Although autism is a common neurodevelopmental disorder, the multiple factors behind its onset are still not fully understood. Animal models of idiopathic autism,[1] especially mice, are often used to help researchers understand the complicated mechanisms behind the disorder, with BTBR/J being the m
which connects the left and right hemispheres of the brain, was impaired in BTBR/J mice but not in BTBR/R mice.
Figure 3. a. AGM. B. Yolk sac: For BTBR/R autism model mice, genes with increased expression are indicated in pink and genes with decreased expression are in light blue. c-f. Comparison of gene expression levels in each cluster. In BTBR/R mice, there were changes in the expression of various genes that are indicative of endogenous retrovirus activation. Credit: Lin, CW., Ellegood, J., Tamada, K. et al.
Figure 5. In BTBR autism model mice , retrovirus activation makes copy number variations occur easily. In other words, they could be said to evolve at a faster speed than normal mice. The supporting evidence for this is that although BTBR/J and BTBR/R mice share a common ancestry, a mere 30 years of being raised in different environments has led not only to behavioral differences between the two species but also significant differences in brain structure . Credit: Lin, CW., Ellegood, J.
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