Acetamiprid mediates cognitive dysfunction through the gut-brain axis: Synaptic damage and immune-mediated...

Area of Science:

• Neuroscience
• Toxicology
• Microbiology

Background:

• Neonicotinoid pesticides like acetamiprid are widely used.
• Exposure to acetamiprid may increase the risk of nervous system diseases and impact cognitive function.
• Clarification of acetamiprid's effects on cognition and underlying mechanisms is needed.

Purpose of the Study:

• To evaluate the effects of acetamiprid on cognitive dysfunction in a mouse model.
• To investigate the underlying mechanisms of acetamiprid-induced cognitive impairment, focusing on the gut-brain axis.

Main Methods:

• A mouse model was used, with acetamiprid administered via drinking water.
• Evaluated cognitive function, specifically spatial learning and memory.
• Assessed changes in hippocampal and synaptic structures, intestinal flora composition and diversity, and systemic immune responses.
• Fecal microbiota transplantation was performed to assess its restorative effects.

Main Results:

• Acetamiprid exposure damaged hippocampal and synaptic structures, leading to impaired spatial learning and memory in mice.
• Acetamiprid altered intestinal flora composition and diversity, inducing a systemic immune response along the gut-brain axis.
• Fecal microbiota transplantation restored gut microbiota homeostasis, reduced synaptic damage, and improved spatial learning and memory.
• Restoration of intestinal barrier function prevented harmful substance entry, reducing blood-brain barrier damage and gut-brain immune response.

Conclusions:

• Acetamiprid exposure causes cognitive dysfunction through damage to the gut-brain axis, including the gut microbiota, neurotransmitters, and immune factors.
• Fecal microbiota transplantation can mitigate acetamiprid-induced cognitive deficits by restoring gut homeostasis and protecting the gut-brain axis.
• This study highlights novel mechanisms linking acetamiprid exposure to cognitive impairment via gut-brain axis disruption.