Posted tagged ‘neuroscience’

Awe, anxiety, joy: Researchers identify 27 categories for human emotions

September 11, 2017

Scores of words describe the wide range of emotions we experience. And as we grasp for words to describe our feelings, scientists are similarly struggling to comprehend how our brain processes and connects these feelings.

Now, a new study from the University of California, Berkeley challenges the assumptions traditionally made in the science of emotion. It was published recently in the Proceedings of the National Academy of Sciences.

Past research has generally categorized all emotions into six to 12 groups, such as happiness, sadness, anger, fear, surprise and disgust. However, the Berkeley researchers identified 27 distinct categories of emotions.

They asked a diverse group of over 850 men and women to view a random sampling of 2185 short, silent videos that depicted a wide range of emotional situations — including births, endearing animals, natural beauty, vomit, warfare and natural disasters, to name just a few. The participants reported their emotional response after each video — using a variety of techniques, including independently naming their emotions or ranking the degree they felt 34 specific emotions. The researchers analyzed these responses using statistical modeling.

The results showed that participants generally had a similar emotional response to each of the videos, and these responses could be categorized into 27 distinct groups of emotions. The team also organized and mapped the emotional responses for all the videos, using a particular color for each of the 27 categories. They created an interactive map that includes links to the video clips and lists their emotional scores.

“We sought to shed light on the full palette of emotions that color our inner world,” said lead author Alan Cowen, a graduate student in neuroscience at the UC Berkeley, in a recent news release.

In addition, the new study refuted the traditional view that emotional categories were entirely distinct islands. Instead, they found many categories to be linked by fuzzy boundaries. For example, there are smooth gradients between emotions like awe and peacefulness, they said.

Cowen explained in the release:

“We don’t get finite clusters of emotions in the map because everything is interconnected. Emotional experiences are so much richer and more nuanced than previously thought.

Our hope is that our findings will help other scientists and engineers more precisely capture the emotional states that underlie moods, brain activity and expressive signals, leading to improved psychiatric treatments, an understanding of the brain basis of emotion and technology responsive to our emotional needs.”

The team hopes to expand their research to include other types of stimuli such as music, as well as participants from a wider range of cultures using languages other than English.

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

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Artificial Intelligence can help predict who will develop dementia, a new study finds

August 29, 2017

 

If you could find out years ahead that you were likely to develop Alzheimer’s, would you want to know?

Researchers from McGill University argue that patients and their families could better plan and manage care given this extra time. So the team has developed new artificial intelligence software that uses positron emission tomography (PET) scans to predict whether at-risk patients will develop Alzheimer’s within two years.

They retrospectively studied 273 individuals with mild cognitive impairment who participated in the Alzheimer’s Disease Neuroimaging Initiative, a global research study that collects imaging, genetics, cognitive, cerebrospinal fluid and blood data to help define the progression of Alzheimer’s disease.

Patients with mild cognitive impairment have noticeable problems with memory and thinking tasks that are not severe enough to interfere with daily life. Scientists know these patients have abnormal amounts of tau and beta-amyloid proteins in specific brain regions involved in memory, and this protein accumulation occurs years before the patients have dementia symptoms.

However, not everyone with mild cognitive impairment will go on to develop dementia, and the McGill researchers aimed to predict which ones will.

First, the team trained their artificial intelligence software to identify patients who would develop Alzheimer’s, by identifying key features in the amyloid PET scans of the ADNI participants. Next, they assessed the performance of the trained AI using an independent set of ADNI amyloid PET scans. It predicted Alzheimer’s progression with an accuracy of 84 percent before symptom onset, as reported in a recent paper in Neurobiology of Aging.

The researchers hope their new AI tool will help improve patient care, as well as accelerate research to find a treatment for Alzheimer’s disease by identifying which patients to select for clinical trials.

“By using this tool, clinical trials could focus only on individuals with a higher likelihood of progressing to dementia within the time frame of the study. This will greatly reduce the cost and time necessary to conduct these studies,” said Serge Gauthier, MD, a senior author and professor of neurology and neurosurgery and of psychiatry at McGill, in a recent news release.

The new AI tool is now available to scientists and students, but the McGill researchers need to conduct further testing before it will be approved and available to clinicians.

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

Strong association between vision loss and cognitive decline

August 22, 2017

Photo by Les Black

In a nationally representative sample of older adults in the United States, Stanford researchers found a strong relationship between visual impairment and cognitive decline, as recently reported in JAMA Ophthalmology.

The research team investigated this association in elderly populations by analyzing two large US population data sets — over 30,000 respondents from the National Health and Aging Trends Study (NHATS) and almost 3,000 respondents from the National Health and Nutrition Examination Study (NHANES) — which both included measurements of cognitive and vision function.

“After adjusting for hearing impairment, physical limitations, patient demographics, socioeconomic status and other clinical comorbidities, we found an over two-fold increase in odds of cognitive impairment among patients with poor vision,” said Suzann Pershing, MD, assistant professor of ophthalmology at Stanford and chief of ophthalmology for the VA Palo Alto Health Care System. “These results are highly relevant to an aging US population.”

Previous studies have shown that vision impairment and dementia are conditions of aging, and their prevalence is increasing as our populations become older. However, the Stanford authors noted that their results are purely observational and do not establish a causative relationship.

The complexity of the relationship between vision and cognition was discussed in a related commentary by Jennifer Evans, PhD, an assistant professor of epidemiology at the London School of Hygiene and Tropical Medicine. She stated that this association could arise owing to problems with measuring vision and cognitive impairment tests in this population. “People with vision impairment may find it more difficult to complete the cognitive impairment tests and … people with cognitive impairment may struggle with visual acuity tests,” she wrote.

Assuming the association between vision and cognitive impairment holds, Evans also raised questions relevant patient care, such as: Which impairment developed first? Would successful intervention for visual impairment reduce the risk of cognitive impairment? Is sensory impairment an early marker of decline?

Pershing said she plans to follow up on the study:

“I am drawn to better understand the interplay between neurosensory vision, hearing impairment and cognitive function, since these are likely synergistic and bidirectional in their detrimental effects. For instance, vision impairment may accelerate cognitive decline and cognitive decline may lead to worsening ability to perform visual tasks. Ultimately, we can aim to better identify impairment and deliver treatments to optimize all components of patients’ health.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

Study shows link between playing football and neurodegenerative disease

July 25, 2017

You’ll likely hear quite a bit this week about a new study that suggests football players have an increased risk of developing chronic traumatic encephalopathy, or CTE, which is a progressive degenerative brain disease associated with repetitive head trauma.

As reported today in JAMA, researchers from the Boston University CTE Center and the VA Boston Healthcare System found pathological evidence of CTE in 177 of the 202 former football players whose brains were donated for research — including 117 of the 119 who played professionally in the United States or Canada. Their study nearly doubles the number of CTE cases described in literature.

The co-first author, Daniel Daneshvar, MD, PhD, is a new resident at Stanford in the orthopaedic surgery’s physical medicine and rehabilitation program, which treats traumatic brain injury and sports injury patients. He recently spoke with me about the study that he participated in while at BU.

“I really enjoyed playing football in high school. I think it’s an important sport for team building, learning leadership and gaining maturity,” he explained. “That being said, I think this study provides evidence of a relationship between playing football and developing a neurodegenerative disease. And that is very concerning, since we have kids as young as 8 years old potentially subjecting themselves to risk of this disease.”

The researchers studied the donated brains of deceased former football players who played in high school, college and the pros. They diagnosed CTE based on criteria recently defined by the National Institutes of Health. Currently, CTE can only be confirmed postmortem.

The study found evidence of mild CTE in three of the 14 former high school players and severe CTE in the majority of former college, semiprofessional and professional players. However, the researchers are quick to acknowledge that their sample is skewed, because brain bank donors don’t represent the overall population of former football players. Daneshvar explained:

“The number of NFL players with CTE is certainly less than the 99 percent that we’re reporting here, based on the fact that we have a biased sample. But the fact that 110 out of the 111 NFL players in our group had CTE means that this is in no way a small problem amongst NFL players.”

The research team also performed retrospective clinical evaluations, speaking with the players’ loved ones to learn their athletic histories and disease symptoms. Daneshvar worked on this clinical component — helping to design the study, organize the brain donations, conduct the interviews and analyze the data. The clinical assessment and pathology teams worked independently, blind to each other’s results.

“It’s difficult to determine after people have passed away exactly what symptoms they initially presented with and what their disease course was,” he told me. “We developed a novel mechanism for this comprehensive, retrospective clinical assessment. I was one of the people doing the phone interviews with the participant’s family members and friends to assess cognitive, behavioral, mood and motor symptoms.”

At this point, there aren’t any clinical diagnosis criteria for CTE, Daneshvar said. Although the current study wasn’t designed to establish these criteria, the researchers are going to use this data to correlate the clinical symptoms that a patient suffers through in life and their pathology at time of death, Daneshvar said. He went on to explain:

“The important thing about this study is that it isn’t just characterizing disease in this population. It’s about learning as much as we can from this methodologically rigorous cohort going forward, so we can begin to apply the knowledge that we’ve gained to help living athletes.”

Daneshvar and his colleagues are already working on a new study to better understand the prevalence and incidence of CTE in the overall population of football players. And they have begun to investigate what types of risk factors affect the likelihood of developing CTE.

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

The implications of male and female brain differences: A discussion

July 17, 2017

Photo by George Hodan

Men and women are equal, but they and their brains aren’t the same, according to a growing pile of scientific evidence. So why is most research still performed on only male animals and men? A panel of researchers explored this question and its implications on a recent episode of KALW’s City Visions radio show.

“It’s important to study sex differences because they are everywhere affecting everything,” said panelist Larry Cahill, PhD, a professor of neurobiology and behavior at the University of California, Irvine. “Over the last 20 years in particular, neuroscientists and really medicine generally have discovered that there are sex differences of all sizes and shapes really at every level of brain function. And we can’t truly treat women equally if we continue to essentially ignore them, which is what we’ve been doing.”

Neuropsychiatrist and author Louann Brizendine, MD, went on to say that many prescription medicines are only tested on male animals and men, even birth control pills designed for women. This is because the researchers don’t want the fluctuations of hormones associated with the menstrual cycle to “mess up” the research data, she said.

However, this practice can lead to dangerous side effects for women, she explained. For example, the U.S. Food and Drug Administration determined that many women metabolized the common sleep aid, Ambien, more slowly than men so the medication remained at a high level in their blood stream in the morning, which impaired activities like driving. After reassessing the clinical data on Ambien, Brizendine said, the FDA reset the male dose to 10 mg and the female dose down to 5 mg.

Niaro Shah, MD, PhD, a professor of psychiatry and behavioral sciences and of neurobiology at Stanford, said this action by the FDA was a sign of progress. “Decisions like what were made about Ambien represent people starting slowly to wake up and realize that we’ve been assuming that we don’t have to worry fundamentally about sex. And in not worrying about it, we are disproportionally harming women. Bare in mind, women absolutely, clearly and disproportionally bear the brunt of side effects of drugs and medicine.” In fact, he explained, eight out of ten drugs are withdrawn from the market due to worse side effects in women. He later added, “This issue is deeply affecting medical health, especially for women.”

So why are most researchers still studying only male animals or men?

According to Cahill, researchers have a deeply ingrained bias against studying sex differences, believing that sex differences aren’t fundamental because they aren’t shared by both men and women. He also said that resistance to this research boils down to the implicit and false assumption that equal has to mean the same. “If a neuroscientist shows that males and females (be that mice or monkeys or humans) are not the same in some aspect of brain function, then [many people think] the neuroscientist is showing that they are not equal — and that is false.”

Cahill offered advice for consumers: “You can go to the FDA website and for almost any approved drug you can get the essentials on how the testing was done. You’re going to find a mixed bag. For some drugs, you’re going to find there is pretty darn good evidence that the drug probably has roughly equal effects in men and women. On the other hand, you’re going to find a lot of cases when the testing was done mostly or exclusively in males and basically people don’t know [the effects in women].”

“You should be discerning and do your homework,” Brizendine agreed.

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

Unable to smell? One Stanford researcher is working to improve therapies

February 13, 2017

I don’t often think about my sense of smell, unless I’m given a fragrant flower or walk past someone smoking. But the ability to smell is both critical and underappreciated, according to Zara Patel, MD, a Stanford assistant professor of otolaryngology, head and neck surgery.

A smell begins when a molecule — say, from a flower — stimulates the olfactory nerve cells found high up in the nose. These nerve cells then send information to the brain, where the specific smell is identified. Anything that interferes with these processes, such as nasal congestion or damage to the nerve cells, can lead to a loss of smell.

I recently spoke with Patel about the loss of the sense of smell, a condition known as anosmia.

How does losing the sense of smell impact patients?

“If asked which sense they’d give up first, most people would likely choose their sense of smell. It’s only after the loss of olfaction that its significant impact on our lives is appreciated. Our sense of smell plays a key role in a vast array of basic human interactions, such as what attracts us to sexual partners, what keeps us in committed relationships and how maternal bonding occurs with newborns. It’s also one of our most basic protective mechanisms that allows us to wake up in the midst of a fire and prevents us from eating spoiled food. And importantly — keeping in mind that our ability to taste is highly dependent on our ability to smell — the inability to enjoy food and related social activities often causes social isolation, depression and malnutrition.”

What causes olfactory loss?

“There are over 100 reasons why people can lose their sense of smell. However, the majority of people lose it from sinonasal inflammatory disease, post-viral infections, traumas or tumors. Unfortunately, olfactory loss is often of “idiopathic” origin, meaning we just don’t know what caused it. That is why research in this area is so important.

It’s also important to be treated as early as possible. It is always frustrating to see someone who lost their sense of smell over a year ago, but they weren’t referred to me at the time or were told that nothing could be done. Those are missed opportunities that will negatively impact those patients for the rest of their lives.”

How do you treat patients who can no longer smell?

“The treatment really depends on the reason for loss, and may include surgery or medications. For those who lose the ability to smell after trauma, post-viral infection or when we don’t know why it happened, olfactory training can be used, which is a very simple protocol that patients can do at home. The patients smell several essentials oils in a structured way twice a day, every day, over a long period of time. The oils — rose, eucalyptus, clove and lemon —stimulate different types of olfactory receptor cells in the nose. Although it does not help everyone, it has been shown to be effective in 30 to 50 percent of patients, across multiple origins of loss.

We don’t have an exact understanding of how and why it works. However, a study using functional MRI observed a change in how the brain responds to odors before and after olfactory training. Before the training, there was a chaotic array of random areas lighting up in the brain. After the training, the images showed a renewed pathway to the olfaction center in the brain. We also know that the olfactory nerve has an inherent ability to regenerate. We’re trying to take advantage of this fact and ‘switch on’ those regenerative cells.

I have many patients who have benefited from olfactory training, including some who need their sense of smell for their livelihood — such as chefs or wilderness guides. Being able to get that sense back has allowed them to continue doing what they’re passionate about and has increased their quality of life.”

What are you working on now?

“Although olfactory training has allowed us to help more patients, 30 to 50 percent improvement is still quite low and certainly not the final answer. That’s why the research I’m currently doing has me excited about the potential of using both stem cells and neurostimulation to advance this field. I hope to soon be able to offer alternative interventions to these patients.”

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.

Stanford researchers map brain circuitry affected by Parkinson’s disease

February 2, 2017

In the brain, neurons never work alone. Instead, critical functions of the nervous system are orchestrated by interconnected networks of neurons distributed across the brain — such as the circuit responsible for motor control.

Researchers are trying to map out these neural circuits to understand how disease or injury disrupts healthy brain cell communication. For instance, neuroscientists are investigating how Parkinson’s disease causes malfunctions in the neural pathways that control motion.

Now, Stanford researchers have developed a new brain mapping technique that reveals the circuitry associated with Parkinson’s tremors, a hallmark of the disease. The multi-disciplinary team turned on specific types of neurons and observed how this affected the entire brain, which allowed them to map out the associated neural circuit.

Specifically, they performed rat studies using optogenetics to modify and turn on specific types of neurons in response to light and functional MRI to measure the resulting brain activity based on changes in blood flow. These data were then computationally modeled to map out the neural circuit and determine its function.

The research was led by Jin Hyang Lee, PhD, a Stanford electrical engineer who is an assistant professor of neurology and neurological sciences, of neurosurgery and of bioengineering. A recent Stanford News release explains the results:

“Testing her approach on rats, Lee probed two different types of neurons known to be involved in Parkinson’s disease — although it wasn’t known exactly how. Her team found that one type of neuron activated a pathway that called for greater motion while the other activated a signal for less motion. Lee’s team then designed a computational approach to draw circuit diagrams that underlie these neuron-specific brain circuit functions.”

“This is the first time anyone has shown how different neuron types form distinct whole brain circuits with opposite outcomes,” Lee said in the release.

Lee hopes their research will help improve treatments for Parkinson’s disease by providing a more precise understanding of how neurons work to control motion. In the long run, she also thinks their new brain mapping technique can be used to help design better therapies for other brain diseases.

This is a reposting of my Scope blog story, courtesy of Stanford School of Medicine.


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