Home-Based Brain Stimulation for Treating Depression

Post by Soumilee Chaudhuri

The takeaway

This study tested a non-invasive at-home device that uses a portable version of transcranial direct current stimulation (tDCS) for people with major depressive disorder (MDD). In a 10-week trial, adults with moderate depression who used the device showed more remarkable symptom improvement than those who did not. The device proved safe, effective, and easy to manage from home with remote support, suggesting it could be a valuable new option for treating depression.

What's the science?

Major depressive disorder (MDD) is a severe mental health condition characterized by persistent sadness, loss of interest in daily activities, and disturbances in sleep, appetite, and energy levels. It is typically treated with antidepressant medications and psychotherapy. However, about one-third of people with MDD do not fully respond to these treatments. Transcranial direct current stimulation (tDCS) is a non-invasive alternative that uses a mild electrical current to stimulate specific brain areas involved in mood regulation. This is typically done by placing electrodes on the scalp of one's head, with one electrode applying a small positive current and the other using an opposing current. This stimulative process can help improve brain function by adjusting the excitation level of these critical brain regions. Additionally, tDCS is portable and potentially more accessible, and previous studies have shown that it can improve depression symptoms, but most have required in-person visits. Therefore, this study aimed to test whether a 10-week at-home version of tDCS, with remote monitoring, could be an effective and practical solution for treating depression.

How did they do it?

The study enrolled one hundred seventy-four participants (120 women, 54 men) with a mean age of 37.63 years, all of whom met the criteria for MDD as defined by the Diagnostic and Statistical Manual of Mental Disorders. The participants were randomly assigned to one of two groups: the active tDCS treatment group and the placebo (sham) group, where the device did not work. Both groups had 87 people each, and the treatment lasted for 10 weeks. Most participants were on stable medication or therapy before joining the study.

What did they find?

Over 10 weeks, participants who received active tDCS demonstrated significant improvements in depression-related outcomes, including reductions in overall symptom severity and higher rates of response to treatment or remission, compared to those receiving the sham treatment. On average, scores on the Hamilton Depression Rating Scale (HDRS) in people in the active group went down by approximately 9 points, in contrast with a decrease of 7 points in the placebo group. The active treatment group had more participants (58%) whose symptoms improved by at least half, compared to just 38% in the placebo group. The active tDCS group also exhibited 2 to 3 times higher symptom improvement rates than the sham group. As the study included individuals with varying types of depression, including first-episode depression, recurrent depression, and treatment-resistant depression, these results indicated that tDCS was beneficial across all subgroups of MDD. Compared to prior studies in the field with shorter treatment protocols, the current study's 10-week treatment period showed better results in decreasing symptoms of depression. Additionally, while some participants experienced mild side effects, such as skin irritation at the stimulation site, these were rare and were not serious or long-term.

What's the impact?

This study aimed to evaluate the effectiveness of a 10-week home-based transcranial direct current stimulation (tDCS) as a treatment for Major Depressive Disorder (MDD) in adults. The results provide strong evidence that home-based tDCS is an effective and safe intervention for reducing depressive symptoms. This makes it a promising alternative for individuals with MDD, including those with treatment-resistant forms of the disorder or who might not have easy access to traditional in-person therapy. The findings of this study could significantly impact the field of depression treatment, offering a new, accessible, and effective option for those who do not respond to traditional therapies. 

Access the original scientific publication here

Sleep Loss Affects Developing Synapses in the Brain

Post by Baldomero B. Ramirez Cantu

The takeaway

Sleep is essential for brain health, especially during development. This study found that sleep deprivation disrupts key processes in brain maturation, with juvenile mice showing significantly higher vulnerability than adults. 

What's the science?

Sleep is crucial for lifelong cognitive health, particularly during brain development. Synapses in the brain undergo significant transformations during youth, shifting from high synapse formation in juveniles to stability in adulthood. Neurodevelopmental conditions like autism spectrum disorder (ASD) often show early-life sleep disturbances, making sleep loss during sensitive developmental periods an important focus. This week in PNAS, Gay et al. investigated the molecular and behavioral impact of sleep deprivation (SD) across developmental stages in mice, analyzing differences in how juvenile, adolescent, and adult brains respond to sleep loss.

How did they do it?

The study involved juvenile, adolescent, and adult mice, which underwent a 4 or 6 hour sleep deprivation session at the start of the light phase. Researchers assessed memory using a novel object recognition (NOR) task, where only juveniles showed cognitive impairment after SD, indicating that adults were more resilient to the deprivation.

For molecular analysis, the team collected forebrain synaptic proteins from each age group under sleep, wake, and SD conditions, using mass spectrometry to quantify thousands of proteins and phosphoproteins. Statistical analysis revealed that SD in juveniles led to broad changes in synapse-related proteins involved in growth and plasticity, whereas adolescents and adults had fewer alterations. Further analysis highlighted that the SD-sensitive proteins in juveniles strongly overlapped with autism risk genes, suggesting that early sleep disruption may interact with genetic vulnerabilities during brain development.

What did they find?

Juvenile mice exposed to SD showed cognitive impairments in memory tasks, whereas adults remained largely unaffected. At the synaptic level, SD was associated with protein and phosphorylation changes in juvenile mice, including upregulation of proteins linked to synaptogenesis and neural activity. These responses overlapped with ASD risk genes, suggesting a potential interaction between developmental sleep loss and ASD susceptibility.

What's the impact?

The findings underscore the role of sleep in neural development and the potential risks posed by sleep loss in youth, with implications for neurodevelopmental disorders like ASD. These insights could guide public health recommendations for pediatric sleep hygiene and inform approaches to ASD prevention and treatment by emphasizing sleep as a crucial factor in brain health.

Access the original scientific publication here. 

A Brain Pathway That Regulates Eating

Post by Rebecca Hill

The takeaway

Overeating leading to obesity can be caused by mutations in brain signaling molecules. One neural circuit in the hypothalamus regulates this overeating behavior.

What's the science?

The brain regulates eating by taking signals from our body about our internal state and processing them into behavioral responses such as eating. Brain-derived neurotrophic factor (BDNF) is a signaling molecule in the brain expressed in the hypothalamus, the brain area responsible for regulating hunger, and other bodily functions. This week in Nature, Kosse and colleagues studied which specific pathway in the brain controls our eating and jaw movements.

How did they do it?

Using optogenetics, a technique that uses light to control the activity of certain cells in the brain, the authors activated or inhibited the activity of BDNF cells in the hypothalamus of mice. The authors fasted mice before the experiment to make sure the mice would be hungry enough to eat. They then measured how much food mice ate to determine how this affected the feeding behavior controlled by these cells. The authors also specifically examined this effect in obese mice to determine if feeding behavior changed after BDNF cell activity was inhibited.

What did they find?

When the authors activated BDNF cells in the hypothalamus, fasted mice did not increase feeding behavior. This means that even though mice had a drive to eat, BDNF cell activity prevented them from feeding. When the authors inhibited BDNF cells in the hypothalamus, mice ate more due to more jaw movements triggered by this neural pathway. When BDNF cell activity was inhibited in obese mice, mice continued feeding behavior despite not needing to eat. This means that the BDNF cell pathway in the hypothalamus processes input about the energy state of an animal and outputs feeding behavior from it. 

What's the impact?

This study is the first to find a neural pathway linked to feeding behavior in which its breakdown leads to obesity. Obesity is a widespread issue, with many struggling to overcome eating behaviors. With the information found in this study, we may be able to develop more effective treatments for overeating behaviors.

Access the original scientific publication here