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Synaptic loss and progression in mice infected with Angiostrongylus cantonensis in the early stage
Kai-Yuan Jhan1, Pi-Kai Chang2, Chien-Ju Cheng2
1Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, 333, Taiwan.
Background:
Angiostrongylus cantonensis is also known as rat lungworm. Infection with this parasite is a zoonosis that can cause eosinophilic meningitis and/or eosinophilic meningoencephalitis in humans and may lead to fatal outcomes in severe cases. In this study, we explored the mechanisms of the impairments in the cognitive functions of mice infected with A. cantonensis.
Methods:
In infected mice with different infective intensities at different timepoint postinfection, loss and recovery of cognitive functions such as learning and memory abilities were determined. Neuronal death and damage to synaptic structures were analyzed by Western blotting and IHC in infected mice with different infection intensities at different timepoint postinfection.
Results:
The results of behavioral tests, pathological examinations, and Golgi staining showed that nerve damage caused by infection in mice occurred earlier than pathological changes of the brain. BDNF was expressed on 14 day post-infection. Cleaved caspase-3 increased significantly in the late stage of infection. However, IHC on NeuN indicated that no significant changes in the number of neurons were found between the infected and uninfected groups.
Conclusions:
The synaptic loss caused by the infection of A. cantonensis provides a possible explanation for the impairment of cognitive functions in mice. The loss of cognitive functions may occur before severe immunological and pathological changes in the infected host.
Insights
Rat lungworm (Angiostrongylus cantonensis) infection impairs cognitive function in mice. Synaptic loss, not neuronal death, explains these cognitive deficits, which appear early in infection.
Area of Science:
- Neuroscience
- Parasitology
- Zoonotic diseases
Background:
- Angiostrongylus cantonensis, or rat lungworm, causes zoonotic parasitic infections.
- Infection can lead to eosinophilic meningitis and meningoencephalitis in humans, with severe cases being fatal.
- This study investigates the mechanisms behind cognitive function impairment in mice infected with A. cantonensis.
Purpose of the Study:
- To explore the mechanisms underlying cognitive function impairments in mice infected with Angiostrongylus cantonensis.
- To determine the relationship between infection intensity, time post-infection, and cognitive deficits.
- To analyze neuronal and synaptic changes associated with A. cantonensis infection.
Main Methods:
- Assessed learning and memory abilities in infected mice at various intensities and timepoints.
- Utilized Western blotting and immunohistochemistry (IHC) to analyze neuronal death and synaptic damage.
- Conducted pathological examinations and Golgi staining to evaluate nerve damage and brain pathology.
Main Results:
- Nerve damage occurred earlier than observable brain pathological changes.
- Brain-Derived Neurotrophic Factor (BDNF) expression was noted at 14 days post-infection.
- Cleaved caspase-3 significantly increased in late-stage infections, while neuron numbers remained unchanged.
Conclusions:
- Synaptic loss resulting from A. cantonensis infection is a likely cause of cognitive function impairment in mice.
- Cognitive function decline may precede significant immunological and pathological alterations in the host.
- Early synaptic damage offers a potential explanation for early cognitive deficits in rat lungworm infections.
