DATE: April 15, 2025 at 02:00AM
SOURCE: PSYPOST.ORG

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TITLE: ALS breakthrough: Ashwagandha-derived drug shows promise in slowing progression of amyotrophic lateral sclerosis

URL: https://www.psypost.org/als-breakthrough-ashwagandha-derived-drug-shows-promise-in-slowing-progression-of-amyotrophic-lateral-sclerosis/

Every year roughly 1,000 Canadians are diagnosed with amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). Some 4,000 Canadians are currently living with the disease.

There are few effective treatments available to slow the progression of ALS and, unfortunately, most sufferers die within two to five years of being diagnosed.

As neuroscience researchers, we are dedicated to finding ways to reduce the symptoms of ALS. In this article, we discuss the promising results of one of our recent studies.

ALS, a complex disease

ALS is a neurodegenerative disease. Sufferers gradually lose the ability to perform voluntary movements due to loss of communication between the nervous system and muscles.

Our scientific understanding of ALS has evolved considerably since the disease was first described by the neurologist Jean-Martin Charcot, in 1874.

Today it is widely recognized that ALS affects several types of cells, including immune cells, muscle cells, glial cells (those that surround and insulate neurons) and neurons. However, for reasons that are still unknown, motor neurons, the cells responsible for controlling voluntary and involuntary movement, are particularly vulnerable.

Targeting motor neurons

Motor neurons have a complex morphology with projections that transmit information, resembling the branches of a tree. The neurons connect the brain and spinal cord to the muscles. These neuronal connections with the muscles are responsible for voluntary movements such as walking, speaking and eating.

In ALS, motor neurons degenerate and die, which leads to muscle weakness and, ultimately, paralysis. Because ALS is a complex disease with few effective therapies, there is an urgent need to better understand it in order to develop more therapeutic strategies.

Our research team in the Department of Psychiatry and Neuroscience at Université Laval is dedicated to understanding the early pathological changes that occur in motor neurons before they die. Our aim is to identify and develop therapeutic interventions that can reverse these early changes and slow the progression of the disease.

How do neurons lose their connectivity?

Using the mouse as a model, we carried out genetic modifications to recreate the motor and cognitive disability brought about by ALS.

In doing so, we discovered that changes in the morphology of motor neurons in the brain occur early in the disease process. This happens even before any changes in motor function have been seen.

We also discovered that a decline in motor functions was associated with the degeneration of motor neurons and the loss of synapses. Synapses are the places where motor neurons communicate, thus connecting the brain and spinal cord to the muscles.

Our study also found that astrocytes and microglia, the immune cells of the brain and spinal cord, were highly activated while synapse loss was underway and motor function was declining.

The over-activation of astrocytes and microglia, which can be described as neuroinflammation, changes the morphology of motor neurons and impairs their interconnectivity. These changes affect the neuronal network and disrupt the transmission of information.

Can we restore motor neuron connectivity?

We then wondered whether, by blocking neuroinflammation (for example, the activation of astrocytes and microglia), it would be possible to restore the morphology and connectivity of motor neurons.

In an attempt to answer this question, we tested the efficacy of a semisynthetic drug based on withaferin A, an extract of the ashwagandha plant which has been used for thousands of years in traditional Indian medicine.

The results of our study show that by blocking the activation of astrocytes and microglia, and thereby preventing inflammation, the morphology of motor neurons and their synaptic connections could be restored.

These promising results coincide with cognitive and motor improvements observed in our ALS mouse model.

Inflammation and loss of synapses are common to several neurodegenerative diseases, including ALS, Alzheimer’s and Parkinson’s disease.

As a result, therapeutic approaches that block inflammation and encourage the restoration of neuronal morphology and synaptic connections could have a wider application in the treatment of neurodegenerative diseases.

Future work by our team will aim to further develop treatment strategies that target inflammation and restore synaptic function in ALS sufferers.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

URL: https://www.psypost.org/als-breakthrough-ashwagandha-derived-drug-shows-promise-in-slowing-progression-of-amyotrophic-lateral-sclerosis/

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DATE: April 15, 2025 at 12:15AM
SOURCE: PSYPOST.ORG

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TITLE: Brain imaging method detects genetic markers of autism with over 90% accuracy

URL: https://www.psypost.org/brain-imaging-method-detects-genetic-markers-of-autism-with-over-90-accuracy/

A new study published in Science Advances introduces a powerful brain imaging technique that can detect autism-linked genetic variations with up to 95% accuracy. This approach, developed by researchers from multiple universities, including Johns Hopkins and Carnegie Mellon, analyzes structural brain images to identify specific genetic patterns associated with autism, potentially offering a way to detect the condition earlier and more objectively than current behavior-based methods.

Autism spectrum disorder is a neurodevelopmental condition characterized by differences in social communication, interaction, and the presence of restricted interests or repetitive behaviors. It is understood to result from a complex interplay of genetic predispositions and environmental influences. Currently, autism is diagnosed based on observing an individual’s behavior, a process that can take time and may not occur until certain developmental milestones are missed.

However, research increasingly points to a strong genetic component in autism. Understanding this genetic basis offers a potential pathway to better comprehend the condition’s origins, potentially leading to more personalized approaches and earlier support. This study explored a “genetics-first” avenue, focusing on specific genetic alterations known as copy number variations. These variations involve segments of a person’s genetic code being deleted or duplicated. Certain copy number variations are known to substantially increase the likelihood of developing autism.

The researchers aimed to see if unique patterns in brain structure, visible through imaging, could be directly linked to these specific genetic variations, providing a potential biological marker, sometimes called an endophenotype, that connects genes to observable traits.

To investigate this possibility, the research team, involving experts from Carnegie Mellon University, the University of California San Francisco, and the Johns Hopkins University School of Medicine, utilized a specialized computer modeling technique they developed called transport-based morphometry. This method stands apart from many other image analysis techniques because its mathematical underpinnings are based on modeling the movement and distribution of mass, akin to how substances move within biological tissues. It essentially quantifies the shape and form (morphometry) of the brain based on these modelled transport processes.

The researchers applied this technique to analyze brain scans from a group of 206 individuals sourced from the Simons Variation in Individuals Project. This cohort included 48 individuals with a deletion in a specific genetic region known as 16p11.2, 40 individuals with a duplication in the same region (both variations are strongly associated with increased autism risk), and 118 control participants without these specific genetic changes.

The control group was carefully selected to match the other participants in terms of age, sex, handedness, and non-verbal intelligence scores, and they were screened to exclude individuals with related neurological conditions or family histories of autism. High-resolution structural brain images (T1-weighted magnetic resonance imaging scans) were obtained for all participants using standardized procedures across different imaging sites.

The images underwent preprocessing steps to isolate brain tissue (gray matter and white matter), adjust for overall brain size differences, and normalize the data before the transport-based morphometry analysis was performed separately on gray matter and white matter distributions. The system was trained using machine learning principles to distinguish the brain structure patterns characteristic of the deletion group, the duplication group, and the control group.

The analysis revealed distinct patterns in brain structure associated with the 16p11.2 copy number variations. The transport-based morphometry system was highly effective at identifying which genetic group an individual belonged to based solely on their brain scan. When analyzing white matter structure, the system achieved an average accuracy of 94.6% in correctly classifying individuals into the deletion, duplication, or control group on previously unseen test data. Analyzing gray matter structure yielded an average accuracy of 88.5%. These results significantly outperformed classification attempts using only basic information like age, gender, or overall brain volume.

A key capability of the transport-based morphometry technique is that it is generative, meaning it allowed the researchers not just to classify the scans but also to visualize the specific brain structure differences driving the classifications. The analysis indicated that the 16p11.2 variations were associated with widespread, or diffuse, changes across the brain, rather than being confined to just one or two small areas.

There was a dose-dependent relationship observed: individuals with the 16p11.2 deletion tended to have larger overall brain volumes and relatively more gray matter tissue compared to controls, while those with the duplication tended to have smaller brain volumes and relatively less gray matter tissue. The visualization also revealed specific regional patterns.

For instance, areas involved in language processing, emotional regulation, visuospatial skills, and integrating information from multiple senses showed distinct patterns of relative tissue expansion or contraction depending on whether an individual had the deletion or duplication. Often, the effect was reciprocal, meaning a region might show relative expansion in the deletion group and relative contraction in the duplication group compared to controls. Some differences were also noted between the left and right sides of the brain.

Importantly, the researchers explored associations between these identified brain structure patterns and participants’ behavioral or cognitive characteristics. They found a strong association between one specific brain pattern (identified along what the researchers termed discriminant direction 1) and the presence of articulation disorders – difficulties producing speech sounds correctly.

This pattern was particularly prominent in individuals with the 16p11.2 deletion. Another distinct brain pattern (associated with discriminant direction 2) showed a significant association with participants’ intelligence quotient scores, explaining roughly 17-20% of the variation in full-scale, verbal, and nonverbal intelligence quotient measures across the groups. These findings suggest that the structural brain differences linked to the 16p11.2 copy number variations are related to observable functional outcomes.

The researchers acknowledge some limitations to their study. The participants were recruited through clinical genetics centers and patient networks, which might mean the sample doesn’t represent the full spectrum of individuals with these genetic variations, potentially missing those with milder or different presentations (ascertainment bias). The study focused on one specific genetic region, 16p11.2, and didn’t explore interactions with other genes.

While the study included individuals from childhood through adulthood, assuming relative stability of these brain patterns, further research focusing on early development is warranted. Also, while associations between brain structure patterns and behavioral measures like articulation or intelligence quotient were found, this type of study cannot establish a cause-and-effect relationship.

Future research could apply this transport-based morphometry approach to investigate other genetic variations linked to autism and related neurodevelopmental conditions. Larger studies involving more diverse populations and prospective studies tracking individuals over time are needed to validate these findings and explore their potential clinical utility for early detection, prognosis, or monitoring responses to interventions. Such work could significantly advance a genetics-first approach to understanding and supporting individuals with autism.

The study, “Discovering the gene-brain- behavior link in autism via generative machine learning,” was authored by Shinjini Kundu, Haris Sair, Elliott H. Sherr, Pratik Mukherjee, and Gustavo K. Rohde.

URL: https://www.psypost.org/brain-imaging-method-detects-genetic-markers-of-autism-with-over-90-accuracy/

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DATE: April 14, 2025 at 08:00PM
SOURCE: PSYPOST.ORG

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TITLE: Food insecurity is associated with cognitive disengagement in adolescents

URL: https://www.psypost.org/food-insecurity-is-associated-with-cognitive-disengagement-in-adolescents/

Adolescents who live in food-insecure households may be more likely to experience symptoms of cognitive disengagement, such as excessive daydreaming, confusion, and sluggish thinking, according to new research published in Research on Child and Adolescent Psychopathology. In contrast, the study found no clear relationship between food insecurity and symptoms of attention-deficit/hyperactivity disorder (ADHD), despite some previous studies suggesting a link. These findings suggest food insecurity may affect mental health in subtle and under-recognized ways, particularly through its relationship with cognitive disengagement syndrome, a condition closely related to but distinct from ADHD.

ADHD is one of the most common mental health conditions in childhood, typically involving high levels of inattention, impulsivity, and hyperactivity. Researchers have long studied how environmental stressors might contribute to these symptoms, and nutrition has emerged as a key area of interest. Food insecurity — defined as limited or uncertain access to adequate food — is one such stressor, affecting nearly 14 million households in the United States.

More than half of these households include children. Although earlier studies have linked food insecurity to behavioral and emotional problems in children, few have investigated how it relates to ADHD. Even fewer have looked at how food insecurity might relate to symptoms of cognitive disengagement syndrome, a condition marked by mental confusion, hypoactivity, and persistent daydreaming. This study aimed to address these gaps.

Researchers at Cincinnati Children’s Hospital Medical Center conducted the study with a group of 136 adolescents between the ages of 10 and 12. Participants and their caregivers were recruited through social media, community postings, and hospital networks. Roughly half of the participants had a formal diagnosis of ADHD. To be included in the study, children had to meet basic criteria including a minimum score on a vocabulary test and the ability to complete study tasks in English. Adolescents with more severe developmental or psychiatric disorders were excluded.

To measure food insecurity, parents answered two questions from a national screening tool assessing whether their household had worried about running out of food or had experienced food shortages over the past year. These responses were combined into a single score, with higher scores indicating more severe food insecurity. About 15 percent of the sample met the criteria for experiencing food insecurity, a rate nearly identical to national averages.

To measure symptoms of ADHD and cognitive disengagement syndrome, the researchers used standardized questionnaires filled out by three informants: parents, teachers, and the adolescents themselves. These surveys asked about specific behaviors related to attention problems, hyperactivity, and cognitive disengagement symptoms like frequent daydreaming, getting lost in thought, or seeming mentally confused. The team also accounted for factors like age, sex, race, ethnicity, psychiatric medication use, and family income.

Initial statistical analyses showed that food insecurity was significantly related to higher levels of cognitive disengagement symptoms across all three reporting sources: parents, teachers, and the adolescents themselves. These associations held up even after accounting for differences in age, sex, race, ethnicity, and medication use. However, once family income was included in the models, only the teacher- and adolescent-reported cognitive disengagement symptoms remained significantly associated with food insecurity. Parent-reported symptoms no longer showed a unique association.

Importantly, none of the ADHD symptom scores were significantly linked to food insecurity when all other factors were taken into account. This held true for both dimensions of ADHD: inattentiveness and hyperactivity/impulsivity. The only exception was a modest correlation between teacher-reported inattention and food insecurity, which did not hold up in the full statistical models. Similarly, food insecurity was not associated with symptoms of anxiety or depression reported by any informant.

These results suggest that food insecurity may be more strongly associated with internal, withdrawn forms of mental disengagement than with the outwardly visible behaviors typical of ADHD. One possibility is that food insecurity, through its effects on diet quality and stress, may impair cognitive functions like focus and attention in subtle ways that manifest as daydreaming or mental fog. Research shows that proper nutrition is important for brain development and cognitive functioning, and hunger or poor diet could contribute to the kinds of slow, internally focused thinking seen in cognitive disengagement syndrome.

Another explanation may involve how children psychologically respond to the stress of food insecurity. Adolescents are more aware of family hardships than younger children and may cope with distress by turning inward. Qualitative research suggests that some children respond to hunger by retreating into imagination, even creating imaginary friends or fantasizing about food to comfort themselves. Such coping strategies could increase the likelihood of behaviors that resemble the symptoms of cognitive disengagement.

Sleep could also be an important link. Studies in adults and young children have found that food insecurity can disrupt sleep, and other research has shown that poor sleep quality is associated with more pronounced symptoms of cognitive disengagement. In this view, food insecurity may impact adolescents’ mental functioning by interfering with sleep, which in turn contributes to greater cognitive sluggishness and disconnection from the external world.

Despite these insights, the study had several limitations. The research design was cross-sectional, meaning that all data were collected at one time. This limits the ability to determine whether food insecurity causes cognitive disengagement symptoms or whether another underlying factor explains both. The food insecurity measure was brief and based solely on caregiver reports, which may differ from how adolescents themselves perceive and are affected by food-related hardship. Moreover, the study sample came from relatively well-educated and higher-income families, with only a small proportion reporting food insecurity. This means the findings might not fully apply to more economically vulnerable populations, where the effects of food insecurity may be more pronounced.

Even so, the study makes an important contribution by identifying a potential relationship between food insecurity and a form of mental disengagement that has received little attention in the context of socioeconomic hardship. The findings suggest that cognitive disengagement syndrome may be especially sensitive to environmental stressors like food insecurity, even when accounting for family income and ADHD symptoms.

The study, “Examining ADHD and Cognitive Disengagement Syndrome Symptoms in Relation to Food Insecurity in Early Adolescents,” was authored by Cathrin D. Green, Andrew C. Martinez, and Stephen P. Becker.

URL: https://www.psypost.org/food-insecurity-is-associated-with-cognitive-disengagement-in-adolescents/

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DATE: April 14, 2025 at 06:00PM
SOURCE: PSYPOST.ORG

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TITLE: Scientists tested three wake-up routines. One type of bedroom lighting clearly stood out.

URL: https://www.psypost.org/scientists-tested-three-wake-up-routines-one-type-of-bedroom-lighting-clearly-stood-out/

Many people struggle with grogginess in the morning, a common experience known as sleep inertia. A new study published in Building and Environment suggests that a simple change to your bedroom lighting might help. Researchers from Osaka Metropolitan University found that exposing sleepers to a moderate amount of natural morning light—specifically starting 20 minutes before waking—led to improved alertness and reduced sleepiness compared to no light or longer light exposure starting at dawn. The findings suggest that carefully timed exposure to natural light could be a practical, energy-efficient way to enhance morning wakefulness.

The researchers were interested in finding better ways to help people transition from sleep to wakefulness, especially in modern environments where many sleep indoors with limited exposure to natural light. While previous research has focused heavily on artificial lighting—such as dawn simulation devices that mimic sunlight—this team wanted to explore whether natural light might offer more effective or more realistic benefits in everyday life. Given that people’s biological clocks evolved under natural lighting conditions, the team hypothesized that natural light, when appropriately timed and controlled, could improve the process of waking up.

To test this, the researchers designed a controlled laboratory experiment that mimicked an ordinary bedroom environment. The study was led by Xiaorui Wang, a graduate student in the School of Human Life and Ecology, and Professor Daisuke Matsushita. Nineteen university students aged 20 to 30 participated in the study. Each participant stayed in a specially outfitted sleep lab on three separate nights. The researchers used motorized curtains to expose participants to different types of natural light before waking.

The experiment tested three conditions. In one condition (called IA), participants were exposed to natural light for 20 minutes before their scheduled wake-up time. In another condition (IB), participants received natural light from dawn (when the sun was just below the horizon) until waking. In the third condition (CC), participants received no natural light before waking. The same participants experienced all three conditions, one each night, in a rotating order to reduce bias. This design allowed the researchers to compare the effects of the lighting conditions on the same individuals, which helps control for personal differences in sleep habits or physiology.

After waking, the researchers measured participants’ sleepiness, alertness, and fatigue using both self-report and biological tools. Subjective sleepiness was assessed using the Karolinska Sleepiness Scale, and alertness was measured with a reaction time test known as the Psychomotor Vigilance Test. For objective data, the researchers recorded brainwave activity with electroencephalograms (EEGs), and heart rate variability with wearable sensors to assess physiological fatigue.

The results showed that natural light exposure had a measurable effect on awakening quality. Both light exposure conditions (IA and IB) were associated with less subjective sleepiness than the no-light condition. However, the 20-minute pre-wake exposure (IA) was most effective overall. Participants in the IA condition had significantly lower objective and subjective sleepiness and responded faster in the alertness test compared to when they received no light. The IB condition, which exposed participants to light starting at dawn and potentially for a longer period, also helped reduce subjective sleepiness and improve alertness—but to a lesser extent than IA.

Interestingly, the longer duration of light exposure in the IB condition did not enhance wakefulness and in some cases may have been less helpful. The researchers suggested that early or prolonged light exposure might lead to more frequent awakenings during sleep, reducing total sleep time and affecting how refreshed participants felt. Indeed, participants in the IA condition slept slightly longer in the final 90 minutes before waking compared to those in the IB condition.

Fatigue levels, as measured through heart rate variability and self-report, did not show consistent differences across the three conditions. This suggests that while light can help people feel more awake and alert, it may not directly reduce feelings of physical tiredness or physiological fatigue in the short term. However, there was some indication that increased natural light exposure was associated with lower fatigue-related indicators, though these findings were not statistically strong enough to draw firm conclusions.

The study also explored how the amount and timing of natural light exposure influenced outcomes. Measurements of illuminance—the brightness of the light—confirmed that the IA and IB conditions both significantly increased light levels in the bedroom compared to the CC condition. However, there was no meaningful difference in brightness between IA and IB, highlighting that duration and timing, rather than brightness alone, may be more important for waking quality.

While the findings suggest practical benefits of morning natural light, the researchers noted several limitations. The participants were young adults with relatively consistent sleep patterns, and all had late bedtime habits typical of college students. These results may not generalize to older adults, people with sleep disorders, or individuals with different routines. In addition, while the controlled lab environment helped isolate the effects of light, it does not capture the full complexity of real-world sleep environments, which vary in terms of noise, temperature, and distractions.

The researchers also pointed out that the study did not include a washout period between conditions, which might have affected the results slightly. Although the crossover design helped minimize individual differences, some carryover effects from the previous night’s condition could not be completely ruled out.

Despite these limitations, the study makes an important contribution to understanding how natural light can support better sleep-wake transitions. By showing that just 20 minutes of light exposure before waking can improve how people feel and function in the morning, the research points to practical changes that could be implemented in everyday bedrooms using automated curtains or smart lighting systems.

Future research will need to explore how these findings apply across different age groups, housing types, and seasons. The team also hopes to examine how other properties of light, such as spectrum and direction, interact with timing and intensity to affect waking. These insights could help guide the development of more responsive and personalized lighting systems that support human health and well-being.

The ultimate goal is to help people wake up feeling better by working with, rather than against, the rhythms of the natural environment. By aligning light exposure with the body’s internal clock, simple changes to how morning light is managed in the bedroom may offer a low-cost, energy-efficient way to ease the daily transition from sleep to wakefulness. “In the future, we hope to control natural light in the sleep environment as it changes with the seasons and time of day, and to clarify how to introduce natural light that is suitable for a more comfortable awakening,” Matsushita said.

The study, “Natural light control to improve awakening quality,” was authored by Xiaorui Wang, Yangcheng Gu, Jihui Yuan, and Daisuke Matsushita.

URL: https://www.psypost.org/scientists-tested-three-wake-up-routines-one-type-of-bedroom-lighting-clearly-stood-out/

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