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SYNAPTIC PROTEIN ACCUMULATION IN C58/J MICE CORRELATES WITH TYPE I INTERFERON-MEDIATED CHANGES IN THE CX3CL1-CX3CR1 PATHWAY
Juan Duarteand 7 co-authors
Instituto de Investigaciones Biomédicas, UNAM
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-678
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Date TBA
Board: PS01-07AM-678
Event Information
Poster Board
PS01-07AM-678
Poster
View posterAbstract
Autism spectrum disorder (ASD) comprises a heterogeneous set of neurodevelopmental disorders which feature deficits in social and communicative skills as well as repetitive behaviors or restricted interest. Postmortem brain tissues from people with ASD show biological traits dissimilar to those of neurotypical individuals, such as an increased dendritic spine density and a reduced dendritic length and complexity. Microglia are the main phagocytes in the brain parenchyma and, among other relevant tasks, they have been shown to prune synaptic terminals during critical developmental periods; however, the implication of microglial synaptic pruning in ASD has been poorly investigated.
We evaluated the hippocampal content of synaptic proteins synaptophysin-1 and Homer1 in male mice of the inbred C58/J strain, a model of idiopathic autism. We found that both proteins accumulate across development when compared to C57BL/6J mice, reaching a significant difference in adulthood. We sought to correlate these changes with alterations in microglial phagocytic capacity, however, we only observed a slight decrease in the CA3 subregion of the hippocampus of C58/J mice. To delve into a mechanistic pathway to explain the increased content of synaptic proteins, we profiled the transcriptomics of the hippocampus of C58/J adult, male mice and we found that gene modules related to type I interferons are differentially regulated in our mouse model of autism. Moreover, changes in the type I interferon response seem to be correlated with the content of chemokine CX3CL1 and receptor CX3CR1, which suggests further alterations of this relevant neuron-microglia crosstalk pathway in the context of ASD.
We evaluated the hippocampal content of synaptic proteins synaptophysin-1 and Homer1 in male mice of the inbred C58/J strain, a model of idiopathic autism. We found that both proteins accumulate across development when compared to C57BL/6J mice, reaching a significant difference in adulthood. We sought to correlate these changes with alterations in microglial phagocytic capacity, however, we only observed a slight decrease in the CA3 subregion of the hippocampus of C58/J mice. To delve into a mechanistic pathway to explain the increased content of synaptic proteins, we profiled the transcriptomics of the hippocampus of C58/J adult, male mice and we found that gene modules related to type I interferons are differentially regulated in our mouse model of autism. Moreover, changes in the type I interferon response seem to be correlated with the content of chemokine CX3CL1 and receptor CX3CR1, which suggests further alterations of this relevant neuron-microglia crosstalk pathway in the context of ASD.
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