The brain cells meant to help us think and feel better may actually be making depression worse. Major depressive disorder (MDD) is a mental health condition that affects millions of people worldwide, causing a loss of interest in activities that were once enjoyable and leading to significant impairments in social and occupational functioning.

Research has shown that immune factors and cells, such as microglial cells, play a crucial role in driving neuroinflammation, which contributes to the development of MDD. However, a team of researchers led by Dr. Gaurav Singhal has shed light on the exact role of astrocytes, a specialized type of glial cell, in neural growth and development.

In their study, published in Neuroprotection, the research team conducted an in-depth review of literature to understand the role of astrocytes in neuroinflammation and MDD. They found that astrocytes are key to maintaining the structural integrity of synaptic junctions between neurons, promoting neurite growth and synapse formation.

However, changes in astrocyte morphology and function were associated with poor synaptic connectivity, contributing to the development of depressive symptoms. The researchers also discovered a critical mechanism involving activated microglia and astrocytes that resulted in sustained neuroinflammation in MDD.

The first step of this mechanism was the release of pro-inflammatory cytokines from activated microglia cells, which induced the secretion of additional inflammatory chemicals from astrocytes, amplifying neuroinflammation. Elaborating on the molecular crosstalk between microglia and astrocytes during MDD, Dr. Singhal explained that increased intracellular calcium levels within astrocytes can induce the release of adenosine triphosphate (ATP), which triggers a delayed calcium response in microglial cells.

Following multiple cycles of astrocyte-released ATP-based activation, microglial cells eventually undergo apoptosis or programmed cell death. Preclinical studies involving murine models showed that astrocytic lactate dehydrogenase A enzyme is important for maintaining neuronal excitability, and histone lactylation alters gene expression, contributing to astrocyte-driven neuroinflammation.

This study highlights the molecular mechanisms underlying astrocytic dysfunction, where astrocytes switch from a neuroprotective role to one that promotes neuroinflammation by increasing the expression and secretion of inflammatory cytokines. Understanding these mechanisms can aid in the development of therapeutic approaches to treat depression and other psychiatric disorders.

CRISPR technology has revolutionized genetics research, enabling scientists to edit genes with unprecedented precision. Recently, researchers at Kobe University developed a new method for modifying embryonic stem cells using CRISPR, creating a bank of 63 mouse embryonic stem cell lines containing the mutations most strongly associated with autism spectrum disorder (ASD). This breakthrough achievement has shed light on the hidden causes of ASD.

For decades, scientists have known that genetics play a significant role in the development of ASD. However, pinpointing the precise cause and mechanism remained elusive due to the lack of a standardized biological model for studying the effects of different mutations associated with the disorder. To address this challenge, Takumi Toru and his team at Kobe University embarked on a journey to create a reliable model by combining conventional manipulation techniques for mouse embryonic stem cells with CRISPR gene editing.

The new method proved highly efficient in making genetic variants of these cells, allowing the researchers to produce 63 mouse embryonic stem cell lines containing the mutations most strongly associated with ASD. These cell lines were further developed into various cell types and tissues, even generating adult mice with their genetic variations. The analysis of these cell lines revealed that autism-causing mutations often result in neurons being unable to eliminate misshapen proteins.

This finding is particularly interesting since the local production of proteins is a unique feature in neurons, and a lack of quality control of these proteins may be a causal factor of neuronal defects in ASD. Takumi expects that this achievement will be an invaluable resource for researchers studying autism and searching for drug targets. Moreover, the genetic variants studied are also implicated in other neuropsychiatric disorders such as schizophrenia and bipolar disorder, making this library potentially useful for studying these conditions as well.

This research was funded by various organizations, including the Japan Society for the Promotion of Science and the National Center of Neurology and Psychiatry. The study demonstrates the potential of CRISPR technology to reveal the hidden causes of complex diseases like ASD, paving the way for future discoveries and treatments.

A recent study has shed light on the benefits of getting extra sleep for teenagers, particularly on weekends. Researchers found that teens who got up to two more hours of sleep on weekends than on weekdays exhibited fewer symptoms of anxiety compared to those who didn’t catch up on their sleep.

The American Academy of Sleep Medicine recommends that teenagers aged 13 to 18 years old should aim for 8-10 hours of sleep each night. However, CDC data show that only 23% of high school students get sufficient sleep on average school nights. This can lead to problems such as depression and suicidal thoughts.

In contrast, the study found that moderate catch-up sleep – defined as less than two hours – was associated with lower anxiety symptoms. The researchers emphasized the importance of identifying the right amount of catch-up sleep for teens who restrict their sleep during the week.

Too little or too much sleep variability from weekday to weekend can contribute to symptoms like physical or mental fatigue and feelings of anxiety. Consistently getting sufficient sleep is crucial for overall health outcomes, including improved attention, behavior, learning, memory, emotional regulation, quality of life, and mental and physical health.

The study involved 1,877 adolescents with a mean age of 13.5 years. Sleep duration was estimated using Fitbit devices, while internalizing symptoms were assessed using the Child Behavior Checklist survey. The research abstract was published in an online supplement of the journal Sleep and will be presented at the SLEEP 2025 annual meeting.

The findings suggest that some weekend recovery sleep may be beneficial for teens, and it’s essential to find the perfect balance between weekday and weekend sleep to promote optimal health outcomes. By prioritizing sleep and establishing a consistent sleep schedule, teenagers can better manage anxiety and improve their overall well-being.