychology, added: “This paper is a novel attempt to bring together the micro and macro anatomy of the brain with behaviour. We link visual abilities, the size of brain areas, and the number of neurons that make up those brain areas to provide a framework that ties brain structure and function together.
“The theory of brain size that we discuss can be tested in the future with more behavioural tests of other species, gathering more comparative neuroanatomical data, and by testing other senses and multi-sensory perception, too. We might be able to even predict how well extinct species could sense the world based on fossil data.”
For the study, Dr Alexandra de Sousa, an expert in brain evolution, provided brain size measurements from her and other’s neuroanatomical research. Dr Michael Proulx, an expert in perception, found psychological studies of visual illusions and visual acuity in the same species or general of animals.
The paper ‘What can volumes reveal about human brain evolution? A framework for bridging behavioral, histometric and volumetric perspectives’ is published today in Frontiers in Neuroanatomy – an online, open access journal.
(Source: bath.ac.uk)
People with tinnitus process emotions differently from their peers
Patients with persistent ringing in the ears – a condition known as tinnitus – process emotions differently in the brain from those with normal hearing, researchers report in the journal Brain Research.
Tinnitus afflicts 50 million people in the United States, according to the American Tinnitus Association, and causes those with the condition to hear noises that aren’t really there. These phantom sounds are not speech, but rather whooshing noises, train whistles, cricket noises or whines. Their severity often varies day to day.
University of Illinois speech and hearing science professor Fatima Husain, who led the study, said previous studies showed that tinnitus is associated with increased stress, anxiety, irritability and depression, all of which are affiliated with the brain’s emotional processing systems.
“Obviously, when you hear annoying noises constantly that you can’t control, it may affect your emotional processing systems,” Husain said. “But when I looked at experimental work done on tinnitus and emotional processing, especially brain imaging work, there hadn’t been much research published.”
She decided to use functional magnetic resonance imaging (fMRI) brain scans to better understand how tinnitus affects the brain’s ability to process emotions. These scans show the areas of the brain that are active in response to stimulation, based upon blood flow to those areas.
Three groups of participants were used in the study: people with mild-to-moderate hearing loss and mild tinnitus; people with mild-to-moderate hearing loss without tinnitus; and a control group of age-matched people without hearing loss or tinnitus. Each person was put in an fMRI machine and listened to a standardized set of 30 pleasant, 30 unpleasant and 30 emotionally neutral sounds (for example, a baby laughing, a woman screaming and a water bottle opening). The participants pressed a button to categorize each sound as pleasant, unpleasant or neutral.
The tinnitus and normal-hearing groups responded more quickly to emotion-inducing sounds than to neutral sounds, while patients with hearing loss had a similar response time to each category of sound. Over all, the tinnitus group’s reaction times were slower than the reaction times of those with normal hearing.
Activity in the amygdala, a brain region associated with emotional processing, was lower in the tinnitus and hearing-loss patients than in people with normal hearing. Tinnitus patients also showed more activity than normal-hearing people in two other brain regions associated with emotion, the parahippocampus and the insula. The findings surprised Husain.
“We thought that because people with tinnitus constantly hear a bothersome, unpleasant stimulus, they would have an even higher amount of activity in the amygdala when hearing these sounds, but it was lesser,” she said. “Because they’ve had to adjust to the sound, some plasticity in the brain has occurred. They have had to reduce this amygdala activity and reroute it to other parts of the brain because the amygdala cannot be active all the time due to this annoying sound.”
Because of the sheer number of people who suffer from tinnitus in the United States, a group that includes many combat veterans, Husain hopes her group’s future research will be able to increase tinnitus patients’ quality of life.
“It’s a communication issue and a quality-of-life issue,” she said. “We want to know how we can get better in the clinical realm. Audiologists and clinicians are aware that tinnitus affects emotional aspects, too, and we want to make them aware that these effects are occurring so they can better help their patients.”
Researchers publish one of the longest longitudinal studies of cognition in MS
Researchers at Kessler Foundation and the Cleveland Clinic have published one of the longest longitudinal studies of cognition in multiple sclerosis (MS). The article, “Cognitive impairment in multiple sclerosis: An 18-year follow-up study,” was epublished by Multiple Sclerosis and Related Disorders on April 13, 2014. Results provide insight into the natural evolution of cognitive changes over time, an important consideration for researchers and clinicians. Authors are Lauren B. Strober, PhD, of Kessler Foundation and Stephen M. Rao, PhD, Jar-Chi Lee, Elizabeth Fisher, PhD, and Richard Rudick, MD, of the Cleveland Clinic.
“While cognitive impairment is known to affect 40 to 65% of individuals with MS, few studies have followed the pattern of cognitive decline over time, which is important for understanding long-term care and outcomes associated with MS,” said Dr. Strober, senior research scientist at Kessler Foundation. “Our study was based on a unique sample of 22 patients who underwent neuropsychological testing at entry into the original phase 3 clinical trial of intramuscular interferon beta-1a, and again at 18-year followup.”
At baseline, 9 patients (41%) had cognitive impairment; at 18-year followup, 13 patients (59%), were found to be impaired. Significant declines over time were found in information processing speed, auditory attention, memory, episodic learning and visual construction. Decline was steeper in the unimpaired than in the impaired group, as indicated by the Symbol Digit Modalities Test (SDMT).
"These longitudinal data contribute substantially to our knowledge of the course of cognitive decline in MS,” noted John DeLuca, PhD, VP of Research & Training at Kessler Foundation. “In light of the young age at diagnosis, this perspective is fundamental to the development of rehabilitation strategies that meet the needs of people dealing with the cognitive effects of MS.”
The study was funded by Biogen Idec.
Neural sweet talk: Taste metaphors emotionally engage the brain
So accustomed are we to metaphors related to taste that when we hear a kind smile described as “sweet,” or a resentful comment as “bitter,” we most likely don’t even think of those words as metaphors. But while it may seem to our ears that “sweet” by any other name means the same thing, new research shows that taste-related words actually engage the emotional centers of the brain more than literal words with the same meaning.
Researchers from Princeton University and the Free University of Berlin report in the Journal of Cognitive Neuroscience the first study to experimentally show that the brain processes these everyday metaphors differently than literal language. In the study, participants read 37 sentences that included common metaphors based on taste while the researchers recorded their brain activity. Each taste-related word was then swapped with a literal counterpart so that, for instance, “She looked at him sweetly” became “She looked at him kindly.”
The researchers found that the sentences containing words that invoked taste activated areas known to be associated with emotional processing, such as the amygdala, as well as the areas known as the gustatory cortices that allow for the physical act of tasting. Interestingly, the metaphorical and literal words only resulted in brain activity related to emotion when part of a sentence, but stimulated the gustatory cortices both in sentences and as stand-alone words.
Metaphorical sentences may spark increased brain activity in emotion-related regions because they allude to physical experiences, said co-author Adele Goldberg, a Princeton professor of linguistics in the Council of the Humanities. Human language frequently uses physical sensations or objects to refer to abstract domains such as time, understanding or emotion, Goldberg said. For instance, people liken love to a number of afflictions including being “sick” or shot through the heart with an arrow. Similarly, “sweet” has a much clearer physical component than “kind.” The new research suggests that these associations go beyond just being descriptive to engage our brains on an emotional level and potentially amplify the impact of the sentence, Goldberg said.
"You begin to realize when you look at metaphors how common they are in helping us understand abstract domains," Goldberg said. "It could be that we are more engaged with abstract concepts when we use metaphorical language that ties into physical experiences."
If metaphors in general elicit an emotional response from the brain that is similar to that caused by taste-related metaphors, then that could mean that figurative language presents a “rhetorical advantage” when communicating with others, explained co-author Francesca Citron, a postdoctoral researcher of psycholinguistics at the Free University’s Languages of Emotion research center.
"Figurative language may be more effective in communication and may facilitate processes such as affiliation, persuasion and support," Citron said. "Further, as a reader or listener, one should be wary of being overly influenced by metaphorical language."
Colloquially, metaphors seem to be employed precisely to evoke an emotional reaction, yet the actual emotional effect of figurative phrases on the person hearing them has not before been deeply explored, said Benjamin Bergen, an associate professor of cognitive science at the University of California-San Diego who studies language comprehension, and metaphorical language and thought.
"There’s a lot of research on the conceptual effects of metaphors, such as how they allow people to think about new or abstract concepts in terms of concrete things they’re familiar with. But there’s very little work on the emotional impact of metaphor," said Bergen, who had no role in the research but is familiar with it.
"Emotional impact seems to be one of the main reasons people use metaphors to begin with. For instance, a senator might describe a bill as ‘job-killing’ to evoke an emotional reaction," he said. "These results suggest that using certain metaphorical expressions induces more of an emotional reaction than saying the same thing literally. Those expressions that have this property are likely to have the effects on reasoning, inference, judgment and decision-making that emotion is known to have."
The brain areas that taste-related words did not stimulate are also an important outcome of the study, Citron said. Existing research on metaphors and neural processing has shown that figurative language generally requires more brainpower than literal language, Citron and Goldberg wrote. But these bursts of neural activity have been related to higher-order processing from thinking through an unfamiliar metaphor.
The brain activity Citron and Goldberg observed did not correlate with this process. In order to create the metaphorical- and literal-sentence stimuli, they had a group of people separate from the study participants rate sentences for familiarity, apparent arousal, imageability — which is how easily a phrase can be imagined in the reader’s mind — and how positive or negative each sentence was interpreted as being. The metaphorical and literal sentences were equal on all of these factors. In addition, each metaphorical phrase and its literal counterpart were rated as being highly similar in meaning.
These steps helped to ensure that the metaphorical and literal sentences were equally as easy to comprehend. Thus, the brain activity the researchers recorded was not likely to be in response to any additional difficulty study participants had in understanding the metaphors.
"It is important to rule out possible effects of familiarity, since less familiar items may require more processing resources to be understood and elicit enhanced brain responses in several brain regions," Citron said.
Citron and Goldberg plan to follow up on their results by examining if figurative language is remembered more accurately than literal language, if metaphors are more physically stimulating, and if metaphors related to other senses also provoke an emotional response from the brain.
Deep Brain Stimulation Improves Non Motor Symptoms in Parkinson’s Disease as well as Motor Symptoms
Deep brain stimulation (DBS) has become a well-recognized non-pharmacologic treatment that improves motor symptoms of patients with early and advanced Parkinson’s disease. Evidence now indicates that DBS can decrease the number and severity of non motor symptoms of patients with Parkinson’s disease (PD) as well, according to a review published in the Journal of Parkinson’s Disease.
“Non motor features are common in PD patients, occur across all disease stages, and while well described, are still under-recognized when considering their huge impact on patients’ quality of life,” says Lisa Klingelhoefer, MD, a fellow at the National Parkinson Foundation International Centre of Excellence, Department of Neurology, King’s College Hospital and King’s College, London.
For example, DBS of the subthalamic nucleus (STN) is effective for alleviating sleep problems and fatigue associated with PD, producing noticeable long-term improvements in sleep efficiency and the quality and duration of continuous sleep. DBS also decreases nighttime and early morning dystonia and improves nighttime mobility. “DBS can contribute to better sleep, less daytime somnolence, improved mobility, and less need for dopamine replacement therapy,” says Dr. Klingelhoefer.
The effects of DBS on some other non motor symptoms of PD are less clear cut and transient worsening of neuropsychological and psychiatric symptoms have been reported. For instance, behavioral disorders such as impulsivity (e.g. hypersexuality, pathological gambling, and excessive eating) can occur or worsen in PD patients after STN DBS. While pre-existing drug-induced psychotic symptoms like hallucinations often disappear after STN DBS, transient psychotic symptoms such as delirium may emerge in the immediate post-operative period. Similarly, conflicting reports have found that STN DBS improves, worsens, or does not change mood disorders such as depression, mania, or anxiety.
“Further work is required in order to fully understand the mechanisms and impact of DBS of the STN or other brain structures on the non motor symptoms of PD,” concludes Dr. Klingelhoefer. She suggests that in the future, non motor symptoms of PD may become an additional primary indication for DBS.
PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most characteristic symptoms are movement-related, such as involuntary shaking and muscle stiffness. Non motor symptoms, such as worsening depression, anxiety, olfactory dysfunction, sweating, bladder and bowel dysfunction, and sleep disturbances, can appear prior to the onset of motor symptoms.
3-D Computer Model May Help Refine Target for Deep Brain Stimulation Therapy for Dystonia
Although deep brain stimulation can be an effective therapy for dystonia – a potentially crippling movement disorder – the treatment isn’t always effective, or benefits may not be immediate. Precise placement of DBS electrodes is one of several factors that can affect results, but few studies have attempted to identify the “sweet spot,” where electrode placement yields the best results.
Researchers led by investigators at Cedars-Sinai, using a complex set of data from records and imaging scans of patients who have undergone successful DBS implantation, have created 3-D, computerized models that map the brain region involved in dystonia. The models identify an anatomical target for further study and provide information for neurologists and neurosurgeons to consider when planning surgery and making device programming decisions.
“We know DBS works as a treatment for dystonia, but we don’t know exactly how it works or why some patients have better, quicker results than others. Patient age, disease duration and other underlying factors have a role, and we believe electrode positioning and device programming are critical, but there is no consensus on ideal device placement and optimal programming strategies,” said Michele Tagliati, MD, director of the Movement Disorders Program in the Department of Neurology at Cedars-Sinai.
“This modeling paves the way for the construction of practical therapeutic and investigational targets,” added Tagliati, senior author of an article now available on the online edition of Annals of Neurology.
Medications usually are the first line of treatment for dystonia and several other movement disorders, but if drugs fail – as frequently happens – or side effects are excessive, neurologists and neurosurgeons may supplement them with deep brain stimulation. Electrical leads are implanted deep in the brain, and a pulse generator is placed near the collarbone. The device is later programmed with a remote, hand-held controller.
To calm the disorganized muscle contractions of dystonia, doctors generally target a brain structure called the globus pallidus, but studies on precise positioning of electrode contacts and the best programming parameters – such as the intensity and frequency of electrical stimulation – are rare and conflicting. Finding the most effective settings can take months of fine-tuning.
In this retrospective study, investigators examined a database of 94 patients with the most common genetic form of dystonia, DYT1, who had been treated with DBS for at least a year. They selected 21 patients who had good responses to treatment, compiled their demographic and treatment information, and used magnetic resonance imaging scans to create 3-D anatomical models with a fine grid to show exact location of relevant brain structures.
The investigators then simulated the placement of electrodes as they were positioned in the patients’ brains and input the actual stimulation parameters into a computer program – a “volume of tissue activation” model – which calculated detailed information specific to each patient and each electrode. The model draws on principles of neurophysiology – the way nerve cells respond to DBS – the biophysics of voltage distribution from electrodes, and the anatomy of the globus pallidus and surrounding structures.
“We found that clinicians were applying relatively large amounts of energy to wide swaths of the globus pallidus, but the area in common among most individuals was much smaller. We interpret this as being the potential ‘target within the target,’ and if our results are validated in further research and clinical practice, computer modeling may offer a physiologically-based, data-driven, visualized approach to clinical decision-making,” Tagliati said.
(Source: newswise.com)
Neuroscientists explain how mutated X-linked mental retardation protein impairs neuronal function
There are new clues about malfunctions in brain cells that contribute to intellectual disability and possibly other developmental brain disorders.
(Image caption: False color image of a mouse hippocampal neuron (cell
body is at lower right) with branchlike dendrites that provide surfaces at which projections from other neurons can connect, by forming synapses. Van Aelst and colleagues have shown that when the OPHN1 protein is mutated, interfering with its ability to interact with another protein called Homer1b/c, AMPA receptors don’t recycle to the surface at synapses at the rate they normally do. This adversely impacts synaptic plasticity, the process by which neurons adjust the strength of their connections. Such pathology may play a role in X-linked mental retardation.)
Professor Linda Van Aelst of Cold Spring Harbor Laboratory (CSHL) has been scrutinizing how the normal version of a protein called OPHN1 helps enable excitatory nerve transmission in the brain, particularly at nerve-cell docking ports containing AMPA receptors (AMPARs). Her team’s new work, published June 24 in the Journal of Neuroscience, provides new mechanistic insight into how OPHN1 defects can lead to impairments in the maturation and adjustment of synaptic strength of AMPAR-expressing neurons, which are ubiquitous in the brain and respond to the excitatory neurotransmitter glutamate.
Mutations in a gene called oligophrenin-1 (OPHN1) – located on the X chromosome – have previously been linked to X-linked intellectual disability (also known as X-linked mental retardation), a condition that affects boys disproportionately and could account for as much as one-fifth of all intellectual disability among males.
Several different mutations in the OPHN1 gene have been identified to date, all of which perturb nerve cells’ manufacture of OPHN1 protein. Previously, Van Aelst and colleagues demonstrated that OPHN1 has a vital role in synaptic plasticity, the process through which adjacent nerve cells adjust the strength of their connections. Cells in the brain are constantly adjusting connection strength as they respond to streams of stimuli.
The new discovery shows how OPHN1 is involved in the trafficking of AMPARs, an essential feature of plasticity in neurons. Neurons move receptors away from synapses into their interior and then back to the surface of synapses to control connection strength. At the synaptic surface, receptors provide an opportunity for the docking of neurotransmitters, in this case glutamate molecules. After a cell has fired, surface receptors are typically brought back into the interior, where they are recycled for future use.
When OPHN1 is misshapen or missing due to genetic mutation, the CSHL team demonstrated, it can no longer properly perform its role in receptor recycling, thus also impairing neurons’ ability to maintain strong long-term connections with their neighbors, called long-term potentiation.
Van Aelst’s new experiments explain how OPHN1 in complex with another protein called Homer1b/c should normally interact with an area called the endocytic zone (EZ) to provide a pool of AMPARs to be brought to the synapse at a location called the post-synaptic density (PSD). When OPHN1 is mutated, the pool does not form and receptors needed for strengthening synapses are not available. Long-term potentiation is impaired.
“This suggests a previously unknown way in which genetic defects in OPHN1 can lead to dysfunctions in the glutamate system,” says Dr. Van Aelst. “Our earlier studies had already shown that OPHN1 is essential in stabilizing AMPA receptors at the synapse. Together, these two essential roles suggest how defective OPHN1 protein may contribute to pathology that underlies X-linked intellectual disability.”
(Source: cshl.edu)
Study shows how brain tumor cells move and damage tissue, points to possible therapy
Researchers at the University of Alabama at Birmingham have shed new light on how cells called gliomas migrate in the brain and cause devastating tumors. The findings, published June 19, 2014 in Nature Communications, show that gliomas — malignant glial cells — disrupt normal neural connections and hijack control of blood vessels.
The study provides insight into the mechanisms of how glioma cells spread throughout the brain as a devastating form of brain cancer, and potentially offers a tantalizing opportunity for therapy.
A hallmark of gliomas is that the cells can migrate away from a central tumor, invading healthy brain tissue. Even if a tumor mass is surgically removed, malignant cells that have migrated are left behind, and can grow into a new tumor.
To grow, glioma cells need access to nutrients in the blood supply, and it is known that gliomas travel along blood vessels within the brain. Now, researchers in the lab of neuroscientist Harald Sontheimer, Ph.D., professor in the UAB Department of Neurobiology, have discovered that, as they move, gliomas dislodge astrocytic endfeet, which play a critical role in regulating blood flow in the brain.
Astrocytes are star-shaped cells in the brain that surround blood vessels and connect to them through projections called endfeet, which extend from the astrocyte and latch onto the vessel wall. The surface of nearly every blood vessel in the brain is covered by endfeet, which regulate the smooth muscle cells on the walls of blood vessels. Through that connection, instructions can be given to the muscle cells to constrict the blood vessel and limit blood flow, or dilate the vessel and increase blood flow.
Sontheimer, director of the UAB Center for Glial Biology in Medicine, says that, as a person performs different neurological functions, blood flow needs to be increased to the areas responsible for that function and correspondingly decreased in other areas to maintain balance.
The arrival of a glioma cell changes all that.
“Glioma cells traveling along blood vessels literally cut the connection of astrocytic endfeet with the vessels and push them out of the way,” said Sontheimer. “By disrupting this important neural connection, adverse cognitive effects could be expected. Additionally, our study showed that gliomas then take control of the blood vessels for their own ends. And those ends are primarily to obtain nutrients from blood so that they can continue to grow and spread.”
Sontheimer’s team says the glioma cells tend to congregate at blood vessel junctions, almost as if camping alongside a stream where it joins a river. The ready supply of nutrients would allow the cell to grow into a larger tumor mass.
By traveling on the outside of a blood vessel, glioma cells are able to access nutrients from the blood stream. As a side effect to that process, they damage the blood brain barrier. The barrier, a layer of endothelial cells, protects the brain by restricting passage of harmful substances from the blood stream into brain tissue.
“We found that, when gliomas push away the astrocytic endfeet, damage occurs to the integrity of the endothelial cells that make up the blood brain barrier,” said Stefanie Robel, Ph.D., a postdoctoral researcher in Sontheimer’s lab and co-first author of the study. “The barrier becomes weakened, and begins to leak. A leak across the barrier can cause severe damage to brain tissue.”
“That leakage appears to be a consequence of glioma cells’ migrating along the blood vessels in their search for nutrients,” said Stacey Watkins, an M.D./Ph.D. student in Sontheimer’s lab and co-first author. “When glioma cells contact the vessels, they have direct access to nutrients.”
But amid the deleterious effects that Sontheimer’s team observed — shearing away the endfeet from their blood vessels, disrupting normal brain activity, hijacking control of blood vessels and causing leaks in the blood brain barrier — he says there may be a silver lining. The idea that gliomas cause the blood brain barrier to become porous and leak might open up a new avenue to kill the malignant cells as they migrate.
Chemotherapy, usually delivered intravenously, is not considered an effective strategy for killing gliomas. Chemotherapeutic agents are very effective in killing cancer cells elsewhere in the body, but the predominant belief is that such drugs will not pass the blood brain barrier and thus will not reach their target.
“Chemotherapy is typically not tried in cases of glioma until after other therapies such as surgery and radiation have been employed,” Sontheimer said. “Our findings, which suggest that gliomas actually weaken the blood brain barrier and cause leakage, might indicate that high-dose, intravenous chemotherapy used early on following a diagnosis of brain cancer would be beneficial.”
The study, funded by the National Institutes of Health and the American Brain Tumor Association, was conducted on a clinically relevant mouse model of human malignant glioma.
Sontheimer says logical next steps would be to further examine the cognitive impact of severing the astrocytic endfeet connection to blood vessels.
Those with episodic amnesia are not ‘stuck in time,’ says philosopher Carl Craver
In 1981, a motorcycle accident left Toronto native Kent Cochrane with severe brain damage and dramatically impaired episodic memory. Following the accident, Cochrane could no longer remember events from his past. Nor could he predict specific events that might happen in the future.
When neuroscientist Endel Tulving, PhD, asked him to describe what he would do tomorrow, Cochrane could not answer and described his state of mind as “blank.”
Psychologists and neuroscientists came to know Cochrane, who passed away earlier this year, simply as “KC.” Many scientists have described KC as “stuck in time,” or trapped in a permanent present.
It has generally been assumed that people with episodic amnesia experience time much differently than those with more typical memory function.
However, a recent paper in Neuropsychologia co-authored by Carl F. Craver, PhD, professor of philosophy and of philosophy-neuroscience-psychology, both in Arts & Sciences at Washington University in St. Louis, disputes this type of claim.
“It’s our whole way of thinking about these people that we wanted to bring under pressure,” Craver said. “There are sets of claims that sound empirical, like ‘These people are stuck in time.’ But if you ask, ‘Have you actually tested what they know about time?’ the answer is no.”
Time and consciousness
A series of experiments convinced Craver and his co-authors that although KC could not remember specific past experiences, he did in fact have an understanding of time and an appreciation of its significance to his life.
Interviews with KC by Craver and his colleagues revealed that KC retained much of what psychologists refer to as “temporal consciousness.” KC could order significant events from his life on a timeline, and he seemed to have complete mastery of central temporal concepts.
For example, KC understood that events in the past have already happened, that they influence the future, and that once they happen, they cannot be changed.
He also knew that events in the future don’t remain in the future, but eventually become present. Even more interestingly, KC’s understanding of time influenced his decision-making.
If KC truly had no understanding of time, Craver argues, then he and others with his type of amnesia would act as if only the present mattered. Without understanding that present actions have future consequences or rewards, KC would have based his actions only upon immediate outcomes. However, this was not the case.
On a personality test, KC scored as low as possible on measures of hedonism, or the tendency to be a self-indulgent pleasure-seeker.
In systematic tests of his decision-making, carried out with WUSTL’s Len Green, PhD, professor of psychology, and Joel Myerson, PhD, research professor of psychology, and researchers at York University in Toronto, KC also showed that he was willing to trade a smaller, sooner reward for a larger, later reward.
In other words, KC’s inability to remember past events did not affect his ability to appreciate the value of future rewards.
‘Questions are now wide open’
KC’s case reveals how much is left to discover about memory and how it relates to human understanding of time.
“If you think about memory long enough it starts to sound magical,” Craver said. “How is it that we can replay these events from our lives? And what’s going on in our brains that allows us to re-experience these events from our past?”
Craver hopes that this article — the last to be published about KC during his lifetime — brings these types of questions to the forefront.
“These findings open up a whole new set of questions about people with amnesia,” Craver said. “Things that we previously thought were closed questions are now wide open.”
Study finds association between maternal exposure to agricultural pesticides, autism in offspring
Pregnant women who lived in close proximity to fields and farms where chemical pesticides were applied experienced a two-thirds increased risk of having a child with autism spectrum disorder or other developmental delay, a study by researchers with the UC Davis MIND Institute has found. The associations were stronger when the exposures occurred during the second and third trimesters of the women’s pregnancies.
The large, multisite California-based study examined associations between specific classes of pesticides, including organophosphates, pyrethroids and carbamates, applied during the study participants’ pregnancies and later diagnoses of autism and developmental delay in their offspring. It is published online today in Environmental Health Perspectives.
“This study validates the results of earlier research that has reported associations between having a child with autism and prenatal exposure to agricultural chemicals in California,” said lead study author Janie F. Shelton, a UC Davis graduate student who now consults with the United Nations. “While we still must investigate whether certain sub-groups are more vulnerable to exposures to these compounds than others, the message is very clear: Women who are pregnant should take special care to avoid contact with agricultural chemicals whenever possible.”
California is the top agricultural producing state in the nation, grossing $38 billion in revenue from farm crops in 2010. Statewide, approximately 200 million pounds of active pesticides are applied each year, most of it in the Central Valley, north to the Sacramento Valley and south to the Imperial Valley on the California-Mexico border. While pesticides are critical for the modern agriculture industry, certain commonly used pesticides are neurotoxic and may pose threats to brain development during gestation, potentially resulting in developmental delay or autism.
The study was conducted by examining commercial pesticide application using the California Pesticide Use Report and linking the data to the residential addresses of approximately 1,000 participants in the Northern California-based Childhood Risk of Autism from Genetics and the Environment (CHARGE) Study. The study includes families with children between 2 and 5 diagnosed with autism or developmental delay or with typical development. It is led by principal investigator Irva Hertz-Picciotto, a MIND Institute researcher and professor and vice chair of the Department of Public Health Sciences at UC Davis. The majority of study participants live in the Sacramento Valley, Central Valley and the greater San Francisco Bay Area.
Twenty-one chemical compounds were identified in the organophosphate class, including chlorpyrifos, acephate and diazinon. The second most commonly applied class of pesticides was pyrethroids, one quarter of which was esfenvalerate, followed by lambda-cyhalothrin permethrin, cypermethrin and tau-fluvalinate. Eighty percent of the carbamates were methomyl and carbaryl.
For the study, researchers used questionnaires to obtain study participants’ residential addresses during the pre-conception and pregnancy periods. The addresses then were overlaid on maps with the locations of agricultural chemical application sites based on the pesticide-use reports to determine residential proximity. The study also examined which participants were exposed to which agricultural chemicals.
“We mapped where our study participants’ lived during pregnancy and around the time of birth. In California, pesticide applicators must report what they’re applying, where they’re applying it, dates when the applications were made and how much was applied,” Hertz-Picciotto said. “What we saw were several classes of pesticides more commonly applied near residences of mothers whose children developed autism or had delayed cognitive or other skills.”
The researchers found that during the study period approximately one-third of CHARGE Study participants lived in close proximity – within 1.25 to 1.75 kilometers – of commercial pesticide application sites. Some associations were greater among mothers living closer to application sites and lower as residential proximity to the application sites decreased, the researchers found.
Organophosphates applied over the course of pregnancy were associated with an elevated risk of autism spectrum disorder, particularly for chlorpyrifos applications in the second trimester. Pyrethroids were moderately associated with autism spectrum disorder immediately prior to conception and in the third trimester. Carbamates applied during pregnancy were associated with developmental delay.
Exposures to insecticides for those living near agricultural areas may be problematic, especially during gestation, because the developing fetal brain may be more vulnerable than it is in adults. Because these pesticides are neurotoxic, in utero exposures during early development may distort the complex processes of structural development and neuronal signaling, producing alterations to the excitation and inhibition mechanisms that govern mood, learning, social interactions and behavior.
“In that early developmental gestational period, the brain is developing synapses, the spaces between neurons, where electrical impulses are turned into neurotransmitting chemicals that leap from one neuron to another to pass messages along. The formation of these junctions is really important and may well be where these pesticides are operating and affecting neurotransmission,” Hertz-Picciotto said.
Research from the CHARGE Study has emphasized the importance of maternal nutrition during pregnancy, particularly the use of prenatal vitamins to reduce the risk of having a child with autism. While it’s impossible to entirely eliminate risks due to environmental exposures, Hertz-Picciotto said that finding ways to reduce exposures to chemical pesticides, particularly for the very young, is important.
“We need to open up a dialogue about how this can be done, at both a societal and individual level,” she said. “If it were my family, I wouldn’t want to live close to where heavy pesticides are being applied.”
(Source: ucdmc.ucdavis.edu)