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PsyPost – Psychology News Daily Digest (Unofficial)

 

(https://www.psypost.org/hippocampal-neurogenesis-decreases-ptsd-symptoms-in-mice-study-finds/) Hippocampal neurogenesis decreases PTSD symptoms in mice, study finds
Dec 9th 2024, 08:00

A study on mice found that interventions increasing the creation of new neurons in the hippocampus (hippocampal neurogenesis) weaken memories of traumatic events and reduce PTSD symptoms. The research was published in (https://doi.org/10.1038/s41380-024-02585-7) Molecular Psychiatry.
Early researchers of brain development believed that the brain stops creating new neurons once a person reaches adulthood. However, newer studies indicate that even adult brains continue to produce new neurons, particularly in the hippocampus. This process is referred to as hippocampal neurogenesis.
Estimates suggest that 700 new neurons are generated daily in each hemisphere, amounting to an annual turnover of 1.75% of neurons. However, the survival and possibly the generation rate of these neurons depend on their incorporation into brain circuits. Studies indicate that new neurons die off if they are not integrated into brain circuits by the time they are one week old.
The hippocampus plays a critical role in the formation, organization, and retrieval of long-term memories. Integration of new neurons into neural circuits in this region may aid in forming new memories but could also facilitate forgetting existing memories through remodeling neural circuits.
Study author Risako Fujikawa and colleagues explored whether promoting forgetting by stimulating the hippocampus to produce new neurons could help in forgetting maladaptive memories associated with conditions like posttraumatic stress disorder (PTSD). PTSD is a psychiatric disorder that can occur in individuals who have experienced or witnessed traumatic events.
The researchers conducted a study on mice aged 8–12 weeks at the start of the experiments. The mice were housed in cages with 2–5 mice per cage and had free access to food and water. PTSD-like symptoms were induced in these mice using a combination of two traumatic events.
The first event involved delivering a high-intensity foot shock in a specially designed box. A mouse was placed in the “safe” part of the box, and after 10 seconds, the door to a second compartment was opened. One second after the mouse entered the second compartment, the door was closed, and a two-second electric shock was delivered to its feet. Following the shock, the mouse remained in the compartment for 10 seconds before being returned to its home cage. To induce PTSD-like symptoms, the mice received a second treatment, referred to as a “reminder shock,” in a new box. This procedure is known as the double trauma PTSD paradigm.
To assess the severity of PTSD-like symptoms, the researchers used behavioral tests, including open-field exploration and conditioned place preference. They then conducted experiments aimed at stimulating hippocampal neurogenesis through genetic manipulation, optogenetics, and exercise using running wheels. Afterward, the researchers analyzed the mice’s brain tissues.
The results showed that the double trauma paradigm produced lasting behavioral effects. Mice with access to running wheels for 30 days exhibited fewer PTSD-like behaviors than sedentary mice. Further analysis revealed that exercise led to a threefold increase in the number of new neurons in the hippocampus.
Additional experiments involved genetic manipulation to induce hippocampal neurogenesis and promote the integration of new neurons into neural circuits. These interventions weakened trauma memories (evidenced by reduced recall of features associated with shock locations) and decreased PTSD-like symptoms in the mice.
“We showed that elevating hippocampal neurogenesis [generation of new neurons in the hippocampus] attenuated PTSD-related behavioral phenotypes [behaviors] in mice. In this paradigm, consecutive traumatic experiences lead to a constellation of behavioral phenotypes associated with PTSD including deficient extinction, threat generalization and anxiety-like behavior,” the study authors concluded.
“Elevation of hippocampal neurogenesis weakened the original trauma memory, and blunted the associated deficient extinction, threat generalization, and anxiety-like phenotypes [PTSD-like behaviors]. These beneficial effects were observed using a range of interventions to manipulate hippocampal neurogenesis, including voluntary exercise and more neurogenesis-specific interventions that promote hyper-integration of new neurons into hippocampal circuits.”
The study sheds light on a neural mechanism that could potentially be leveraged to alleviate PTSD symptoms in humans. However, it is important to note that the research was conducted on mice, not humans. While mice and humans share many physiological similarities, they are distinct species, and the findings may not directly translate to humans.
The paper, “(https://doi.org/10.1038/s41380-024-02585-7) Neurogenesis-dependent remodeling of hippocampal circuits reduces PTSD-like behaviors in adult mice,” was authored by Risako Fujikawa, Adam I. Ramsaran, Axel Guskjolen, Juan de la Parra, Yi Zou, Andrew J. Mocle, Sheena A. Josselyn, and Paul W. Frankland.

(https://www.psypost.org/neuroscientists-just-turned-a-major-alzheimers-theory-on-its-head/) Neuroscientists just turned a major Alzheimer’s theory on its head
Dec 9th 2024, 06:00

A recent study published in (https://academic.oup.com/brain/article/147/10/3513/7754406) Brain
challenges long-held assumptions about Alzheimer’s disease treatment. Researchers at the University of Cincinnati found that new monoclonal antibody drugs may slow cognitive decline by increasing levels of a critical brain protein called amyloid-beta 42 (Aβ42), rather than simply reducing amyloid plaques in the brain. This discovery shifts the focus from plaque buildup to the potential role of Aβ42 in maintaining brain health.
Alzheimer’s disease is the most common form of dementia, characterized by progressive memory loss, cognitive decline, and changes in behavior. The condition gradually impairs daily functioning and quality of life, affecting millions of people worldwide. At a biological level, Alzheimer’s is marked by two main features: the buildup of amyloid plaques outside neurons and neurofibrillary tangles of tau protein inside neurons.
Amyloid-beta is a protein fragment naturally produced in the brain during normal cell processes. It exists in several forms, but two variants, Aβ40 and Aβ42, are of particular interest in Alzheimer’s research. Aβ40 is the more common form, comprising about 90% of all amyloid-beta produced and considered relatively benign under normal conditions. Aβ42, although less abundant, is more prone to clumping and forming plaques. This increased aggregation potential has made Aβ42 the focus of theories about Alzheimer’s pathology.
The amyloid cascade hypothesis, first proposed in the early 1990s, has dominated the field for decades. According to this theory, Alzheimer’s begins when Aβ42 molecules stick together to form clumps called oligomers. These oligomers aggregate into amyloid plaques, which are thought to disrupt neuronal communication, trigger inflammation, and eventually lead to the widespread damage seen in Alzheimer’s. Support for this hypothesis came from genetic studies showing that mutations in genes affecting amyloid production are linked to rare, inherited forms of Alzheimer’s.
Despite the appeal of the amyloid cascade hypothesis, efforts to treat Alzheimer’s by removing amyloid plaques have largely failed. Over 30 clinical trials targeting amyloid have either shown no significant cognitive benefits or, in some cases, worsened symptoms. This has led researchers to question whether plaques are the root cause of Alzheimer’s or a secondary byproduct of the disease. Observations that many older individuals with plaques never develop dementia have further fueled this debate.
Neurology professor Alberto J. Espay and his team hypothesized that the loss of normal, soluble Aβ42 in the brain, rather than the buildup of plaques, might drive Alzheimer’s pathology. Research supporting this idea suggests that Aβ42 plays a critical role in maintaining neuronal health and synaptic function. Its depletion, not its aggregation, may be what leads to cognitive decline.
The researchers also noted that some newly approved monoclonal antibody treatments (aducanumab, lecanemab, and donanemab) unintentionally increased Aβ42 levels in cerebrospinal fluid, which correlated with cognitive improvements. These findings prompted the team to investigate whether raising Aβ42 levels might explain the benefits of these treatments, offering a fresh perspective on the disease’s underlying mechanisms.
“Most anti-Aβ interventions had succeeded in clearing the brain from amyloid plaques, yet they were either futile or statistically favored the placebo group,” explained Espay, the director and endowed chair of the Gardner Family Center for Parkinson’s Disease and Movement Disorders and co-author of (https://amzn.to/3Zt7cZ5) Brain Fables, the Hidden History of Neurodegenerative Diseases and a Blueprint to Conquer Them.
“I was interested in finding out what made aducanumab, lecanemab, and donanemab special. Along the way, I learned that along with removing amyloid, virtually all monoclonal anti-Aβ antibodies also increase Aβ42 in cerebrospinal fluid.”
“I was interested in finding out whether one could explain the cognitive outcomes from the opposite end of protein homeostasis—by the increases in Aβ42. This is at the core of the two opposing hypotheses in neurodegeneration in general and Alzheimer’s disease in particular: one posits that the disease is caused by the accumulation of amyloid plaques (so-called amyloid cascade hypothesis); the other that the disease is caused by the loss of Aβ42 as it transforms into amyloid plaques (the proteinopenia hypothesis). I have (https://www.sciencedirect.com/science/article/pii/S1568163723002714) reviewed data in favor of the latter.”
In their new study, Espay and his colleagues analyzed data from 24 randomized clinical trials of monoclonal antibody drugs designed to target amyloid plaques. These trials included nearly 26,000 patients diagnosed with early or moderate Alzheimer’s disease. The researchers focused on changes in two key biomarkers: amyloid plaque levels (measured through imaging) and cerebrospinal fluid levels of Aβ42. They also examined cognitive performance using standardized tests like the Alzheimer’s Disease Assessment Scale and the Clinical Dementia Rating.
The team used statistical methods to compare the cognitive outcomes of patients treated with monoclonal antibodies against changes in amyloid plaques and Aβ42 levels. By evaluating the relationship between these biomarkers and cognitive improvement, the researchers aimed to determine which factor was more closely linked to slowing cognitive decline.
The results showed that increases in Aβ42 levels were just as strongly associated with cognitive improvement as the reduction of amyloid plaques. In fact, drugs that raised Aβ42 levels showed a consistent correlation with better cognitive outcomes. Conversely, treatments that lowered Aβ42 levels—such as certain enzyme inhibitors—worsened cognitive performance.
The researchers proposed that amyloid plaques might not directly cause Alzheimer’s symptoms. Instead, plaques could represent a protective response by the brain to stress or injury. The real issue, they suggested, might be the depletion of soluble Aβ42, which plays a critical role in neuron health and synaptic function. When Aβ42 levels drop below a critical threshold, cognitive decline appears to accelerate.
The findings highlight that “there are two sides to any story,” Espay told PsyPost. “We have thought that the only explanation for any potential benefit of the newly approved monoclonal antibodies for Alzheimer’s is that they are good at removing amyloid plaques from the brain. Yet many other interventions have done that in the past, to no avail. The alternative explanation for any benefit is the increase in the levels of Aβ42 in cerebrospinal fluid, which most antibodies accomplish (remarkably, such data is mostly confined to the supplementary materials of the trial reports).”
But the study, like all research, has limitations. The researchers relied on aggregated data from clinical trials, which may limit the precision of their analyses. “We don’t have individual-level data, as these are not shared by the companies that own the data. This meant we worked with lowered power to find significant differences,” Espay explained.
In other words, the researchers had to base their conclusions on group-level trends rather than detailed, individualized information. This limitation reduces the ability to account for variations in how different patients respond to treatments, potentially obscuring important nuances that could refine their findings or reveal more precise relationships between biomarkers and cognitive outcomes.
The study also raises practical challenges. Monoclonal antibody treatments, while effective at increasing Aβ42 levels, carry risks, including brain inflammation and shrinkage. Looking forward, Espay hopes “to test the potential benefits of directly increasing Aβ42 without the toxicities imposed upon the brain by removing amyloid (quite a toxic enterprise).”
“There is resistance to looking at Alzheimer’s as a loss, which is paradoxical,” he added. “We have long become too comfortable with the idea that Alzheimer’s is about a ‘gain’—of the amyloid plaques. But in fact, amyloid forms as a reaction to many things. And if too much of it is necessary in such a reaction, less of the normal protein from which it comes (Aβ42) remains.”
The study, “(https://doi.org/10.1093/brain/awae216) Increases in amyloid-β42 slow cognitive and clinical decline in Alzheimer’s disease trials,” was authored by Jesus Abanto, Alok K. Dwivedi, Bruno P. Imbimbo, and Alberto J. Espay.

(https://www.psypost.org/emotion-dysregulation-is-a-core-component-of-adhd-study-finds/) Emotion dysregulation is a core component of ADHD, study finds
Dec 8th 2024, 14:00

An analysis of data from the Adolescent Brain Cognitive Development Study (ABCD) study found that emotion dysregulation mediates the association between a smaller surface area of the right pars orbitalis region of the inferior frontal gyrus and ADHD symptoms one year later. This finding suggests that emotion dysregulation is a core component of ADHD and may also serve as a pathway leading to the development of the disorder. The research was published in (https://www.nature.com/articles/s44220-024-00251-z) Nature Mental Health.
Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by persistent patterns of inattention, hyperactivity, and impulsivity that interfere with daily functioning. Individuals with ADHD often struggle to focus on tasks, organize activities, and regulate their impulses. Symptoms typically begin in childhood, though they can persist into adolescence and adulthood. Most often, the disorder is diagnosed when a child starts school, as the symptoms interfere with expected behaviors in school settings.
ADHD affects approximately 6%-7% of children and adolescents, but its causes are not fully understood. The predominant view is that ADHD results from a combination of specific cognitive impairments and motivational dysfunctions. However, these characteristics are absent in about 30% of ADHD cases, and they cannot reliably predict how ADHD symptoms will progress over time.
Study author Wenjie Hou and colleagues hypothesized that emotion dysregulation might represent a third neuropsychological pathway to ADHD, distinct from cognitive impairment and motivational dysfunction. The authors explain that critical brain regions for emotion regulation include the inferior frontal gyrus, the orbitofrontal cortex, the anterior cingulate cortex, the amygdala, and the ventral striatum. Many of these regions are not part of the classic cognitive control neural circuits previously linked to ADHD in other studies.
The researchers analyzed data from 672 individuals with ADHD who participated in the ABCD study, a large longitudinal study tracking brain development and mental health in 11,877 children from 22 sites across the United States.
Additionally, the researchers conducted a separate analysis using data from the ADHD-200 study, which included 263 individuals with ADHD and 409 children without the disorder. The participants in this group had an average age of 11-12 years.
Participants completed assessments of ADHD symptoms using the ADHD scale of the Child Behavior Checklist. Cognitive functioning was measured through a battery of seven cognitive tasks, while motivational dysfunction was assessed using the Reward Sensitivity Scale, adapted from the PhenX toolkit. Emotion dysregulation was reported by parents/guardians using the Difficulty in Emotion Regulation Scale. In the ABCD group, emotion dysregulation was assessed when the children were 13 years old, while cognitive and motivational data were collected when they were 12.
The researchers also used participants’ magnetic resonance imaging (MRI) data and white blood cell counts from the ABCD study. Gene expression in the cerebral cortex was analyzed using data from the Allen Human Brain Atlas.
The results showed that emotion dysregulation was not associated with cognitive performance or motivational dysfunction from the previous year. In the ABCD group, ADHD symptom severity was more strongly associated with emotion dysregulation than with cognitive performance or motivational dysfunction. Among the 350 children with very severe ADHD symptoms, 21% exhibited neither cognitive nor motivational deficits. Furthermore, children with persistent ADHD symptoms did not differ significantly in cognitive or motivational assessments from those whose symptoms had remitted. However, the group with persistent symptoms showed stronger emotion dysregulation scores, indicating that emotion dysregulation can be considered a core symptom of ADHD.
Analysis of neuroimaging data revealed that emotion dysregulation has a distinct neural correlate. Children with more severe emotion dysregulation tended to have a smaller surface area (but not cortical thickness) in the right orbital part of the inferior frontal gyrus.
The researchers tested a statistical model suggesting that a smaller surface area in this brain region leads to stronger emotion dysregulation, which, in turn, contributes to worse inattention symptoms. According to the model, while this pathway is plausible, there is also a direct link between inattention and the surface area of this brain region that is not mediated by emotion dysregulation.
The researchers also identified and tested similar statistical models linking the structural characteristics of specific brain areas to inattention through cognitive functioning and motivational dysfunction.
“We have shown, using a large sample and a second independent clinical sample, that emotion dysregulation is a core symptom and a route to ADHD, which may not respond to the current pharmacological treatments for ADHD,” the study authors concluded.
The study provides new insights into the neuropsychological underpinnings of ADHD symptoms. However, the design of the study does not allow for definitive cause-and-effect inferences to be drawn from the results.
The paper, “(https://doi.org/10.1038/s44220-024-00251-z) Emotion dysregulation and right pars orbitalis constitute a neuropsychological pathway to attention deficit hyperactivity disorder,” was authored by Wenjie Hou, Barbara J. Sahakian, Christelle Langley, Yuqing Yang, R. A. I. Bethlehem, and Qiang Luo.

(https://www.psypost.org/lab-grown-mini-brains-shed-light-on-severe-autism-and-offer-hope-for-treatment/) Lab-grown “mini-brains” shed light on severe autism and offer hope for treatment
Dec 8th 2024, 12:00

Researchers at Scripps Research Institute have used patient-derived stem cells to create brain organoids—also called “mini-brains”—to investigate a rare and severe form of autism spectrum disorder (ASD) linked to intellectual disability. These models provided insights into how a specific genetic mutation disrupts brain development and allowed the team to test an experimental drug, NitroSynapsin, which reversed some of the identified dysfunctions.
The study, published in (https://www.nature.com/articles/s41380-024-02761-9) Molecular Psychiatry, sheds light on the molecular effects of mutations in the MEF2C gene, a key regulator in brain development. It also suggests that targeting imbalances caused by such mutations later in life could mitigate some ASD symptoms, offering hope for future therapies.
ASD is a complex neurodevelopmental condition characterized by challenges with social interaction, communication, and repetitive or restricted behaviors. It varies widely in severity and can be accompanied by intellectual disabilities, sensory sensitivities, and medical issues such as epilepsy. Despite extensive research, the exact causes of autism remain elusive.
Genetic mutations are thought to play a significant role, with hundreds of genes implicated. However, the molecular mechanisms that connect these genetic changes to autism’s behavioral and neurological symptoms are poorly understood, creating barriers to developing effective treatments.
One specific genetic condition associated with autism is MEF2C haploinsufficiency syndrome. This rare disorder results from a mutation in one copy of the MEF2C gene, which disrupts its ability to produce sufficient levels of a protein critical for brain development and function. Individuals with MEF2C haploinsufficiency often experience severe developmental delays, limited or absent speech, stereotypic movements, and frequent seizures.
The MEF2C gene is a key regulator of other genes that influence brain cell development and synaptic function, making it an important area of study. However, how exactly this mutation leads to the severe symptoms seen in patients remained unclear, limiting the ability to design targeted therapies.
The motivation behind the study was to bridge this knowledge gap and explore whether the disruptions caused by MEF2C mutations could be mitigated or reversed. By studying patient-derived brain models, the researchers aimed to better understand how the mutation affects the development and function of neural circuits. Additionally, the researchers sought to evaluate the therapeutic potential of NitroSynapsin, an experimental drug, to determine whether it could address the neural dysfunctions caused by MEF2C mutations.
“Our group was the first to discover and clone the transcription factor named MEF2C some years ago, but more recently we and others recognized its importance not only in development, maintenance and aging resilience in the nervous system, but also to the development of a severe form of ASD and developmental intellectual disability in individuals bearing certain mutation in one copy of the gene encoding MEF2C (termed MEF2C haploinsufficiency),” said (https://www.scripps.edu/faculty/lipton/) Stuart A. Lipton, the Step Family Foundation Endowed Professor and co-director of the Neurodegeneration New Medicines Center at Scripps Research, a clinical neurologist, and senior author of the new research.
“Importantly, MEF2C also directs the expression of many other genes involved in ASD, so finding a treatment or cure for MEF2C haploinsufficiency might also help these other children. Given the very high prevalence of ASD now, affecting approximately 1 in every 36 children, this could prove very important.”
To understand how mutations in the MEF2C gene lead to severe autism symptoms, the researchers used cells from patients with MEF2C haploinsufficiency syndrome. They transformed these cells into induced pluripotent stem cells, which can develop into any cell type, including brain cells. Using these stem cells, they created lab-grown “mini-brains” (organoids) and 2D cell cultures that mimic human brain development.
“We could reproduce essential aspects of the brains of patients to study their electrical activity and other properties,” Lipton said. “We actually brought kids into the lab to see their own mini-brains and that was quite emotional for the children and families alike.”
These models allowed the team to observe how the mutation affected brain cell growth and function. They also compared the patient-derived cells to genetically edited “control” cells without the MEF2C mutation, ensuring a precise understanding of the mutation’s effects. To test potential treatments, they exposed the mini-brains to NitroSynapsin, a drug designed to regulate brain cell communication.
The researchers found that the MEF2C mutation caused an imbalance in brain cell development. Normally, a balanced mix of neurons (nerve cells) and astrocytes (support cells) is crucial for proper brain function. However, the patient-derived mini-brains produced fewer neurons and more astrocytes, disrupting this balance. This imbalance hindered the formation of healthy neural circuits, a foundational aspect of brain development.
The neurons that did form displayed hyperactive behavior. Electrophysiological recordings showed that these neurons fired excessively and out of sync with one another, mimicking the neural overactivity associated with seizures in patients. At the molecular level, the mutation disrupted the expression of genes essential for neural communication and synaptic function. One key discovery was an increase in excitatory signaling and a decrease in inhibitory signaling, creating an imbalance that could explain many of the symptoms observed in MEF2C haploinsufficiency syndrome.
The researchers discovered that MEF2C mutations disrupted the expression of specific microRNAs—small molecules that help regulate gene activity—important for brain development. In patient-derived cells, the levels of microRNAs such as miR-4273 and miR-663 were significantly reduced.
“In our study, a few specific miRNAs appear to be important in telling developing brain cells whether to become glial cells, excitatory neurons, or inhibitory neurons,” Lipton said. “Mutations in MEFC2 alter the expression of these miRNAs which, in turn, prevent the developing brain from making proper nerve cells and proper connections or synapses between nerve cells.”
When the researchers applied NitroSynapsin to the mini-brains, they found that it helped restore balance in neural activity. The drug reduced the excessive firing of neurons and corrected the imbalance between excitatory and inhibitory signals. These changes brought the activity of patient-derived mini-brains closer to that of the control models. This finding suggests that NitroSynapsin might hold therapeutic potential for addressing neural dysfunctions caused by MEF2C mutations.
Lipton was surprised by “the fact that correcting excitatory/inhibitory imbalance of electrical signals in human mini-brains, made from stem cells of patients with this form of ASD, could have such a large effect on phenotypes associated with the condition.”
However, the organoids, while advanced, cannot fully replicate the complexity of a human brain or its environment. Additionally, the findings are specific to MEF2C mutations and may not generalize to other forms of autism. Further research is needed to confirm these results.
“We have now developed our new drugs in mouse models and using human cerebral organoids of ‘mini-brains’ but real human trials are needed to test the new drugs,” Lipton said. “We are raising funds for this right now.” The long-term goal is to “complete a human clinical trial testing our new lead drug to improve the lives of children with ASD.”
The study, “(https://doi.org/10.1038/s41380-024-02761-9) Dysregulation of miRNA expression and excitation in MEF2C autism patient hiPSC-neurons and cerebral organoids,” was authored by Dorit Trudler, Swagata Ghatak, Michael Bula, James Parker, Maria Talantova, Melissa Luevanos, Sergio Labra, Titas Grabauskas, Sarah Moore Noveral, Mayu Teranaka, Emily Schahrer, Nima Dolatabadi, Clare Bakker, Kevin Lopez, Abdullah Sultan, Parth Patel, Agnes Chan, Yongwook Choi, Riki Kawaguchi, Pawel Stankiewicz, Ivan Garcia-Bassets, Piotr Kozbial, Michael G. Rosenfeld, Nobuki Nakanishi, Daniel H. Geschwind, Shing Fai Chan, Wei Lin, Nicholas J. Schork, Rajesh Ambasudhan, and Stuart A. Lipton.

(https://www.psypost.org/laughter-yoga-boosts-well-being-and-reduces-stress-in-nursing-students-study-finds/) Laughter yoga boosts well-being and reduces stress in nursing students, study finds
Dec 8th 2024, 10:00

A new study published in (https://iaap-journals.onlinelibrary.wiley.com/doi/10.1111/aphw.12610) Applied Psychology: Health and Well-Being has found that laughter yoga boosts well-being and reduces stress in nursing students, offering a potential aid to the mental health challenges common in higher education. While the findings suggest benefits for stress and emotional health, the research shows no measurable impact on students’ academic self-confidence.
Nursing students often face high levels of stress due to the demands of rigorous academic programs and intense clinical training. This heightened stress can negatively affect mental well-being, leading to issues like burnout, anxiety, and depression. Recognizing this, researchers Merve Altiner Yas and Olga Incesu from Istanbul University-Cerrahpaşa explored whether laughter yoga could help alleviate some of these pressures.
Laughter yoga is a unique exercise routine that combines breathing techniques from traditional yoga with voluntary laughter. It operates on the principle that the brain cannot distinguish between real and simulated laughter, meaning participants can reap emotional and physiological benefits even if they start with forced laughter.
In this study, 83 final-year nursing students participated. The group was divided into an intervention group (41 participants), who attended five weekly 40-minute laughter yoga sessions, and a control group (42 participants), who did not receive any intervention. The laughter yoga sessions incorporated clapping, deep breathing exercises, and playful activities designed to elicit laughter.
The results were promising. Students in the laughter yoga group showed significant improvements in their well-being scores, with many reporting feeling happier and less stressed after the sessions. Stress levels also declined in this group, although the researchers found no difference in perceived stress levels between the laughter yoga and control groups at the study’s conclusion.
Interestingly, academic self-efficacy — a student’s confidence in their ability to perform academic tasks — remained unchanged. This finding might reflect the short duration of the intervention, or the already high levels of academic confidence reported by the students at the start of the study.
While the results highlight the potential of laughter yoga to support mental health, the researchers note some limitations. The self-reported nature of the data introduces the possibility of bias, and the researchers were not blinded in this single-blinded study.
Despite these caveats, the study authors concluded with some benefits of their research: “laughter yoga can be utilized to support mental well-being in senior nursing students as a beneficial, non-pharmacological, and cost-effective approach. Moreover, community mental health nurses and educators can plan regular laughter yoga programs for promoting mental health and well-being in universities.”
The study, “(https://doi.org/10.1111/aphw.12610) The Effect of Laughter Yoga on Well-Being, Perceived Stress, and Academic Self-Efficacy in Nursing Students,” was authored by Merve Altiner Yas and Olga Incesu.

(https://www.psypost.org/18-month-olds-tailor-communication-to-others-knowledge-new-study-finds/) 18-month-olds tailor communication to others’ knowledge, new study finds
Dec 8th 2024, 08:00

A recent study explored whether 18-month-old infants can adjust their communication based on what they believe their partner knows. The findings suggest that even at this young age, infants tailor their pointing gestures to provide relevant information when their partner lacks it. This ability reflects a sophisticated understanding of others’ mental states, highlighting the early development of skills crucial for human communication. The findings were published in (https://direct.mit.edu/opmi/article/doi/10.1162/opmi_a_00166/124957/Infants-Produce-Optimally-Informative-Points-to) Open Mind: Discoveries in Cognitive Science.
Human communication relies on the ability to share and interpret information effectively. This often involves understanding what others know—or don’t know—and adjusting behavior accordingly. While adults naturally modify their communication to suit their audience, little is known about when this skill begins to develop. Researchers aimed to determine whether infants, who are just beginning to communicate, could similarly adapt their actions based on others’ knowledge.
“Human communication is unparalleled in the animal kingdom. To understand what makes it unique, we can investigate how it differs from animal communication systems,” said study author Tibor Tauzin, a postdoctoral researcher affiliated with the (https://psy-ling.univie.ac.at/en/babelfisch-lab/) Babelfisch Lab at the University of Vienna.
“We hypothesized that human infants already have the ability to recognize that, in order to communicate effectively, they must consider the knowledge others possess. This led us to investigate whether infants point more accurately to an object when interacting with someone who has incorrect or no knowledge about it.”
The research consisted of three experiments, each testing how infants adapted their gestures depending on what their partner could see or knew.
In Experiment 1, the researchers investigated whether 18-month-old infants could adapt their pointing gestures to make their intentions clear in situations where a simple point could be ambiguous. Infants were seated across from an experimenter at a table, with two objects—one being the “target” that the infant wanted and the other a “distractor”—placed on the table. The objects were arranged in three different ways: the target closer to the infant, the target farther away but behind the distractor, and the target alone.
The experimenter asked the infant to show her where the desired object was. If the infant pointed to the target, the experimenter activated it to produce lights and sounds, providing positive feedback. If the infant pointed to the distractor, which could not activate the effects, the experimenter expressed mild disappointment.
The results showed that when the target was behind the distractor, infants spontaneously modified their gestures to avoid ambiguity, pointing higher or at an angle to clearly indicate the desired object. This demonstrated that infants could adjust their communication based on the spatial arrangement of objects to ensure clarity.
In Experiment 2, the researchers tested whether infants could take into account what their communicative partner did or did not know about the objects’ locations. This time, the objects were hidden under opaque cups. The infants interacted with two experimenters: one who had seen the objects being hidden and one who had not. In one condition, the same experimenter who hid the objects returned and asked the infant to indicate the target’s location. In another condition, a different experimenter, who had no prior knowledge of the objects’ placement, entered and made the same request.
The researchers found that infants pointed more frequently at the target and used clearer, more modified gestures when interacting with the uninformed experimenter, suggesting that they recognized the partner’s lack of knowledge and adapted their communication to fill in the informational gap.
In Experiment 3, the researchers examined whether infants could correct a communicative partner who held incorrect information about the target’s location. After one experimenter placed and hid the objects, another experimenter entered and visibly swapped their positions under the cups. In one condition, the first experimenter returned, unaware of the swap, and asked the infant to indicate the target’s location. In another condition, the experimenter who had witnessed the swap returned and made the same request.
The findings revealed that infants were more likely to point at the target and use modified gestures when interacting with the misinformed experimenter. This indicated that infants understood the experimenter’s incorrect belief and adjusted their communication to correct it.
“Our findings suggest that human infants can understand when their communicative partner has inaccurate or no information about a relevant fact,” Tauzin told PsyPost. “Moreover, they do not merely recognize that someone is missing crucial information; they actively try to help their communicative partners by providing additional details.”
“In this way, infants communicate in a manner similar to adults, who share more detailed information with others lacking the relevant background knowledge. For example, an adult might say, ‘The tool is in the bottom drawer in the cabinet on the left-hand side,’ rather than simply stating, ‘The tool is in the drawer’ when their partner is ignorant about the fact that the tool can be found in one specific place.”
The results of these experiments have significant implications for understanding early human communication. They suggest that even at 18 months, infants possess a sophisticated ability to infer and act upon their communicative partner’s mental states, including their knowledge and beliefs.
“One of the most striking aspects of our study is that, according to the standard view, only children aged 4 and older are thought to have the ability to recognize when others possess incorrect knowledge about a particular fact—an ability known as ‘mentalization,” Tauzin explained. “However, our results suggest that even infants can understand when someone holds a false belief about reality and take this into account during interactions with that person.”
The study sheds new light on the communicative abilities of 18-month-old infants but there are limitations to consider. First, the study focused on a specific form of communication (pointing) in a controlled setting. It is unclear how these skills generalize to other forms of interaction or more naturalistic environments. Second, the sample size was relatively small, with 24 to 48 participants per experiment, though appropriate for the study’s design.
“The aim of our study was to determine whether human infants are able to recognize that others have incorrect or incomplete information about a fact during a communicative interaction with an adult,” Tauzin noted. “Our findings demonstrate that infants can use mentalization to communicate effectively with others. However, our results do not suggest that infants can use mentalization for other purposes, such as predicting the future behavior of others based on their knowledge and beliefs.”
Future research could explore whether these abilities extend to younger infants or involve other types of communicative gestures, such as vocalizations. Additionally, examining the neural mechanisms behind this behavior could provide insights into the development of human social cognition.
“Our research group also conducted a similar experiment with non-human primates (chimps, gorillas, orangutans, and bonobos), where we found that, in contrast to humans, they cannot understand when their communicative partner is ignorant of a relevant fact,” Tauzin added. “Even when motivated to share precise information they alone possessed about the location of hidden food, the primates failed to do so. This suggests that human communication may be fundamentally different from that of other animals, as humans have the ability to mentalize—that is, to understand that knowledge and beliefs is guiding the behavior of others.”
The study, “(https://doi.org/10.1162/opmi_a_00166) Infants Produce Optimally Informative Points to Satisfy the Epistemic Needs of Their Communicative Partner,” was authored by Tibor Tauzin, Josep Call, and György Gergely.

Forwarded by:
Michael Reeder LCPC
Baltimore, MD

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