therapeutic action: synaptic plasticity enhancement

Reelin cells and sex-dependent synaptopathology in autism following postnatal immune activation

Researchers found that infections in newborn mice, particularly males, can disrupt brain development and lead to autism-like behaviors by damaging special brain cells called Reelin+ cells that help synapses mature properly. These damaged synapses failed to develop normally, resulting in social withdrawal and repetitive behaviors similar to autism in humans. Importantly, the study found that male mice were much more susceptible to this immune-triggered damage than female mice. The findings suggest that Reelin could be a promising therapeutic target for treating autism in children who experienced infections early in life.

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The progress of the microbe-gut-brain axis in sepsis-associated encephalopathy

Sepsis can cause brain dysfunction called sepsis-associated encephalopathy, leading to memory problems and confusion in about one-third to two-thirds of sepsis patients. The bacteria in your gut communicate with your brain through multiple pathways, and when sepsis disrupts this communication, it causes harmful inflammation in the brain. Treatments like probiotics and transplanting healthy gut bacteria from donors show promise in animal studies and early human trials for improving memory and cognitive function after sepsis.

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Reprogramming astrocytic NDRG2/NF-κB/C3 signaling restores the diabetes-associated cognitive dysfunction

This study found that regular exercise helps protect the brain of diabetic people from cognitive decline by boosting a protein called NDRG2 in astrocytes (brain support cells). The research shows that NDRG2 works by blocking harmful immune responses that damage synapses (connections between brain cells). In diabetic mice, exercise improved memory and learning ability while increasing NDRG2 levels, while blocking this protein reversed these benefits.

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