Immunohistochemical detection of 4-hydroxynonenal protein adducts in Parkinson disease

Immunohistochemical detection of 4-hydroxynonenal protein adducts in Parkinson disease

Vol. 93, pp. 2696–2701, April 1996 | ASAKO YORITAKA*, NOBUTAKA HATTORI†, KOJI UCHIDA‡, MASASHI TANAKA§, EARL R. STADTMAN¶, AND YOSHIKUNI MIZUNO*
This study investigates the presence of oxidative stress in nigral neurons of Parkinson's disease (PD) patients using immunohistochemical detection of 4-hydroxynonenal (HNE) protein adducts. HNE is a marker of oxidative stress-induced cellular damage. The researchers used polyclonal antibodies against HNE-modified proteins to label oxidative damage in control subjects (ages 18-99) and PD patients (ages 57-78). They found that 58% of nigral neurons in PD patients were positively stained for HNE-modified proteins, compared to only 9% in control subjects, with a statistically significant difference (Mann–Whitney U test; P < 0.01). In contrast, oculomotor neurons showed no or weak staining in both PD and control subjects. The results suggest that oxidative stress within nigral neurons may contribute to their death in PD. The study also highlights the potential of developing drugs to prevent lipid peroxidation as a neuroprotective treatment for PD.This study investigates the presence of oxidative stress in nigral neurons of Parkinson's disease (PD) patients using immunohistochemical detection of 4-hydroxynonenal (HNE) protein adducts. HNE is a marker of oxidative stress-induced cellular damage. The researchers used polyclonal antibodies against HNE-modified proteins to label oxidative damage in control subjects (ages 18-99) and PD patients (ages 57-78). They found that 58% of nigral neurons in PD patients were positively stained for HNE-modified proteins, compared to only 9% in control subjects, with a statistically significant difference (Mann–Whitney U test; P < 0.01). In contrast, oculomotor neurons showed no or weak staining in both PD and control subjects. The results suggest that oxidative stress within nigral neurons may contribute to their death in PD. The study also highlights the potential of developing drugs to prevent lipid peroxidation as a neuroprotective treatment for PD.
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