Moreover, studies revealed that Hapln2 overexpression contributes to neurodegeneration in Parkinson’s disease, Alzheimer’s disease as well as schizophrenia, most likely via dysfunction of the ubiquitin-proteasome pathway (UPP) (Lam et al., 2000; Bousman et al., 2010; Shen et al., 2013), which prevents accumulation of potentially toxic proteins within neurons and balances protein synthesis with degradation (for review see Wang et al., 2019). This evidence concerns the gene HAPLN2 and early-onset autosomal dominant Alzheimer disease.