Giamanco and Matthews (2012) demonstrated in cell cultures that Acan and hyaluronan are sufficient for base PNN assembly in the absence of glia-derived components Hapln1 and tenascin-R (Giamanco and Matthews, 2012). In contrast, Suttkus et al. (2014) have shown that Tn-R and Hapln1 deficiency has a detrimental impact and results in the loss of neuroprotective characteristics of PNNs (Suttkus et al., 2014). However, on the mRNA level, our findings did not indicate significant differences in Hapln1 or Acan expression in aging or stroke. Here, ACAN is linked to stroke disorder.