HAPLN2 and Parkinson disease: 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).