This reduction may be linked to CRS-induced decreases in either the expression or release of BDNF (Ju et al. 2022) or it could result from elevated glucocorticoid (GC) levels caused by CRS, which impair glucocorticoid receptor (GR)–tropomyosin receptor kinase B (TrkB) interactions, disrupting BDNF functions in the brain (Chiba et al. 2012). Here, NTRK2 is linked to congenital rubella syndrome.