Posts tagged science
Articles and news from the latest research reports.
A New Wrinkle in Parkinson’s Disease Research
The active ingredient in an over-the-counter skin cream might do more than prevent wrinkles. Scientists have discovered that the drug, called kinetin, also slows or stops the effects of Parkinson’s disease on brain cells.
Scientists identified the link through biochemical and cellular studies, but the research team is now testing the drug in animal models of Parkinson’s. The research is published in the August 15, 2013 issue of the journal Cell.
“Kinetin is a great molecule to pursue because it’s already sold in drugstores as a topical anti-wrinkle cream,” says HHMI investigator Kevan Shokat of the University of California, San Francisco. “So it’s a drug we know has been in people and is safe.”
Parkinson’s disease is a degenerative disease that causes the death of neurons in the brain. Initially, the disease affects one’s movement and causes tremors, difficulty walking, and slurred speech. Later stages of the disease can cause dementia and broader health problems. In 2004, researchers studying an Italian family with a high prevalence of early-onset Parkinson’s disease discovered mutations in a protein called PINK1 associated with the inherited form of the disease.
Since then, studies have shown that PINK1 normally wedges into the membrane of damaged mitochondria inside cells that causes another protein, Parkin, to be recruited to the mitochondria, which are organelles responsible for energy generation. Neurons require high levels of energy production, therefore when mitochondrial damage occurs, it can lead to neuronal death. However, when Parkin is present on damaged mitochondria, studding the mitochondrial surface, the cell is able to survive the damage. In people who inherit mutations in PINK1, however, Parkin is never recruited to the organelles, leading to more frequent neuronal death than usual.
Shokat and his colleagues wanted to develop a way to turn on or crank up PINK1 activity, therefore preventing an excess of cell death, in those with inherited Parkinson’s disease. But turning on activity of a mutant enzyme is typically more difficult than blocking activity of an overactive version.
“When we started this project, we really thought that there would be no conceivable way to make something that directly turns on the enzyme,” says Shokat. “For any enzyme we know that causes a disease, we have ways to make inhibitors but no real ways to turn up activity.”
His team expected it would have to find a less direct way to mimic the activity of PINK1 and recruit Parkin. In the hopes of more fully understanding how PINK1 works, they began investigating how PINK1 binds to ATP, the energy molecule that normally turns it on. In one test, instead of adding ATP to the enzymes, they added different ATP analogues, versions of ATP with altered chemical groups that slightly change its shape. Scientists typically must engineer new versions of proteins to be able to accept these analogs, since they don’t fit into the typical ATP binding site. But to Shokat’s surprise, one of the analogs—kinetin triphosphate, or KTP—turned on the activity of not only normal PINK1, but also the mutated version, which doesn’t bind ATP.
“This drug does something that chemically we just never thought was possible,” says Shokat. “But it goes to show that if you find the right key for the right lock, you’ll be able to open the door.”
To test whether the binding of KTP to PINK1 led to the same consequences as the usual ATP binding, Shokat’s group measured the activity of PINK1 directly, as well as the downstream consequences of this activity, including the amount of Parkin recruited to the mitochondrial surface, and the levels of cell death. Adding the precursor of KTP, kinetin, to cells—both those with PINK1 mutations and those with normal physiology—amplified the activity of PINK1, increased the level of Parkin on damaged mitochondria, and decreased levels of neuron death, they found.
“What we have here is a case where the molecular target has been shown to be important to Parkinson’s in human genetic studies,” says Shokat. “And now we have a drug that specifically acts on this target and reverses the cellular causes of the disease.”
The similar results in cells with and without PINK1 mutations suggest that kinetin, which is a precursor to KTP, could be used to treat not only Parkinson’s patients with a known PINK1 mutation, but to slow progression of the disease in those without a family history by decreasing cell death.
Shokat is now performing experiments on the effects of kinetin in mice with various forms of Parkinson’s disease. However, the usefulness of animal models in Parkinson’s research has been debated, and therefore the positive results from the cellular data, he says, is as good an indicator as results in animals that this drug has potential to treat Parkinson’s in humans. Initial human studies will likely focus on the small population of patients with PINK1 mutations, and if successful in that group the drug could later be tested in a wider array of Parkinson’s patients.
(Source: hhmi.org)
A Genetic Answer to the Alzheimer’s Riddle?
What if we could pinpoint a hereditary cause for Alzheimer’s, and intervene to reduce the risk of the disease? We may be closer to that goal, thanks to a team at the University of Kentucky. Researchers affiliated with the UK Sanders-Brown Center on Aging have completed new work in Alzheimer’s genetics; the research is detailed in a paper published today in the Journal of Neuroscience.
Emerging evidence indicates that, much like in the case of high cholesterol, some Alzheimer’s disease risk is inherited while the remainder is environmental. Family and twin studies suggest that about 70 percent of total Alzheimer’s risk is hereditary.
Recently published studies identified several variations in DNA sequence that each modify Alzheimer’s risk. In their work, the UK researchers investigated how one of these sequence variations may act. They found that a “protective” genetic variation near a gene called CD33 correlated strongly with how the CD33 mRNA was assembled in the human brain. The authors found that a form of CD33 that lacked a critical functional domain correlates with reduced risk of Alzheimers disease. CD33 is thought to inhibit clearance of amyloid beta, a hallmark of Alzheimers disease.
The results obtained by the UK scientists indicate that inhibiting CD33 may reduce Alzheimer’s risk. A drug tested for acute myeloid leukemia targets CD33, suggesting the potential for treatments based on CD33 to mitigate the risk for Alzheimer’s disease. Additional studies must be conducted before this treatment approach could be tested in humans.
Study debunks controversial MS theory
There is no evidence that impaired blood flow or blockage in the veins of the neck or head is involved in multiple sclerosis, says a McMaster University study.
The research, published online by PLOS ONE Wednesday, found no evidence of abnormalities in the internal jugular or vertebral veins or in the deep cerebral veins of any of 100 patients with multiple sclerosis (MS) compared with 100 people who had no history of any neurological condition.
The study contradicts a controversial theory that says that MS, a chronic, neurodegenerative and inflammatory disease of the central nervous system, is associated with abnormalities in the drainage of venous blood from the brain. In 2008 Italian researcher Paolo Zamboni said that angioplasty, a blockage clearing procedure, would help MS patients with a condition he called chronic cerebrospinal venous insufficiency (CCSVI). This caused a flood of public response in Canada and elsewhere, with many concerned individuals lobbying for support of the ‘Liberation Treatment’ to clear the veins, as advocated by Zamboni.
“This is the first Canadian study to provide compelling evidence against the involvement of CCSVI in MS,” said principal investigator Ian Rodger, a professor emeritus of medicine in the Michael G. DeGroote School of Medicine. “Our findings bring a much needed perspective to the debate surrounding venous angioplasty for MS patients”.
In the study all participants received an ultrasound of deep cerebral veins and neck veins as well as a magnetic resonance imaging (MRI) of the neck veins and brain. Each participant had both examinations performed on the same day. The McMaster research team included a radiologist and two ultrasound technicians who had trained in the Zamboni technique at the Department of Vascular Surgery of the University of Ferrara.
(Source: dailynews.mcmaster.ca)
Brain scans could predict response to antipsychotic medication
Researchers from King’s College London and the University of Nottingham have identified neuroimaging markers in the brain which could help predict whether people with psychosis respond to antipsychotic medications or not.
In approximately half of young people experiencing their first episode of a psychosis (FEP), the symptoms do not improve considerably with the initial medication prescribed, increasing the risk of subsequent episodes and worse outcome. Identifying individuals at greatest risk of not responding to existing medications could help in the search for improved medications, and may eventually help clinicians personalize treatment plans.
In a study published today in JAMA Psychiatry, researchers used structural Magnetic Resonance Imaging (MRI) to scan the brains of 126 individuals – 80 presenting with FEP, and 46 healthy controls. Participants had an MRI scan shortly after their FEP, and another assessment 12 weeks later, to establish whether symptoms had improved following the first treatment with antipsychotic medications.
The researchers examined a particular feature of the brain called “cortical gyrification” - the extent of folding of the cerebral cortex and a marker of how it has developed. They found that the individuals who did not respond to treatment already had a significant reduction in gyrification across multiple brain regions, compared to patients who did respond and to individuals without psychosis. This reduced gyrification was particularly present in brain areas considered important in psychosis, such as the temporal and frontal lobes. Those who responded to treatment were virtually indistinguishable from the healthy controls.
The researchers also investigated whether the differences could be explained by the type of diagnosis of psychosis (eg. with or without affective symptoms, such as depression or elated mood). They found that reduced gyrification predicted non-response to treatment independently of the diagnosis.
Dr Paola Dazzan from the Department of Psychosis Studies at King’s College London’s Institute of Psychiatry, and senior author of the paper, says: “Our study provides crucial evidence of a neuroimaging marker that, if validated, could be used early in psychosis to help identify those people less likely to respond to medications. It is possible that the alterations we observed are due to differences in the way the brain has developed early on in people who do not respond to medication compared to those who do.”
She continues:”There have been few advances in developing novel anti-psychotic drugs over the past 50 years and we still face the same problems with a sub-group of people who do not respond to the drugs we currently use. We could envisage using a marker like this one to identify people who are least likely to respond to existing medications and focus our efforts on developing new medication specifically adapted to this group. In the longer term, if we were able to identify poor responders at the outset, we may be able to formulate personalized treatment plans for that individual patient.”
Dr Lena Palaniyappan from the University of Nottingham adds: “All of us have complex and varying patterns of folding in our brains. For the first time we are showing that the measurement of these variations could potentially guide us in treating psychosis. It is possible that people with specific patterns of brain structure respond better to treatments other than antipsychotics that are currently in use. Clearly, the time is ripe for us to focus on utilising neuroimaging to guide treatment decisions.”
Psychosis is a term used to indicate mental health disorders that present with symptoms like hallucinations (such as hearing voices) or delusions (unshakeable beliefs based on the person’s altered perception of reality, which may not correspond to the way others see the world). Psychotic episodes are present in conditions such as schizophrenia and bipolar disorder.
Approximately 1 in 100 people in England have at least one episode of psychosis throughout their lives. In most cases, psychosis develops during late adolescence (15 or above) or adulthood. Treatment involves a combination of antipsychotic medication, psychological therapies and social support. Many people with psychosis go on to lead ordinary lives and for about 60% of people, the symptoms disappear within 12 months from onset. However, for others, treatment is less straightforward and many do not respond to the initial antipsychotic treatment prescribed by their doctor. Early response to antipsychotic medication is known to be associated with better outcome and fewer subsequent episodes, and intervening early with effective treatments is therefore important.
(Source: kcl.ac.uk)
Two left feet? Study looks to demystify why we lose our balance
It’s always in front of a million people and feels like eternity. You’re strolling along when suddenly you’ve stumbled—the brain realizes you’re falling, but your muscles aren’t doing anything to stop it.
For a young person, a fall is usually just embarrassing. However, for the elderly, falling can be life threatening. Among the elderly who break a hip, 80 percent die within a year.
University of Michigan researchers believe that the critical window of time between when the brain senses a fall and the muscles respond may help explain why so many older people suffer these serious falls. A better understanding of what happens in the brain and muscles during this lag could go a long way toward prevention.
To that end, researchers at the U-M School of Kinesiology developed a novel way of looking at the electrical response in the brain before and during a fall by using an electroencephalogram.
Findings showed that many areas of the brain sense and respond to a fall, but that happens well before the muscles react. Lead researcher Daniel Ferris likened the study method to recording an orchestra with many microphones and then teasing out the sounds of specific instruments. In the study, researchers measured electrical activity in different regions of the brain.
"We’re using an EEG in a way others don’t, to look at what’s going on inside the brain," said Ferris, a professor in kinesiology. "We were able to determine what parts of the brain first identify when you are losing your balance during walking."
During the study, healthy young subjects with electrodes attached to their scalps walked on a balance beam mounted to a treadmill. When participants lost their balance and went off the beam, they simply continued walking on the moving treadmill, thus avoiding injury.
Ferris and colleagues then used a method called independent components analysis to separate and visualize the electrical activity in different parts of the brain. They found that people sense the start of a fall much better with both feet on the ground. Two grounded feet make it easier to determine where the ground is relative to the body, but people aren’t as sure of their stability on one foot.
The researchers were surprised that so many different parts of the brain activate during a fall, and they didn’t expect the brain to recognize a loss of balance as early as it does.
Future studies comparing the elderly with younger subjects could determine if the elderly sense falls too late, in which case, pharmaceuticals might help them regain their balance. If it’s a simple motor problem such as muscles not responding properly, strengthening exercises could help.
Other experiments under the same grant in the Ferris lab look to separate sensory and motor contributions to brain activity during walking.
The study, “Loss of balance during balance beam walking elicits a broadly distributed theta band electrocortical response,” was published in advance online in the Journal of Neurophysiology.
Researchers Building a Computer Chip Based on the Human Brain
Today’s computing chips are incredibly complex and contain billions of nano-scale transistors, allowing for fast, high-performance computers, pocket-sized smartphones that far outpace early desktop computers, and an explosion in handheld tablets.
Despite their ability to perform thousands of tasks in the blink of an eye, none of these devices even come close to rivaling the computing capabilities of the human brain. At least not yet. But a Boise State University research team could soon change that.
Electrical and computer engineering faculty Elisa Barney Smith, Kris Campbell and Vishal Saxena are joining forces on a project titled “CIF: Small: Realizing Chip-scale Bio-inspired Spiking Neural Networks with Monolithically Integrated Nano-scale Memristors.”
Team members are experts in machine learning (artificial intelligence), integrated circuit design and memristor devices. Funded by a three-year, $500,000 National Science Foundation grant, they have taken on the challenge of developing a new kind of computing architecture that works more like a brain than a traditional digital computer.
“By mimicking the brain’s billions of interconnections and pattern recognition capabilities, we may ultimately introduce a new paradigm in speed and power, and potentially enable systems that include the ability to learn, adapt and respond to their environment,” said Barney Smith, who is the principal investigator on the grant.
The project’s success rests on a memristor – a resistor that can be programmed to a new resistance by application of electrical pulses and remembers its new resistance value once the power is removed. Memristors were first hypothesized to exist in 1972 (in conjunction with resistors, capacitors and inductors) but were fully realized as nano-scale devices only in the last decade.
One of the first memristors was built in Campbell’s Boise State lab, which has the distinction of being one of only five or six labs worldwide that are up to the task.
The team’s research builds on recent work from scientists who have derived mathematical algorithms to explain the electrical interaction between brain synapses and neurons.
“By employing these models in combination with a new device technology that exhibits similar electrical response to the neural synapses, we will design entirely new computing chips that mimic how the brain processes information,” said Barney Smith.
Even better, these new chips will consume power at an order of magnitude lower than current computing processors, despite the fact that they match existing chips in physical dimensions. This will open the door for ultra low-power electronics intended for applications with scarce energy resources, such as in space, environmental sensors or biomedical implants.
Once the team has successfully built an artificial neural network, they will look to engage neurobiologists in parallel to what they are doing now. A proposal for that could be written in the coming year.
Barney Smith said they hope to send the first of the new neuron chips out for fabrication within weeks.
Two different versions of the same signaling protein tell a nerve cell which end is which, UA researchers have discovered. The findings could help improve therapies for spinal injuries and neurodegenerative diseases.
University of Arizona scientists have discovered an unknown mechanism that establishes polarity in developing nerve cells. Understanding how nerve cells make connections is an important step in developing cures for nerve damage resulting from spinal cord injuries or neurodegenerative diseases such as Alzheimer’s.
In a study published on Aug. 12 in the journal Proceedings of the National Academy of Sciences, UA doctoral student Sara Parker and her adviser, assistant professor of cellular and molecular medicine Sourav Ghosh, report that the decision which will be the “plus” and the “minus” end in a newborn nerve cell is made by a long and a short version of the same signaling molecule.
Nerve cells – or neurons – differ from many other cells by their highly asymmetric shape: Vaguely resembling a tree, a neuron has one long, trunk-like extension ending in a tuft of root-like bristles. This is called the axon. From the opposite end of the cell body sprout branch-like structures known as dendrites. By connecting the “branches” of their dendrites to the “root tips” of other neurons’ axons, nerve cells form networks, which can be as simple as the few connections involved in the knee-jerk reflex or as complex as those in the human brain.
Parker and her team found that embryonic nerve cells manufacture a well-known signaling enzyme called Atypical Protein Kinase C (aPKC) in two varieties: a full-length one and a truncated one. Both varieties compete to bind the same molecular partner, a protein called Par3. If the short form of aPKC pairs up with Par3, it tells the cell to grow a dendrite, and if the long one pairs up with Par3, it will make an axon instead.
When the researchers blocked the production of the short form, the nerve cell grew multiple axons and no dendrites. When they created an artificial abundance of the short form, dendrites formed at the expense of axons. UA undergraduate student Sophie Hapak performed many of the experiments revealing how the two isoforms compete for Par3.
"We show that wiring a neuronal circuit is much more complex than previously thought," said Ghosh. "The process has a built-in robustness that explicitly defines which part of the cell is ‘positive’ and which is ‘negative.’"
"In order to have a functioning neuronal circuit, you have to have receiving and sending ends," Parker said. "Initially, when a neuron is formed, it lacks the polarity it needs once it develops into a part of a circuit. The mechanism we discovered establishes that polarity."
"How the various brain regions are wired is the basis of emotion, memory and all cognitive functions," said Ghosh, who is a member of the UA’s BIO5 Institute. "Establishing neuronal polarity in single neurons is absolutely essential for neuronal circuits to form."
"If we understand this mechanism, we could think about methods to spur new axons after the original ones were severed in a traumatic spinal cord injury, for example," Ghosh said.
The findings defy conventional wisdom, which maintains that a developing neuron will make dendrites by default unless instructed by the long form of aPKC to make an axon instead. By cultivating and studying neurons just after they formed, Parker and her group found that both forms of aPKC, long and short, are initially distributed equally throughout the cell. These forms subsequently segregate into different parts of the cell as the neuron matures and establishes polarity.
Because the cells were isolated from rat brains and kept in culture, the researchers could demonstrate that no external clues from other cells are needed to instruct a developing neuron. Whether the establishment of polarity is a random process or whether other signals yet to be identified play a role in regulating the abundance of the two aPKC varieties is not known.
Researchers Debunk Myth of “Right-brain” and “Left-brain”Personality Traits
Newly released research findings from University of Utah neuroscientists assert that there is no evidence within brain imaging that indicates some people are right-brained or left-brained.
Chances are, you’ve heard the label of being a “right-brained” or “left-brained” thinker. Logical, detail-oriented and analytical? That’s left-brained behavior. Creative, thoughtful and subjective? Your brain’s right side functions stronger —or so long-held assumptions suggest.
But newly released research findings from University of Utah neuroscientists assert that there is no evidence within brain imaging that indicates some people are right-brained or left-brained.
For years in popular culture, the terms left-brained and right-brained have come to refer to personality types, with an assumption that some people use the right side of their brain more, while some use the left side more.
Following a two-year study, University of Utah researchers have debunked that myth through identifying specific networks in the left and right brain that process lateralized functions. Lateralization of brain function means that there are certain mental processes that are mainly specialized to one of the brain’s left or right hemispheres. During the course of the study, researchers analyzed resting brain scans of 1,011 people between the ages of seven and 29. In each person, they studied functional lateralization of the brain measured for thousands of brain regions —finding no relationship that individuals preferentially use their left -brain network or right- brain network more often.
“It’s absolutely true that some brain functions occur in one or the other side of the brain. Language tends to be on the left, attention more on the right. But people don’t tend to have a stronger left- or right-sided brain network. It seems to be determined more connection by connection, ” said Jeff Anderson, M.D., Ph.D., lead author of the study, which is formally titled “An Evaluation of the Left-Brain vs. Right-Brain Hypothesis with Resting State Functional Connectivity Magnetic Resonance Imaging.” It is published in the journal PLOS ONE this month.
Researchers obtained brain scans for the population they studied from a database called INDI, the International Neuroimaging Data-Sharing Initiative. The participants’ scans were taken during a functional connectivity MRI analysis, meaning a participant laid in a scanner for 5 to 10 minutes while their resting brain activity was analyzed.
By viewing brain activity, scientists can correlate brain activity in one region of the brain compared to another. In the study, researchers broke up the brain into 7,000 regions and examined which regions of the brain were more lateralized. They looked for connections — or all of the possible combinations of brain regions — and added up the number of connections for each brain region that was left- lateralized or right-lateralized. They discovered patterns in brain imaging for why a brain connection might be strongly left- or right-lateralized, said Jared Nielsen, a graduate student in neuroscience who carried out the study as part of his coursework.
“If you have a connection that is strongly left- lateralized, it relates to other strongly lateralized connection only if both sets of connections have a brain region in common,” said Nielsen.
Results of the study are groundbreaking, as they may change the way people think about the old right-brain versus left-brain theory, he said.
“Everyone should understand the personality types associated with the terminology ‘left-brained’ and ‘right-brained’ and how they relate to him or her personally; however, we just don’t see patterns where the whole left-brain network is more connected or the whole right-brain network is more connected in some people. It may be that personality types have nothing to do with one hemisphere being more active, stronger, or more connected,” said Nielsen.
Newly Discovered ‘Switch’ Plays Dual Role In Memory Formation
Researchers at Johns Hopkins have uncovered a protein switch that can either increase or decrease memory-building activity in brain cells, depending on the signals it detects. Its dual role means the protein is key to understanding the complex network of signals that shapes our brain’s circuitry, the researchers say. A description of their discovery appears in the July 31 issue of the Journal of Neuroscience.
“What’s interesting about this protein, AGAP3, is that it is effectively double-sided: One side beefs up synapses in response to brain activity, while the other side helps bring synapse-building back down to the brain’s resting state,” says Richard Huganir, Ph.D., a professor and director of the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine and co-director of the Brain Science Institute at Johns Hopkins. “The fact that it links these two opposing activities indicates AGAP3 may turn out to be central to controlling the strength of synapses.”
Huganir has long studied how connections between brain cells, known as synapses, are strengthened and weakened to form or erase memories. The new discovery came about when he and postdoctoral fellow Yuko Oku, Ph.D., investigated the chain reaction of signals involved in one type of synaptic strengthening.
In a study of the proteins that interact with one of the known proteins from that chain reaction, the previously unknown AGAP3 turned up. It contained not only a site designed to bind another protein involved in the chain reaction that leads from brain stimulation to learning, but also a second site involved in bringing synapse-building activity down to normal levels after a burst of activity.
Although it might seem the two different functions are behaving at cross-purposes, Oku says, it also could be that nature’s bundling of these functions together in a single protein is an elegant way of enabling learning and memory while preventing dangerous overstimulation. More research is needed, Oku says, to figure out whether AGAP3’s two sites coordinate by affecting each other’s activity, or are effectively free agents.
A hypnotic suggestion can generate true and automatic hallucinations
A multidisciplinary group of researchers from Finland (University of Turku and University of Helsinki) and Sweden (University of Skövde) has now found evidence that hypnotic suggestion can modify processing of a targeted stimulus before it reaches consciousness. The experiments show that it is possible to hypnotically modulate even highly automatic features of perception, such as color experience. The results are presented in two articles published in PLoS ONE and International Journal of Clinical and Experimental Hypnosis. The Finnish part of the research is funded by the Academy of Finland.
The nature of hypnotically suggested changes in perception has been one of the main topics of controversy during the history of hypnosis. The major current theories of hypnosis hold that we always actively use our own imagination to bring about the effects of a suggestion. For example the occurrence of visual hallucinations always requires active use of goal directed imagery and can be experienced both with and without hypnosis.
The study published in PLoS ONE was done with two very highly hypnotizable participants who can be hypnotized and dehypnotized by just using a one-word cue.
The researchers measured brains oscillatory activity from the EEG in response to briefly displayed series of red or blue shapes (squares, triangles or circles). The participants were hypnotized and given a suggestion that certain shapes always have a certain color (e.g. all squares are always red). Participant TS-H reported constantly experiencing a change in color immediately when a suggested shape appeared on the screen (e.g. seeing a red square when the real color was blue). The researchers found that this experience was accompanied with enhanced high-frequency brain activity already 1/10 second after the stimulus appeared and it was only seen in response to the shapes mentioned in the suggestion. The second participant did not experience the color change or the enhanced activity. However, she reported a peculiar feeling when a suggestion-relevant shape was presented: “sometimes I saw a shape that was red but my brain told me it had a different color”.
This enhanced oscillatory brain activity is proposed to reflect automatic comparison of input to memory representations. In this case the hypnotic suggestion “all squares are red” led to a memory trace that was automatically activated when a square was presented. Furthermore, for the participant TS-H the effect was strong enough to override the real color of the square. The matching must have occurred preconsciously because of the early timing of the effect and the immediacy of the color change. Also, both participants reported having performed under posthypnotic amnesia without conscious memory of the suggestions.
In the article published in International Journal of Clinical and Experimental Hypnosis TS-H was tested in a similar type of setting, however, only behavioral data, including accuracy and response times in color recognition, were collected. These results further support that a hypnotic suggestion affects her color perception of targeted objects before she becomes conscious of them. Furthermore, TS-H was not capable of changing her experience of visually presented stable images without the use of hypnotic suggestions i.e. by using mere mental imagery.
Importantly, both of these experiments were done by using a posthypnotic suggestion. The effect was suggested during hypnosis but the experience was suggested to occur after hypnosis. Thus all the experiments were carried out while participants were in their normal state of consciousness.
This result indicates that all hypnotic responding can no longer be regarded merely as goal directed mental imagery. It shows that in hypnosis it is possible to create a memory trace that influences early and preconscious stages of visual processing already about 1/10 second after the appearance of a visual target. This result has important implications in psychology and cognitive neuroscience especially when studying visual perception, memory and consciousness.