Decreased cognitive function of ALG13KO female mice may be related to the decreased plasticity of hippocampal neurons

Asparagine-linked glycosylation 13 (ALG13) is an X-linked gene that encodes a protein involved in the glycosylation of the N-terminus. ALG13 deficiency leads to ALG13-congenital disorders of glycosylation (ALG13-CDG), usually in females presenting with mental retardation and epilepsy. Cognitive function is an important function of the hippocampus, and forms the basis for learning, memory and social abilities. However, researchers have not yet investigated the effect of ALG13 on hippocampal cognitive function. In this study, the exploration, learning, memory and social abilities of ALG13 knockout (KO) female mice were decreased in behavioral experiments. Golgi staining demonstrated a decrease in the complexity of hippocampal neurons. Western blot and immunofluorescence staining of the synaptic plasticity factors postsynaptic density protein 95 (PSD95) and synaptophysin (SYP) displayed varying degrees of decline. In other words, the KO of ALG13 may have reduced the expression of PSD95 and SYP in the hippocampus of female mice. Moreover, it may have lowered the synaptic plasticity in various areas of the hippocampus, thus resulting in decreased dendrite length, complexity, and dendrite spine density, which affected the hippocampal function and reduced the cognitive function in female mice.