For example, preclinical animal models having DNA mutations to mimic neurological diseases, such as schizophrenia, cognitive dysfunction, and autism spectrum diseases, were characterized by increasing oxidative stress indicated by high levels of 8-hydroxy-2’-deoxyguanosine immunoreactivity, a marker of DNA oxidative damage, as well as a low percentage of parvalbumin-reactive neurons and parvalbumin-reactive cells surrounded by perineuronal nets [133]. The gene discussed is PVALB; the disease is schizophrenia.